Bacteria on the skin: Our invisible companions influence how quickly wounds heel

A new study suggests microbes living on our skin influence how quickly wounds heal. The findings could lead to new treatments for chronic wounds, which affect 1 in 20 elderly people.We spend our lives covered head-to-toe in a thin veneer of bacteria. But despite a growing appreciation for the valuable roles our resident microbes play in the digestive tract, little is known about the bacteria that reside in and on our skin. A new study suggests the interplay between our cells and these skin-dwelling microbes could influence how wounds heal.”This study gives us a much better understanding of the types of bacterial species that are found in skin wounds, how our cells might respond to the bacteria and how that interaction can affect healing,” said Matthew Hardman, Ph.D., a senior research fellow at The University of Manchester Healing Foundation Centre who led the project. “It’s our hope that these insights could help lead to better treatments to promote wound healing that are based on sound biology.”Chronic wounds — cuts or lesions that just never seem to heal — are a significant health problem, particularly among elderly people. An estimated 1 in 20 elderly people live with a chronic wound, which often results from diabetes, poor blood circulation or being confined to bed or a wheelchair.”These wounds can literally persist for years, and we simply have no good treatments to help a chronic wound heal,” said Hardman, who added that doctors currently have no reliable way to tell whether a wound will heal or persist. “There’s a definite need for better ways to both predict how a wound is going to heal and develop new treatments to promote healing.”The trillions of bacteria that live on and in our bodies have attracted a great deal of scientific interest in recent years. Findings from studies of microbes in the gut have made it clear that although some bacteria cause disease, many other bacteria are highly beneficial for our health.In their recent study, Hardman and his colleagues compared the skin bacteria from people with chronic wounds that did or did not heal. The results showed markedly different bacterial communities, suggesting there may be a bacterial “signature” of a wound that refuses to heal.”Our data clearly support the idea that one could swab a wound, profile the bacteria that are there and then be able to tell whether the wound is likely to heal quickly or persist, which could impact treatment decisions,” said Hardman.The team also conducted a series of studies in mice to shed light on the reasons why some wounds heal while others do not. They found that mice lacking a single gene had a different array of skin microbiota — including more harmful bacteria — and healed much more slowly than mice with a normal copy of the gene.The gene, which has been linked to Chrohn’s disease, is known to help cells recognize and respond to bacteria. …

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Beauty FAQ: Common beauty questions answered

Learn more about Herbalife – Follow @Herbalife on Twitter- Like Herbalife on Facebook- What is Herbalife? More fitness advice – Watch ‘Fit Tips’ Videos on YouTube- Straightforward exercise advice- Get fit = be happy. Positivity advice Nutrition advice for you – Watch ‘Healthy Living’ on YouTube- Dieting advice you might like- Interesting weight loss articles Copyright © 2013 Herbalife International of America, Inc.

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It’s alive! Bacteria-filled liquid crystals could improve biosensing

Plop living, swimming bacteria into a novel water-based, nontoxic liquid crystal and a new physics takes over. The dynamic interaction of the bacteria with the liquid crystal creates a novel form of soft matter: living liquid crystal.The new type of active material, which holds promise for improving the early detection of diseases, was developed by a research collaboration based at Ohio’s Kent State University and Illinois’ Argonne National Laboratory. The team will present their work at the 58th annual Biophysical Society Meeting, held in San Francisco, Feb.15-19.As a biomechanical hybrid, living liquid crystal moves and reshapes itself in response to external stimuli. It also stores energy just as living organisms do to drive its internal motion. And it possesses highly desirable optical properties. In a living liquid crystal system, with the aid of a simple polarizing microscope, you can see with unusual clarity the wake-like trail stimulated by the rotation of bacterial flagella just 24-nanometers thick, about 1/4000th the thickness of an average human hair.You can also control and guide active movements of the bacteria by manipulating variables such as oxygen availability, temperature or surface alignment, thus introducing a new design concept for creating microfluidic biological sensors. Living liquid crystal provides a medium to amplify tiny reactions that occur at the micro- and nano-scales — where molecules and viruses interact — and to also easily optically detect and analyze these reactions. That suits living liquid crystal to making sensing devices that monitor biological processes such as cancer growth, or infection. Such microfluidic technology is of increasing importance to biomedical sensing as a means of detecting disease in its earliest stages when it is most treatable, and most cost-effectively managed.”As far as we know, these things have never been done systematically as we did before in experimental physics,” explained Shuang Zhou, a Ph.D. candidate at Ohio’s Kent State University. …

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Body’s ‘safety procedure’ could explain autoimmune disease

Sep. 5, 2013 — Monash University researchers have found an important safety mechanism in the immune system that may malfunction in people with autoimmune diseases, such as Multiple Sclerosis, potentially paving the way for innovative treatments.Published today in Immunity, the research, led by Head of the Monash Department of Immunology Professor Fabienne Mackay, described for the first time how the body manages marginal zone (MZ) B cells, which form a general first line of attack against germs, but are potentially harmful.MZ B cells are integral to our defenses as they rapidly produce polyreactive antibodies that are capable of destroying a variety of pathogens. This first response gives the body time to put in place an immune reaction specific to the invading microbe.However, MZ B cells have the potential to turn against the body. Some are capable of producing antibodies which attack healthy, rather than foreign, cells — known as an autoimmune response. Bacteria trigger MZ B cells irrespective of whether these cells are dangerous or benign, effectively placing anyone with a bacterial infection at risk of developing an autoimmune disease.Professor Mackay’s team has discovered the mechanism that regulates this response, ensuring that that the majority of infections do not result in the body attacking its own tissue.”We found that while MZ B cells are rapidly activated, they have a very short life span. In fact, the very machinery which triggers a response leads to MZ B cells dying within 24 hours,” Professor Mackay said.”This means that in a healthy person, the potentially harmful immune cells are not active for long enough to cause in tissue damage. We now need to look at whether a malfunction in this safety feature is leading to some autoimmune diseases.”When MZ B cells are activated by bacteria, they express greater amounts of a protein known as TACI. When TACI binds to another protein as part of the immune response, this triggers the activation of the ‘death machinery’ inside MZ B cells. The detection of a pathogen sets of a chain reaction that both activates and then destroys MZ B cells.Professor Mackay said this was an entirely new way of looking at the immune system.”The research suggests that through evolution the immune system has not solely been vulnerable to infections but has learned to take advantage of pathogens to develop its own internal safety processes,” Professor Mackay said.”This says something important about our environment — pathogens are not always the enemy. They can also work hand in hand with our immune system to protect us against some immune diseases.”

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TB and Parkinson’s disease linked by unique protein

Sep. 4, 2013 — A protein at the center of Parkinson’s disease research now also has been found to play a key role in causing the destruction of bacteria that cause tuberculosis, according to scientists led by UC San Francisco microbiologist and tuberculosis expert Jeffery Cox, PhD.The protein, named Parkin, already is the focus of intense investigation in Parkinson’s disease, in which its malfunction is associated with a loss of nerve cells. Cox and colleagues now report that Parkin also acts on tuberculosis, triggering destruction of the bacteria by immune cells known as macrophages. Results appear online today (September 4, 2013) in the journal Nature.The finding suggests that disease-fighting strategies already under investigation in pre-clinical studies for Parkinson’s disease might also prove useful in fighting tuberculosis, according to Cox. Cox is investigating ways to ramp up Parkin activity in mice infected with tuberculosis using a strategy similar to one being explored by his UCSF colleague Kevan Shokat, PhD, as a way to ward off neurodegeneration in Parkinson’s disease.Globally, tuberculosis kills 1.4 million people each year, spreading from person to person through the air. Parkinson’s disease, the most common neurodegenerative movement disorder, also affects millions of mostly elderly people worldwide.Cox homed in on the enzyme Parkin as a common element in Parkinson’s and tuberculosis through his investigations of how macrophages engulf and destroy bacteria. In a sense the macrophage — which translates from Greek as “big eater” — gobbles down foreign bacteria, through a process scientists call xenophagy.Mycobacterium tuberculosis, along with a few other types of bacteria, including Salmonella and leprosy-causing Mycobacterium leprae, are different from other kinds of bacteria in that, like viruses, they need to get inside cells to mount a successful infection.The battle between macrophage and mycobacterium can be especially intense. M. tuberculosis invades the macrophage, but then becomes engulfed in a sac within the macrophage that is pinched off from the cell’s outer membrane. The bacteria often escape this intracellular jail by secreting a protein that degrades the sac, only to be targeted yet again by molecular chains made from a protein called ubiquitin. …

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Stomach bacteria switch off human immune defenses to cause disease

Sep. 2, 2013 — Helicobacter pylori is a bacterium that establishes a life-long stomach infection in humans, which in some cases can lead to duodenal ulcers or stomach cancer. New research, presented at this week’s Society for General Microbiology Autumn Conference, gives us a clearer understanding of how these bacteria can manipulate the human immune system to survive in the mucosal lining of the stomach.Share This:Researchers from the University of Nottingham have shown that H. pylori is able to supress the body’s normal production of ‘human beta defensin 1’ (hβD1), an antimicrobial factor present in the stomach lining that helps prevent bacterial infection. By collecting stomach tissue biopsies from 54 patients at the Queens Medical Centre, Nottingham, the team showed that patients infected with H. pylori had ten times less hβD1 than uninfected patients. Those with the lowest amount of hβD1 had the most bacteria present in their stomach lining.The most damaging strains of H. pylori make a molecular syringe called the cagT4SS, through which bacterial products are injected into cells of the stomach lining. In vitro work using human gastric epithelial cell lines showed that this activates chemical pathways to suppress hβD1 production. These activated pathways are also involved in the stimulation of an inflammatory response, meaning that these H. …

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Mycobacterium tuberculosis: Our African follower for over 70,000 years

Sep. 1, 2013 — Tuberculosis (TB) remains one of deadliest infectious diseases of humans, killing 50% of individuals when left untreated. Even today, TB causes 1-2 million deaths every year mainly in developing countries. Multidrug-resistance is a growing threat in the fight against the disease.An international group of researchers led by Sebastien Gagneux from the Swiss Tropical and Public Health Institute (Swiss TPH) has now identified the origin in time and space of the disease. Using whole-genome sequencing of 259 Mycobacterium tuberculosis strains collected from different parts of the world, they determined the genetic pedigree of the deadly bugs. This genome comparison to be published September 1st in the journal Nature Genetics indicates that TB mycobacteria originated at least 70,000 years ago in Africa.Stunningly close relationship between humans and M. tuberculosisThe researchers compared the genetic evolutionary trees of mycobacteria and humans side-by-side. And to the researcher’s surprise, the phylogenetic trees of humans and the TB bacteria showed a very close match. “The evolutionary path of humans and the TB bacteria shows striking similarities,” says Sebastien Gagneux.This strongly points to a close relationship between the two, lasting tens of thousands of years. Humans and TB bacteria not only have emerged in the same region of the world, but have also migrated out of Africa together and expanded all over the globe.The migratory behaviour of modern humans accompanied with changes in lifestyle has created favourable conditions for an increasingly deadly disease to evolve. …

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A home for the microbiome: Biologists identify how beneficial bacteria reside and thrive in gastrointestinal tract

Aug. 19, 2013 — The human body is full of tiny microorganisms — hundreds to thousands of species of bacteria collectively called the microbiome, which are believed to contribute to a healthy existence. The gastrointestinal (GI) tract — and the colon in particular — is home to the largest concentration and highest diversity of bacterial species. But how do these organisms persist and thrive in a system that is constantly in flux due to foods and fluids moving through it? A team led by California Institute of Technology (Caltech) biologist Sarkis Mazmanian believes it has found the answer, at least in one common group of bacteria: a set of genes that promotes stable microbial colonization of the gut.A study describing the researchers’ findings was published as an advance online publication of the journal Nature on August 18.”By understanding how these microbes colonize, we may someday be able to devise ways to correct for abnormal changes in bacterial communities — changes that are thought to be connected to disorders like obesity, inflammatory bowel disease and autism,” says Mazmanian, a professor of biology at Caltech whose work explores the link between human gut bacteria and health.The researchers began their study by running a series of experiments to introduce a genus of microbes called Bacteriodes to sterile, or germ-free, mice. Bacteriodes, a group of bacteria that has several dozen species, was chosen because it is one of the most abundant genuses in the human microbiome, can be cultured in the lab (unlike most gut bacteria), and can be genetically modified to introduce specific mutations.”Bacteriodes are the only genus in the microbiome that fit these three criteria,” Mazmanian says.Lead author S. Melanie Lee (PhD ’13), who was an MD/PhD student in Mazmanian’s lab at the time of the research, first added a few different species of the bacteria to one mouse to see if they would compete with each other to colonize the gut. They appeared to peacefully coexist. Then, Lee colonized a mouse with one particular species, Bacteroides fragilis, and inoculated the mouse with the same exact species, to see if they would co-colonize the same host. To the researchers’ surprise, the newly introduced bacteria could not maintain residence in the mouse’s gut, despite the fact that the animal was already populated by the identical species.”We know that this environment can house hundreds of species, so why the competition within the same species?” Lee says. …

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Bee venom: Biophysicists zoom in on pore-forming toxin

Aug. 14, 2013 — A new study by Rice University biophysicists offers the most comprehensive picture yet of the molecular-level action of melittin, the principal toxin in bee venom. The research could aid in the development of new drugs that use a similar mechanism as melittin’s to attack cancer and bacteria.The study appears this week in the Proceedings of the National Academy of Sciences.Melittin does its damage by penetrating the outer walls of cells and opening pores that allow the contents of the cell to escape. At low concentrations, melittin forms transient pores. At higher concentrations, the pores become stable and remain open, and at still higher doses, the cell membrane dissolves altogether.”This strategy of opening holes in the cell membrane is employed by a great number of host-defense antimicrobial peptides, many of which have been discovered over the past 30 years,” said Rice’s Huey Huang, the lead investigator of the study. “People are interested in using these peptides to fight cancer and other diseases, in part because organisms cannot change the makeup of their membrane, so it would be very difficult for them to develop resistance to such drugs.”But the clinical use of the compounds is complicated by the lack of consensus about how the peptides work. For example, scientists have struggled to explain how different concentrations of melittin could yield such dramatically different effects, said Huang, Rice’s Sam and Helen Worden Professor of Physics and Astronomy.In the new study, Huang and Rice graduate student Tzu-Lin Sun partnered with colleagues Ming-Tao Lee at the National Synchrotron Radiation Research Center (NSRRC) in Hsinchu, Taiwan, and with Wei-Chin Hung at the Republic of China Military Academy in Fengshan, Taiwan. The team used a combination of experiments to zero in on the molecular activity of melittin at the “minimal inhibitory concentration” (MIC), the lowest concentration that’s been shown to slow the growth of target cell populations. The MIC for melittin is a dose that results in stable pore formation, rather than complete dissolution of the membrane.”We want to understand how pore formation works at this critical concentration, including both at the molecular scale — what are the shapes of the pores themselves — and the cellular scale — how are the pores arranged and distributed over the surface of the membrane,” Huang said.To find the answer, the team correlated the results of two different types of experiments. In the first type, which was conducted at Rice, the team used confocal microscopy to film “giant unilamellar vesicles” (GUVs), synthetic membrane-enclosed structures that are about the same size as a living cell. …

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Bee venom: Biophysicists zoom in on pore-forming toxin

Aug. 14, 2013 — A new study by Rice University biophysicists offers the most comprehensive picture yet of the molecular-level action of melittin, the principal toxin in bee venom. The research could aid in the development of new drugs that use a similar mechanism as melittin’s to attack cancer and bacteria.The study appears this week in the Proceedings of the National Academy of Sciences.Melittin does its damage by penetrating the outer walls of cells and opening pores that allow the contents of the cell to escape. At low concentrations, melittin forms transient pores. At higher concentrations, the pores become stable and remain open, and at still higher doses, the cell membrane dissolves altogether.”This strategy of opening holes in the cell membrane is employed by a great number of host-defense antimicrobial peptides, many of which have been discovered over the past 30 years,” said Rice’s Huey Huang, the lead investigator of the study. “People are interested in using these peptides to fight cancer and other diseases, in part because organisms cannot change the makeup of their membrane, so it would be very difficult for them to develop resistance to such drugs.”But the clinical use of the compounds is complicated by the lack of consensus about how the peptides work. For example, scientists have struggled to explain how different concentrations of melittin could yield such dramatically different effects, said Huang, Rice’s Sam and Helen Worden Professor of Physics and Astronomy.In the new study, Huang and Rice graduate student Tzu-Lin Sun partnered with colleagues Ming-Tao Lee at the National Synchrotron Radiation Research Center (NSRRC) in Hsinchu, Taiwan, and with Wei-Chin Hung at the Republic of China Military Academy in Fengshan, Taiwan. The team used a combination of experiments to zero in on the molecular activity of melittin at the “minimal inhibitory concentration” (MIC), the lowest concentration that’s been shown to slow the growth of target cell populations. The MIC for melittin is a dose that results in stable pore formation, rather than complete dissolution of the membrane.”We want to understand how pore formation works at this critical concentration, including both at the molecular scale — what are the shapes of the pores themselves — and the cellular scale — how are the pores arranged and distributed over the surface of the membrane,” Huang said.To find the answer, the team correlated the results of two different types of experiments. In the first type, which was conducted at Rice, the team used confocal microscopy to film “giant unilamellar vesicles” (GUVs), synthetic membrane-enclosed structures that are about the same size as a living cell. …

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Stressed bacteria stop growing: Mechanism discovered

Aug. 15, 2013 — Whether a man, a mouse or a microbe, stress is bad for you. Experiments in bacteria by molecular biologists in Peter Chien’s lab at the University of Massachusetts Amherst, with others at MIT, have uncovered the mechanism that translates stress, such as exposure to extreme temperature, into blocked cell growth.It turns out that stressful conditions cause some proteins to be literally bent out of shape, or misfolded, and they stop working, says Chien. “You might think of this as microbial temper tantrums. Bacteria deal with stress by destroying proteins. Specifically, we’ve shown that certain kinds of bacteria respond to high temperatures by destroying proteins needed for DNA replication. Therefore, they stop growing. The signal for this destruction turned out to be the buildup of proteins that were misfolded because of the stress.”Under favorable conditions, cells strive to grow, which means initiating DNA replication. But in stressful conditions, cells must prevent the initiation of replication and instead shift their priorities to protective functions.As Chien explains, all cells including bacteria contain a huge variety of proteins, molecules that help cells do all the chemical reactions needed for life. Shape determines what kind of functions each protein can perform. …

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Evolution of hyperswarming bacteria could develop anti-biofilm therapies

Aug. 15, 2013 — The evolution of hyperswarming, pathogenic bacteria might sound like the plot of a horror film, but such bugs really have repeatedly evolved in a lab, and the good news is that they should be less of a problem to us than their less mobile kin. That’s because those hyperswarmers, adorned with multiple whipping flagella, are also much worse at sticking together on surfaces in hard-to-treat biofilms. They might even help us figure out a way to develop anti-biofilm therapies for use in people with cystic fibrosis or other conditions, say researchers who report their findings in Cell Reports, a Cell Press publication, on August 15th.Share This:The findings are also a textbook example of real-time experimental evolution. What’s more, says Joao Xavier of Memorial Sloan Kettering Cancer Center, they are a “unique example of strikingly parallel molecular evolution.”In other words, the evolution that he and his team witnessed was repeatable, all the way down to the molecular level.The researchers didn’t set out with the goal to evolve hyperswarmers, but they did passage Pseudomonas aeruginosa on special plates over a period of days. On those plates, bacteria that could spread out had an advantage in harvesting nutrients from the surface, and within a matter of days, some of those bacteria started hyperswarming.Investigation of the bacteria showed that P. aeruginosa gained its hyperswarming ability through a single point mutation in a flagellar synthesis regulator (FleN). As a result, the bacteria, which usually have one single flagellum, were locked into a multi-flagellated state. They became better at moving around to cover a surface, but much worse at forming densely packed, surface-attached biofilm communities. All told, the researchers saw this new ability independently arise 20 times.”The fact that the molecular adaptations were the same in independent lineages suggests evolution may be, to some extent, predictable,” says Xavier.The findings may be very important because biofilms are a major problem in clinical settings. …

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New gene repair technique promises advances in regenerative medicine

Aug. 12, 2013 — Using human pluripotent stem cells and DNA-cutting protein from meningitis bacteria, researchers from the Morgridge Institute for Research and Northwestern University have created an efficient way to target and repair defective genes.Writing August 12 in the Proceedings of the National Academy of Sciences, the team reports that the novel technique is much simpler than previous methods and establishes the groundwork for major advances in regenerative medicine, drug screening and biomedical research.Zhonggang Hou of the Morgridge Institute’s regenerative biology team and Yan Zhang of Northwestern University served as first authors on the study; James Thomson, director of regenerative biology at the Morgridge Institute, and Erik Sontheimer, professor of molecular biosciences at Northwestern University, served as principal investigators.”With this system, there is the potential to repair any genetic defect, including those responsible for some forms of breast cancer, Parkinson’s and other diseases,” Hou said. “The fact that it can be applied to human pluripotent stem cells opens the door for meaningful therapeutic applications.”Zhang said the Northwestern University team focused on Neisseria meningitidis bacteria because it is a good source of the Cas9 protein needed for precisely cleaving damaged sections of DNA.”We are able to guide this protein with different types of small RNA molecules, allowing us to carefully remove, replace or correct problem genes,” Zhang said. “This represents a step forward from other recent technologies built upon proteins such as zinc finger nucleases and TALENs.”These previous gene correction methods required engineered proteins to help with the cutting. Hou said scientists can synthesize RNA for the new process in as little as one to three days — compared with the weeks or months needed to engineer suitable proteins.Thomson, who also serves as the James Kress Professor of Embryonic Stem Cell Biology at the University of Wisconsin-Madison, a John D. MacArthur professor at UW-Madison’s School of Medicine and Public Health and a professor in the department of molecular, cellular and developmental biology at the University of California, Santa Barbara, says the discovery holds many practical applications.”Human pluripotent stem cells can proliferate indefinitely and they give rise to virtually all human cell types, making them invaluable for regenerative medicine, drug screening and biomedical research,” Thomson says. “Our collaboration with the Northwestern team has taken us further toward realizing the full potential of these cells because we can now manipulate their genomes in a precise, efficient manner.”Sontheimer, who serves as the Soretta and Henry Shapiro Research Professor of Molecular Biology with Northwestern’s department of molecular biosciences, Center for Genetic Medicine and the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, says the team’s results also offer hopeful signs about the safety of the technique.”A major concern with previous methods involved inadvertent or off-target cleaving, raising issues about the potential impact in regenerative medicine applications,” he said. “Beyond overcoming the safety obstacles, the system’s ease of use will make what was once considered a difficult project into a routine laboratory technique, catalyzing future research.”Also contributing to the study, which was supported by funding from sources including the National Institutes of Health, the Wynn Foundation and the Morgridge Institute for Research, were Nicholas Propson, Sara Howden and Li-Fang Chu from the Morgridge Institute for Research.

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Narrower range of helpful bacteria in guts of C-section infants

Aug. 7, 2013 — Decreased gut microbiota diversity delayed Bacteroidetes colonisation and reduced Th1 responses in infants delivered by Caesarean section.The range of helpful bacteria in the guts of infants delivered by caesarean section, during their first two years of life, is narrower than that of infants delivered vaginally, indicates a small study published online in the journal Gut.This has implications for the development of the immune system, say the researchers, particularly as the C-section infants had lower levels of the major group of gut bacteria associated with good gut health, Bacteroidetes phylum, as well as chemicals that help curb allergic responses.The researchers assessed the patterns of bacterial colonisation of the guts of 24 infants, nine of whom had been born by caesarean section one week, and then again at one, three, six, 12 and 24 months after birth.They also took blood samples at six, 12 and 24 months to test for levels of immune system chemicals known as Th1 and 2 associated chemokines. Excess Th2 chemokines have been implicated in the development of allergies, which Th1 responses can counteract, say the authors.The results showed that babies delivered by caesarean section, and who therefore did not pass down the mother’s birth canal, either lacked or acquired late one of the major groups of gut bacteria, the Bacteroidetes, compared with the babies born vaginally.In some C-section infants acquisition of Bacteroidetes did not occur until a year after birth. The total range of bacteria among those born by C-section was also lower than that of their vaginally delivered peers.The differences in bacterial colonisation between the two groups of infants were not down to their mums having been given antibiotics during C-section or after the procedure to prevent infection: the levels and range of bacteria sampled from both sets of mums were similar, the analysis showed.Bacteria are important for priming the immune system to respond appropriately to triggers, and not overreact as is the case in allergies, diabetes, and inflammatory bowel disease, say the authors.This includes the development of immune system T cells and the correct balance between their chemical messengers, Th1 and Th2.The C-section infants had lower circulating levels of Th1 chemical messengers in their blood, indicating an imbalance between Th1 and Th2. “Failure of Th2 silencing during maturation of the immune system may underlie development of Th2-mediated allergic disease,” write the authors.They point out that previous research has indicated that Bacteroides fragilis, one of the many Bacteroidetes, strongly influences the immune system, which ultimately enhances T cell activity and the Th1-Th2 balance.”Thus, the lower abundance of Bacteroides among the C-section infants may be a contributing factor to the observed differences in the Th1-associated chemokines,” they write.

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From harmless colonizers to virulent pathogens: Microbiologists identify what triggers disease

Aug. 6, 2013 — The bacteria Streptococcus pneumoniae harmlessly colonizes the mucous linings of throats and noses in most people, only becoming virulent when they leave those comfortable surroundings and enter the middle ears, lungs or bloodstream. Now, in research published in July in mBio, University at Buffalo researchers reveal how that happens.”We were asking, what is the mechanism behind what makes us sick?” explains Anders P. Hakansson, PhD, assistant professor of microbiology and immunology in the UB School of Medicine and Biomedical Sciences. “We are looking to find ways to interfere with the transition to disease. Few have looked at the specific mechanism that suddenly makes these bacteria leave the nose where they typically prefer to reside and travel into the lungs or the middle ear where they cause disease. If we can understand that process, then maybe we can block it.”Hakansson and his colleagues had previously found that when the pneumococci colonize the nose, they form sophisticated, highly structured biofilm communities.In the current study, the research team grew biofilms of pneumococci on top of human epithelial cells, where the bacteria normally grow. They then infected these bacteria with influenza A virus or exposed them to the conditions that typically accompany the flu, including increased temperature to mimic fever, increased concentrations of ATP (the energy molecule in cells), and the stress hormone norepinephrine, released during flu infection. All three stimuli triggered a sudden release and departure of bacteria from the biofilm in the nose into otherwise normally sterile organs, such as the middle ears and lungs or into the bloodstream. At the same time, the researchers found that the gene expression profile of the bacteria that had dispersed from the biofilms revealed far more virulence.Hakansson says the research demonstrates how the mammalian and bacterial kingdoms interact. …

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More accurate model of climate change’s effect on soil

Aug. 1, 2013 — Scientists from UC Irvine and the National Center for Atmospheric Research have developed a new computer model to measure global warming’s effect on soil worldwide that accounts for how bacteria and fungi in soil control carbon.They found that soil outcomes based on their microbial model were more reliable than those forecast by traditional models. Study results appear online in Nature Climate Change.While standard models project modest carbon losses with global warming, the microbial models generate two novel scenarios: One is that soil around the world will accumulate carbon if microbial growth declines with higher temperatures. The second assumes that microbial growth increases with global warming, resulting in large soil carbon losses, meaning much more carbon will be released into the atmosphere.”The microbial soil model is extremely important to understanding the balance of carbon in the soil versus the atmosphere and how carbon mass in soil is affected by these bacteria and fungi,” said the study’s senior author, Steven Allison, an associate professor of ecology & evolutionary biology and Earth system science at UC Irvine. “Our hope is that this new soil model will be applied to the global Earth system models to better predict overall climate change.”The researchers also discovered that in cases of increased carbon input to soil (such as carbon dioxide or nutrient fertilization), microbes actually released the added carbon to the atmosphere, while traditional models indicate storage of the additional carbon. This, they said, is further evidence that Earth system models should incorporate microbial impact on soil to more accurately project climate change ramifications.”In our microbial model, we directly simulate how the activity of organisms like bacteria and fungi control the storage and losses of soil carbon,” said Will Wieder, a postdoctoral scientist with the National Center for Atmospheric Research in Boulder, Colo. “Now that we can more accurately measure what happens to soil as temperatures increase, we hope to study the potential effects of soil carbon fluctuations within a changing environment.”Gordon Bonan of the National Center for Atmospheric Research also contributed to the study, which was supported by National Science Foundation grants AGS-1020767 and EF-0928388 and the U.S. Department of Energy.

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Newly discovered marine viruses offer glimpse into untapped biodiversity

July 24, 2013 — Studying bacteria from the Baltic Sea, UA researchers have discovered an entire array of previously unknown viruses that barely resemble any of the known bacteria-infecting viruses.Researchers of the University of Arizona’s Tucson Marine Phage Lab have discovered a dozen new types of unknown viruses that infect different strains of marine bacteria.Bacteriophages — viruses that prey on bacteria — are less familiar to most people than their flu- or cold-causing cousins, but they control processes of global importance. For example, they determine how much oxygen goes from the oceans into the atmosphere in exchange for carbon dioxide, they influence climate patterns across Earth and they alter the assemblages of microorganisms competing in the environment.Despite their importance, scientists know almost nothing about “environmental viruses.” This is because most bacteriophages studies focus on those involved in human diseases or food processing.Now, a research team led by Matthew Sullivan, an assistant professor in the UA’s department of ecology and evolutionary biology, has deciphered the genetic makeup of 31 phages infecting a bacterium from the Baltic Sea known as Cellulophaga baltica. This bacterium and its relatives, collectively known as Bacteroidetes, play key roles in complex carbohydrate cycling in environments ranging from the oceans and sea ice to the human gut. The results are published in Proceedings of the National Academy of Science.”All of the phages we found in these bacteria were not previously known to science,” said Sullivan, who is a member of the UA’s BIO5 Institute. “It shows how little we know about what is out there.””Every single one of those groups that we found represents a new genus and their biology is exceptional,” he added. “For example, some have genomes twice as large as those we’ve seen before.””More than 80 percent of the phages’ structural proteins have no known counterparts in other species,” Sullivan said. “We’re breaking new ground with these viruses pretty much everywhere we look.”The analyses also represent what the authors describe as the first glimpse in to the phage side of the rare biosphere.”Anywhere you go, there are some organisms that are abundant and some that are rare,” Sullivan explained. “We tend to study the ones that are abundant because those are the ones we see. These Bacteroidetes phages are ubiquitous, meaning they occur in many parts of the world, but they’re never abundant — at least at the locations and times we’ve sampled so far.””In a random water sample, you might not find any, but if we were to sample an algae bloom, we would expect these rare biosphere organisms to become important. Now that we have them in culture, we can make a bloom happen anytime in the lab, and study them in a way that we haven’t been able to before.”The research illustrates why environmental phages are important: Bacteria like Cellulophaga account for many of the microorganisms that make up marine and freshwater phytoplankton, where they control global cycles of oxygen and carbon, and their boom and bust cycles directly translate into abundance and shortage nutrients, which sustain global food webs and fisheries, for example.The hidden movers and shakers behind these processes are the viruses that infect their bacterial hosts, regulating their populations and swapping genetic material among them. …

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Immunity: A secret to making macrophages

July 18, 2013 — Biologists at the California Institute of Technology (Caltech) have worked out the details of a mechanism that leads undifferentiated blood stem cells to become macrophages — immune cells that attack bacteria and other foreign pathogens. The process involves an unexpected cycle in which cell division slows, leading to an increased accumulation of a particular regulatory protein that in turn slows cell division further. The finding provides new insight into how stem cells are guided to generate one cell type as opposed to another.Previous research has shown that different levels of a key regulatory protein called PU.1, which is involved in the new cycle, are important for the production of at least four different kinds of differentiated blood cells. For example, levels of PU.1 need to increase in order for macrophages to form, but must decrease during the development of another type of white blood cell known as the B cell. Precisely how such PU.1-level changes occur and are maintained in the cells has been unclear. But by observing differentiation in both macrophages and B cells, the Caltech team discovered something unusual in the feedback loop that produces macrophages. Their findings appear in the current issue of Science Express.”Our results explain how blood stem cells and related progenitor cells can differentiate into macrophages and slow down their cell cycle, coordinating these two processes at the same time,” says lead author Hao Yuan Kueh, a postdoctoral scholar at Caltech who works with biologists Michael Elowitz and Ellen Rothenberg, who were both principal investigators on the study. “We are excited about this because it means other systems could also use this mechanism to coordinate cell proliferation with differentiation.”In the study, the researchers captured movies of blood stem cells taken from transgenic mice. The cells expressed a green fluorescent protein that serves as an indicator of PU.1 levels in the cell: the brighter the cells appeared in the movies, the more PU.1 was present. By measuring PU.1 levels over time using this indicator, the scientists were able to monitor changes in the rate of PU.1’s synthesis.PU.1 can work through a positive feedback loop, binding to its own DNA regulatory sequence to stimulate its own production in a self-reinforcing manner. …

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Intestinal bacteria linked to white blood cell cancer

July 16, 2013 — Researchers from UCLA’s Jonsson Comprehensive Cancer Center (JCCC) have discovered that specific types of bacteria that live in the gut are major contributors to lymphoma, a cancer of the white blood cells that are part of the human immune system. The study, led by Robert Schiestl, member of the JCCC and professor of pathology and laboratory medicine, environmental health sciences, and radiation oncology, was published online recently in the journal Cancer Research.In rodents, intestinal bacteria influence obesity, intestinal inflammation, and certain types of epithelial cancers. Those cancers affect the coverings of the stomach, liver or colon. However, little is known about the identity of the bacterial species that promote the growth of or protect the body from cancer, or about their effect on lymphoma.Up to 1,000 different species of bacteria (intestinal microbiota) live in the human gut. Intestinal microbiota number 100 trillion cells; over 90% of the cells in the body are bacteria. The composition of each person’s microbiome — the body’s bacterial make-up — is very different, due to the original childhood source of bacteria, and the effects of diet and lifestyle.Schiestl’s group wanted to determine whether differences in peoples’ microbiomes affect their risk for lymphoma, and whether changing the bacteria can reduce this risk. They studied mice with ataxia-telangiectasia (A-T), a genetic disease that in humans and mice is associated with a high rate of B-cell lymphoma. They discovered that, of mice with A-T, those with certain microbial species lived much longer than those with other bacteria before developing lymphoma, and had less of the gene damage (genotoxicity) that causes lymphoma.”This study is the first to show a relationship between intestinal microbiota and the onset of lymphoma,” Schiestl said. “Given that intestinal microbiota is a potentially modifiable trait, these results hold considerable promise for intervention of B cell lymphoma and other diseases.”The scientists were also able to create a detailed catalog of bacteria types with promoting or protective effects on genotoxicity lymphoma, which could be used in the future to create combined therapies that kill the bacteria that promote cancer (such as antibiotics) and expand the bacteria that protect from cancer (such as probiotics).This work was supported by the National Institutes of Health (NIH), JCCC, the Crohn’s and Colitis Foundation of America, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, the Austrian Federal Ministry of Science and Research, NASA, University of California Toxic Substances Research and Teaching Program, and the UCLA Graduate Division.

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Bacteria communicate to help each other resist antibiotics

July 4, 2013 — New research from Western University unravels a novel means of communication that allows bacteria such as Burkholderia cenocepacia (B. cenocepacia) to resist antibiotic treatment. B. cenocepacia is an environmental bacterium that causes devastating infections in patients with cystic fibrosis (CF) or with compromised immune systems.Dr. Miguel Valvano and first author Omar El-Halfawy, PhD candidate, show that the more antibiotic resistant cells within a bacterial population produce and share small molecules with less resistant cells, making them more resistant to antibiotic killing. These small molecules, which are derived from modified amino acids (the building blocks used to make proteins), protect not only the more sensitive cells of B. cenocepacia but also other bacteria including a highly prevalent CF pathogen, Pseudomonas aeruginosa, and E. coli. The research is published in PLOS ONE.”These findings reveal a new mechanism of antimicrobial resistance based on chemical communication among bacterial cells by small molecules that protect against the effect of antibiotics,” says Dr. Valvano, adjunct professor in the Department of Microbiology and Immunology at Western’s Schulich School of Medicine & Dentistry, currently a Professor and Chair at Queen’s University Belfast. …

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