East African honeybees safe from invasive pests … for now

Several parasites and pathogens that devastate honeybees in Europe, Asia and the United States are spreading across East Africa, but do not appear to be impacting native honeybee populations at this time, according to an international team of researchers.The invasive pests include including Nosema microsporidia and Varroa mites.”Our East African honeybees appear to be resilient to these invasive pests, which suggests to us that the chemicals used to control pests in Europe, Asia and the United States currently are not necessary in East Africa,” said Elliud Muli, senior lecturer in the Department of Biological Sciences, South Eastern Kenya University, and researcher at the International Centre of Insect Physiology and Ecology, Kenya.The team first discovered Varroa mites in Kenya in 2009. This new study also provides baseline data for future analyses of possible threats to African honeybee populations.”Kenyan beekeepers believe that bee populations have been experiencing declines in recent years, but our results suggest that the common causes for colony losses in the United States and Europe — parasites, pathogens and pesticides — do not seem to be affecting Kenyan bees, at least not yet,” said Christina Grozinger, professor of entomology and director of the Center for Pollinator Research, Penn State. “Some of our preliminary data suggest that the loss of habitat and drought impacting flowering plants, from which the bees get all their food, may be the more important factor driving these declines.”According to Harland Patch, research scientist in entomology, Penn State, not only are flowering plants important for honeybees, but the insects are important for plants as well.”Honeybees are pollinators of untold numbers of plants in every ecosystem on the African continent,” Patch said. “They pollinate many food crops as well as those important for economic development, and their products, like honey and wax, are vital to the livelihood of many families. People say the greatest animal in Africa is the lion or the elephant, but honeybees are more essential, and their decline would have profound impacts across the continent.”In 2010, the researchers conducted a nationwide survey of 24 locations across Kenya to evaluate the numbers and sizes of honeybee colonies, assess the presence or absence of Varroa and Nosema parasites and viruses, identify and measure pesticide contaminants in hives and determine the genetic composition of the colonies.”This is the first comprehensive survey of bee health in East Africa, where we have examined diseases, genetics and the environment to better understand what factors are most important in bee health in this region,” said Grozinger. The results appeared today in PLOS ONE.The researchers found that Varroa mites were present throughout Kenya, except in the remote north. In addition, Varroa numbers increased with elevation, suggesting that environmental factors may play a role in honeybee host-parasite interactions. Most importantly, the team found that while Varroa infestation dramatically reduces honeybee colony survival in the United States and Europe, in Kenya, its presence alone does not appear to impact colony size.The scientists found Nosema at three sites along the coast and one interior site. At all of the sites, they found only a small number of pesticides at low concentrations. Of the seven common honeybee viruses in the United States and Europe, the team only identified three species, but, like Varroa, these species were absent from northern Kenya. …

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‘3-D’ test could reduce reliance on animals for testing asthma and allergy medications

To determine whether new medicines are safe and effective for humans, researchers must first test them in animals, which is costly and time-consuming, as well as ethically challenging. In a study published in ACS’ journal Molecular Pharmaceutics, scientists report that they’ve developed a simple, “3D” laboratory method to test asthma and allergy medications that mimics what happens in the body, which could help reduce the need for animal testing.Amir Ghaemmaghami and colleagues note that respiratory conditions, such as asthma and allergies, are becoming more common. These conditions affect the lungs and the airway leading to the lungs, making it difficult to breathe. Every year, respiratory symptoms lead to expensive hospital visits, as well as absences from work and school. Better drugs could provide relief, but before giving new medicines to people, researchers must first test them in animals — a costly and laborious process. Sometimes, researchers will use “2D” tests in which they apply the drug to a layer of human cells in a lab dish instead, but this isn’t an adequate way to tell how a medicine will work in a whole animal or a whole person. So, Ghaemmaghami’s team developed a new, 3D alternative.Their test includes three types of human cells that are typically in a person’s airway. In the body, these cells are close together and are involved in the development of respiratory conditions. The 3D “model” reacted just like a real person’s airway when they exposed it to allergens and bacterial extract. They say that the model has the potential of reducing the need for some animal testing of new drugs for respiratory conditions.Story Source:The above story is based on materials provided by American Chemical Society. …

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Novel battleground for plant-pathogen interactions

Scientists at The Sainsbury Laboratory in Norwich, with collaborators at Michigan State University and the University of Illinois, have unveiled a new way in which plants perceive pathogens to activate immunity. They also show how pathogens inhibit the mechanism to cause disease. It was previously only associated with other processes in mammalian cells.When plants detect microbial molecules, they trigger immune responses to prevent disease. Although several plant immune receptors for these microbial molecules are known, how they are activated once the microbe is recognized is not well understood.In a study published this week in the journal Science, the scientists found that phosphorylation of an amino acid called tyrosine — phosphorylation being a process that can turn molecules on or off — is key for activating plant immune receptors. This mechanism is already known to play an essential role in the activation of mammalian receptors, and its mis-regulation is often linked to important chronic diseases.The current study shows for the first time that the modification occurs in plant immune receptors as well.”This finding opens the door to improving crop disease resistance as we can investigate ways to optimize how plants recognize pathogenic microbes,” says Professor Cyril Zipfel.”It also provides a new link between our understanding of cellular signalling in plant and animal cells.”In the same study, the researchers discovered that pathogenic bacteria use an enzyme secreted within plant cells to derail the plant’s immune response. They use an enzyme to remove tyrosine phosphorylation from immune receptors, quelling the plant’s signalling mechanisms. Inhibiting the immune response allows bacteria to cause disease.”Our research highlights a battle between hosts and pathogens to take control of an important mechanism,” said first author Dr Alberto Macho from The Sainsbury Laboratory.”Control over this mechanism to activate immune receptors determines whether a plant stays healthy or suffers from disease,” he says.Story Source:The above story is based on materials provided by Norwich BioScience Institutes. Note: Materials may be edited for content and length.

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Fighting antibiotic resistance with ‘molecular drill bits’

In response to drug-resistant “superbugs” that send millions of people to hospitals around the world, scientists are building tiny, “molecular drill bits” that kill bacteria by bursting through their protective cell walls. They presented some of the latest developments on these drill bits, better known to scientists as antimicrobial peptides (AMPs), at the 247th National Meeting & Exposition of the American Chemical Society (ACS), the world’s largest scientific society.The meeting features more than 10,000 scientific reports across disciplines from energy to medicine.One of the researchers in the search for new ways to beat pathogenic bacteria is Georges Belfort, Ph.D. He and his team have been searching for a new therapy against the bacteria that cause tuberculosis (TB). It’s a well-known, treatable disease, but resistant strains are cropping up. The World Health Organization estimates that about 170,000 people died from multidrug-resistant TB in 2012.”If the bacteria build resistance to all current treatments, you’re dead in the water,” said Belfort, who is at Rensselaer Polytechnic Institute.To avoid this dire scenario, scientists are developing creative ways to battle the disease. In ongoing research, Belfort’s group together with his wife, Marlene Belfort, and her group at the University at Albany are trying to dismantle bacteria from within. They also decided to attack it from the outside.In their search for a way to do this, they came upon AMPs. Although these naturally occurring, short strings of amino acids are not new — all classes of organisms from humans to bacteria produce them as part of their natural defense strategy — the fight against drug-resistant pathogens has heightened attention on these protective molecules.Researchers began studying them in earnest in the 1980s. By 2010, they had identified nearly 1,000 unique AMPs from many sources, including fly larvae, frog skin and mammalian immune system cells. The molecules come in different shapes, lengths and with other varying traits. …

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Substance in photosynthesis was in play in ancient, methane-producing microbes

An international team of researchers led by scientists at Virginia Tech and the University of California, Berkeley has discovered that a process that turns on photosynthesis in plants likely developed on Earth in ancient microbes 2.5 billion years ago, long before oxygen became available.The research offers new perspective on evolutionary biology, microbiology, and the production of natural gas, and may shed light on climate change, agriculture, and human health.”By looking at this one mechanism that was not previously studied, we will be able to develop new basic information that potentially has broad impact on contemporary issues ranging from climate change to obesity,” said Biswarup Mukhopadhyay, an associate professor of biochemistry at the Virginia Tech College of Agriculture and Life Sciences, and the senior author of the study. He is also a faculty member at the Virginia Bioinformatics Institute. Plant and microbial biology professor emeritus Bob B. Buchanan co-led the research and co-authored the paper.The findings were described this week in an early online edition of the Proceedings of the National Academy of Sciences.This research concerns methane-forming archaea, a group of microbes known as methanogens, which live in areas where oxygen is absent. Methane is the main component of natural gas and a potent greenhouse gas.”This innovative work demonstrates the importance of a new global regulatory system in methanogens,” said William Whitman, a professor of microbiology at the University of Georgia who is familiar with the study, but not connected to it. “Understanding this system will provide the tools to use these economically important microorganisms better.”Methanogens play a key role in carbon cycling. When plants die, some of their biomass is trapped in areas that are devoid of oxygen, such as the bottom of lakes.Methanogens help convert the residual biological material to methane, which other organisms convert to carbon dioxide — a product that can be used by plants.This natural process for producing methane forms the basis for treating municipal and industrial wastes, helps reduce pollution, and provides methane for fuel. The same process allows natural gas production from agricultural residues, a renewable resource.Methanogens also play an important role in agriculture and human health. They live in the digestive systems of cattle and sheep where they facilitate the digestion of feed consumed in the diet.Efforts to control methanogens in specific ways may improve feed utilization and enhance the production of meat and milk, researchers say.Methanogens are additionally a factor in human nutrition. The organisms live in the large intestine, where they enhance the breakdown of food. …

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Uncovering the drivers of honey bee colony declines and losses

Scientists have announced the results of research conducted on honey bee colony declines and the factors attributed to honey bee losses. In a paper published this week in the journal EcoHealth, scientists at EcoHealth Alliance investigated the causes of long-term declines of colony numbers and annual colony losses. The work shows that socioeconomic and political pressures on honey production over the past few decades has caused a long-term reduction in the number of colonies in production in the USA, Europe and many other countries. However, more recently honey bee managers have reported increased losses in their stocks each year (so-called ‘annual colony losses’), and the new research shows that pests, pathogens and management issues likely play a major role in this, and are under researched and poorly understood drivers.Honey bees provide ecosystem services through pollination of crops worth $215 billion annually worldwide. Concern over honey bee declines in recent decades as well as annual losses has sparked debate over their causes and has led to hypotheses that a specific novel syndrome ‘Colony Collapse Disorder’ (CCD) is plaguing bee populations. Many scientists have proposed new drivers such as pollution from pesticides as the cause of these declines. EcoHealth Alliance conducted an in-depth, critical review of the science behind these declines and losses and have shown that:1. The long-term multi-decadal downward trend in the number of bee colonies in many countries reflects a reduction in the profitability of bee keeping due to economic and/or political change, with many bee keepers leaving the profession;2. Data on annual losses is sparse and collected in a non-uniform way that makes comparing the extent and potential cause of losses to those in previous years difficult3. That there are significant inconsistencies with the way researchers (and thus potentially bee keepers) define CCD, suggesting that it may be over-reported; and4. …

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Up close and 3-dimensional: HIV caught in the act inside the gut

HIV infection has many unhealthy consequences on the body, but in particular it messes up the gut. The human intestine has the highest concentration of HIV target cells, the majority of which are destroyed within days of infection, and before CD4 T cell counts drop measurably in the blood. A study published on January 30th in PLOS Pathogens reports the first three-dimensional ultra-structural study of HIV infection in vivo. Not only does it reveal details on how the virus quickly infects immune cells in the gut, using them as virus-producing factories, but it also highlights where the virus “hides out” deep within the intestinal tissue.Pamela Bjorkman, from the Howard Hughes Medical Institute and the California Institute of Technology, USA, and colleagues used electron tomography for a high-resolution study of HIV virus in the guts of “humanized” mice, whose immune system is made up to a large degree of human cells. They infected these “BLT mice” (so-called because they have human bone marrow, thymus, and liver cells) with HIV virus and developed methods that allowed them to safely examine and visualize the three-dimensional architecture of infected parts of the gut.They saw HIV-infected human immune cells, caught virus particles in the act of budding from such cells, and also found groups of free immature and mature viruses. For one infected host cell (turned HIV factory) the researchers counted 63 virus particles it had likely released. The actual number is almost certainly much higher, because the method can only visualize virus particles surrounding the host cell within a relatively small part of the tissue. Nevertheless, they discovered that groups of viruses that were farther from the host cell were more mature than those closer to it, which suggested that the host cell releases new virus in a series of “semi-synchronized” waves.Among the samples, the researchers found some where viruses released from one infected cell seemed directly to attach to a neighboring host cell, presumably infecting it. In addition to such “virological synapses,” they also observed free virus particles that appear to have covered some distance between their “mother” cell and the cell that would become their target to infect.These images provide the first 3D ultrastructural details on HIV infection and virus production in a setting that closely resembles the gut of human patients. Some results confirm earlier findings from in vitro experiments — cells grown and infected in a petri dish — but others are seen for the first time and advance the understanding of how HIV infection spreads in real life.”To me, an important finding is that the majority of the viral transmission events within tissue involved free virus rather than virological synapses,” says Bjorkman. …

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Toxin-emitting bacteria being evaluated as potential multiple sclerosis trigger

Oct. 17, 2013 — A research team from Weill Cornell Medical College and The Rockefeller University has identified a bacterium it believes may trigger multiple sclerosis (MS), a chronic, debilitating disorder that damages myelin forming cells in the brain and spinal cord.Their study, published in PLoS ONE, is the first to identify the bacterium, Clostridium (C.) perfringens type B, in humans.The scientists say their study is small and must be expanded before a definitive connection between the pathogen and MS can be made, but they also say their findings are so intriguing that they have already begun to work on new treatments for the disease.”This bacterium produces a toxin that we normally think humans never encounter. That we identified this bacterium in a human is important enough, but the fact that it is present in MS patients is truly significant because the toxin targets the exact tissues damaged during the acute MS disease process,” say the study’s first author, K. Rashid Rumah, an MD/PhD student at Weill Cornell Medical College, and the study’s senior investigator, Dr. Timothy Vartanian, professor of neurology and neuroscience at Weill Cornell Medical College and director of the Judith Jaffe Multiple Sclerosis Center at New York-Presbyterian Hospital/Weill Cornell Medical Center.”While it is clear that new MS disease activity requires an environmental trigger, the identity of this trigger has eluded the MS scientific community for decades,” Dr. Vartanian says. “Work is underway to test our hypothesis that the environmental trigger for MS lays within the microbiome, the ecosystem of bacteria that populates the gastrointestinal tract and other body habitats of MS patients.”Connection to MS in grazing animalsThe study describes discovery of C. perfringens type B in a 21-year-old woman who was experiencing a flare-up of her MS.The woman was part of the Harboring the Initial Trigger for MS (HITMS) observational trial launched by Dr. Vartanian and K. Rashid Rumah, who works both with Dr. …

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Scientists discover novel functions of platelets

Sep. 1, 2013 — A new finding could lead to novel treatments to reduce bleeding in trauma and severe infections.The research, from Oklahoma Medical Research Foundation scientists Lijun Xia, M.D., Ph.D., Jianxin Fu, M.D., Ph.D., and Brett Herzog, Ph.D., appears in the most recent issue of the journal Nature.One way the immune system keeps a body healthy is through immune surveillance. Lymphocytes, a type of white blood cell, constantly exit the bloodstream and “check in” at the lymph nodes to learn about possible pathogens or abnormal cell growth. The function prepares the immune system to fight infections and dispose of pre-cancerous cells.For years, scientists have wondered how lymphocytes exit the bloodstream at a large volume without causing bleeding. Xia and his team of researchers found that platelets, which normally stop blood loss by clumping and forming plugs in blood vessel holes after injuries, activate a screening process. And this process allows lymphocytes to exit into lymph nodes without letting red blood cells leave the blood vessel.”Platelets are the smallest blood cells that work in clotting to heal cuts because they stick to the site of the injury,” said Xia, a member of OMRF’s Cardiovascular Biology Research Program. “This novel function requires platelets to dump a specific lipid content, but does not need intact platelets because it’s not forming a clot. We never knew they could do this before.”Not only are platelets making it possible for lymphocytes to leave the blood vessel, they’re doing so by going outside the vessel, themselves — another novel finding, he said.When scientists interrupted the process by removing a protein called podoplanin, the screening process stopped working, allowing both lymphocytes and red blood cells to escape. The new study reveals a novel function of platelets independent of their hemostatic role. The findings could alter the ways in which doctors use platelets to treat traumatic injuries and serious infections.Intact platelets that can clot usually only last 5 to 7 days in the blood and cannot be frozen, making storage a problem, Xia said. …

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How to achieve a well-balanced gut: ‘Peacekeeper’ in the gut identified

Aug. 9, 2013 — Creating an environment that nurtures the trillions of beneficial microbes in our gut and, at the same time, protects us against invasion by food-borne pathogens is a challenge. A study published on August 8 in PLOS Pathogens reveals the role of a key player in this balancing act.SIGIRR is a protein present at the surface of the cells that line the gut that dampens the innate (non-specific) immune response of these cells to bacteria. The new study, led by Xiaoxia Li (from the Lerner Research Institute in Cleveland, USA) and Bruce Vallance (from BC’s Childrens’ Hospital and the University of British Columbia in Vancouver, Canada), now shows that SIGIRR function in mice (and presumably also in humans) is necessary to protect the gut against “hostile takeover” by bacteria that cause serious food poisoning and bowel inflammation.The researchers infected mice that were missing the Sigirr gene with bacterial pathogens that cause food poisoning in rodents (either a relative of toxic E. coli or Salmonella Typhimurium). And even though these mice had a much stronger intestinal innate immune response than mice with intact SIGIRR function, they were unable to defend themselves against the pathogens and got much sicker than their normal counterparts.Examining the underlying mechanism, the researchers looked at the beneficial microbes that normally reside in the gut. Often, these can delay or even prevent pathogens from infecting the gut by competing for space and nutrients, in a process called “colonization resistance.” Consistent with this role, the exaggerated antimicrobial responses triggered by the pathogens in the absence of Sigirr caused a rapid and dramatic loss of beneficial microbes from the infected gut. This depletion seems to reduce the ability of the resident good bugs to outcompete the invading bad ones, leaving the gut highly vulnerable to colonization by the toxic pathogens.SIGIRR function in the gut therefore reflects a balancing strategy that sacrifices maximal immune responsiveness in order to protect the beneficial resident microbe populations which, when healthy, provide a strong barrier against toxic foreign invaders and thus protection for their host through colonization resistance.The researchers conclude “Our results suggest our immune system really isn’t very good at preventing food-borne infections, and, through evolution, we have come to rely on our gut microbiota to protect us from many pathogens. If we disrupt this mutualistic relationship (for example, with antibiotics), we leave ourselves highly susceptible to infections.”While being gentle with your beneficial gut flora is clearly a good thing, the researchers also speculate that modulating SIGIRR function within the gut might one day offer therapeutic potential for gastro-intestinal disorders, such as inflammatory bowel disease.

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New modular vaccine design combines best of existing vaccine technologies

July 29, 2013 — A new method of vaccine design, called the Multiple Antigen Presentation System (MAPS), may result in vaccines that bring together the benefits of whole-cell and acellular or defined subunit vaccination. The method, pioneered by researchers at Boston Children’s Hospital, permits rapid construction of new vaccines that activate mulitple arms of the immune system simultaneously against one or more pathogens, generating robust immune protection with a lower risk of adverse effects.As reported by Fan Zhang, PhD, Ying-Jie Lu, PhD, and Richard Malley, MD, from Boston Children’s Division of Infectious Disease, in the Proceedings of the National Academy of Sciences on July 29, the method could speed development of new vaccines for a range of globally serious pathogens, or infectious agents.Broadly speaking, the vaccines available today fall into two categories: whole-cell vaccines, which rely on weakened or killed bacteria or viruses; and acellular or subunit vaccines, which include a limited number of antigens — portions of a pathogen that trigger an immune response. Both approaches have advantages and disadvantages.”Whole-cell vaccines elicit a broad range of immune responses, often just as an infection would, but can cause side effects and are hard to standardize,” said Malley. “Acellular vaccines can provide good early immunity with less risk of side effects, but the immune responses they induce wane with time.”The MAPS method may allow vaccine developers to take a middle ground, where they can link multiple protein and polysaccharide (sugar) antigens from one or more pathogens together in a modular fashion, much as one would connect Lego blocks.The resulting complex — which resembles a scaffold of polysaccharides studded with proteins — can stimulate both antibody and T-cell responses simultaneously much like whole-cell vaccines, resulting in stronger immunity to the source pathogen(s). However, because the composition of a MAPS vaccine is well defined and based on the use of isolated antigens (as one would find with an acellular vaccine) the risk of side effects should be greatly reduced.For instance, mice injected with a MAPS vaccine combining proteins from tuberculosis (TB) and polysaccharides from Streptococcus pneumoniae (pneumococcus) mounted vigorous antibody and T-cell responses against TB, whereas those vaccinated with TB protein antigens alone mounted only an antibody response.Similarly, 90 percent of mice given a MAPS-based vaccine containing multiple pneumococcal polysaccharide and protein antigens were protected from a lethal pneumococcus infection, mounting strong antibody and T-cell responses against the bacteria. By contrast, 30 percent of mice vaccinated with the same antigens in an unbound state survived the same challenge.”The MAPS technology gives you the advantages of: whole-cell vaccines while being much more deliberate about which antigens you include; doing it in a quantitative and precise way; and including a number of antigens so as to try to replicate the effectiveness of whole-cell vaccination,” Malley explained. “The immunogenicity of these constructs is greater than the sum of their parts, somewhat because they are presented to the host as particles.”The system relies on the interactions of two compounds, biotin and rhizavidin, rather than covalent binding as is used in most of the current conjugate vaccines. To build a MAPS vaccine, biotin is bound to the polysaccharide(s) of choice and rhizavidin to the protein(s). The biotin and rhizavidin then bind together through an affinity interaction analogous to Velcro. The construction process is highly efficient, significantly reducing the time and cost of vaccine development and production.While his team’s initial work has focused on bacterial pathogens, Malley believes the technology could impact vaccine development for a broad range of pathogens, in particular those of importance in the developing world. …

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Researchers identify new source of powerful immunity protein

July 10, 2013 — Researchers at UT Southwestern Medical Center report the identification of a new cellular source for an important disease-fighting protein used in the body’s earliest response to infection.The protein interferon-gamma (IFN-γ) keeps viruses from replicating and stimulates the immune system to produce other disease-fighting agents. Neutrophils, the newly identified cellular source of the protein, are the major component of the pus that forms around injured tissue.The researchers also report that the neutrophils appear to produce IFN-γ through a new cellular pathway independent of Toll-like receptors (TLRs): the body’s early warning system for invasion by pathogens. This finding indicates that mammals might possess a second early-alert system — the sort of built-in redundancy engineers would envy, said Dr. Felix Yarovinsky, assistant professor of immunology and senior author of the study published online in the Proceedings of the National Academy of Sciences in June.”We believe our mouse study provides strong evidence that neutrophils, white blood cells created in the bone marrow, produce significant amounts of IFN-γ in response to disease,” Dr. Yarovinsky said. “The finding of a new and essential cellular source for IFN-γ challenges a long-held belief in the field and is significant because neutrophils are the most common kind of white blood cell.”Two pathogens were used in this study: the parasite Toxoplasma gondii — which can cause brain damage in humans and other mammals that have compromised immune systems — and a type of bacterium that causes gastroenteritis, Salmonella typhimurium.Innate immunity is the body’s first line of defense against pathogens, including those that it has never before encountered. Adaptive immunity is the secondary system that battles pathogens to which the body has previously been exposed and to which it has developed antibodies.Textbooks list natural killer (NK) cells and T cells as the body’s significant sources of IFN-γ. Although large numbers of neutrophils have long been observed to congregate at the site of a new infection, they were commonly thought to be first responders or foot soldiers rather than generals in the battle against disease, as this study indicates they are, Dr. Yarovinsky explained.About 20 years ago, there were clinical reports in humans and animals suggesting that neutrophils might produce IFN-γ, but the idea was largely ignored by the scientific community until the last decade, he said.Since then, studies at UT Southwestern and elsewhere have found that mice lacking NK and T cells, and therefore expected to be unable to produce IFN-γ, somehow continued to withstand infections better than mice genetically unable to make any IFN-γ. These observations suggested the possibility of an unknown source of the protein, he explained.In a series of experiments, the UT Southwestern researchers identified neutrophils as the major source of IFN-γ in mice lacking NK and T cells. …

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Early, late first exposure to solid food appears associated with development of Type 1 diabetes

July 8, 2013 — Both an early and late first exposure to solid food for infants appears to be associated with the development of type 1 diabetes mellitus (T1DM), according to a study published by JAMA Pediatrics, a JAMA Network publication.T1DM is increasing around the world with some of the most rapid increase among children younger than 5 years of age. The infant diet has been of particular interest in the origin of the disease, according to the study background.Brittni Frederiksen, M.P.H., Colorado School of Public Health, University of Colorado, Aurora, and colleagues examined the associations between perinatal and infant exposures, especially early infant diet, and the development of T1DM. Newborn screening of umbilical cord blood for diabetes susceptibility in the human leukocyte antigen (HLA) region was performed at St. Joseph’s Hospital in Denver and first-degree relatives of individuals with T1DM were recruited from the Denver area.Both early (less than 4 months of age) and late (greater than or equal to 6 months of age) first exposure to any solid food was associated with development of T1DM (hazard ratio [HR] 1.91, and HR, 3.02, respectively), according to the study results. Early exposure to fruit and late exposure to rice/oat was associated with an increased risk of T1DMB (HR, 2.23 and HR, 2.88, respectively), whereas breastfeeding when wheat /barley (HR, 0.47) were introduced appeared to be associated with a decreased risk, the results also indicate.”Our data suggest multiple foods/antigens play a role and that there is a complex relationship between the timing and type of infant food exposures and T1DM risk. In summary, there appears to be a safe window in which to introduce solid foods between 4 and 5 months of age; solid foods should be introduced while continuing to breastfeed to minimize T1DM risk in genetically susceptible children. These findings should be replicated in a larger cohort for confirmation,” the authors conclude.

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Potential disease-transmission sources in animals ID’d by calculating risk using social network mathematics

June 11, 2013 — Spanish and US scientists have successfully identified animal species that can transmit more diseases to humans by using mathematical tools similar to those applied to the study of social networks like Facebook or Twitter. Their research — recently published in the journal PNAS — describes how parasite-primate interactions transmit diseases like malaria, yellow fever or AIDS to humans. Their findings could make an important contribution to predicting the animal species most likely to cause future pandemics.Professor José María Gómez of the University of Granada Department of Ecology is the principal author of this research, in collaboration with Charles L. Nunn (University of Cambridge, Massachusetts, US) and Miguel Verdú (Spanish National Research Council Desertification Research Center, Valencia, Spain). They propose a criterion to identify disease-transmission agents based on complex network metrics similar to those used to study social networks.As Prof Gómez explains, “most emerging diseases in humans are zoonotic, that is, they are transmitted to humans by animals. To identify animal species that are potential high-risk sources of emerging diseases it’s essential we set up mechanisms that control and observe these diseases.”Study of 150 primate speciesTo conduct their study, the researchers constructed a network in which each node represented one of the approximately 150 non-human primate species about which we have enough data on their parasite fauna. “Each primate species is connected to the other primates as a function of the number of parasites they share. Once the network was constructed, we studied each primate species’ position — whether central or peripheral. A primate’s centrality is measured by its connection intensity with many other primates that are, in turn, closely connected,” says the University of Granada researcher.The article published in PNAS reports the researchers’ discovery that the most central primates could be more capable of transmitting parasites to other species and, therefore, to humans, than the rest. “This is comparable to the idea that, in social networks, web pages that are central and have links to many other pages, spread their contents all through the Web,” José María Gómez affirms.The researchers have confirmed their hypothesis by relating the centrality value of each primate with the number of emerging pathogens shared with humans. …

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Substances in honey increase honey bee detox gene expression

May 1, 2013 — Research in the wake of Colony Collapse Disorder, a mysterious malady afflicting (primarily commercial) honey bees, suggests that pests, pathogens and pesticides all play a role. New research indicates that the honey bee diet influences the bees’ ability to withstand at least some of these assaults. Some components of the nectar and pollen grains bees collect to manufacture food to support the hive increase the expression of detoxification genes that help keep honey bees healthy.

The findings appear in the Proceedings of the National Academy of Sciences.

University of Illinois professor of entomology May Berenbaum, who led the study, said that many organisms use a group of enzymes called cytochrome P450 monooxygenases to break down foreign substances such as pesticides and compounds naturally found in plants, known as phytochemicals. However, honey bees have relatively few genes dedicated to this detoxification process compared to other insect species, she said.

“Bees feed on hundreds of different types of nectar and pollen, and are potentially exposed to thousands of different types of phytochemicals, yet they only have one-third to one-half the inventory of enzymes that break down these toxins compared to other species,” Berenbaum said.

Determining which of the 46 P450 genes in the honey bee genome are used to metabolize constituents of their natural diet and which are used to metabolize synthetic pesticides became a “tantalizing scientific question” to her research team, Berenbaum said.

“Every frame of honey (in the honey bee hive) is phytochemically different from the next frame of honey because different nectars went in to make the honey. If you don’t know what your next meal is going to be, how does your detoxification system know which enzymes to upregulate?” Berenbaum said.

Research had previously shown that eating honey turns on detoxification genes that metabolize the chemicals in honey, but the researchers wanted to identify the specific components responsible for this activity. To do this, they fed bees a mixture of sucrose and powdered sugar, called bee candy, and added different chemical components in extracts of honey. They identified p-coumaric acid as the strongest inducer of the detoxification genes.

“We found that the perfect signal, p-coumaric acid, is in everything that bees eat — it’s the monomer that goes into the macromolecule called sporopollenin, which makes up the outer wall of pollen grains. It’s a great signal that tells their systems that food is coming in, and with that food, so are potential toxins,” Berenbaum said.

Her team showed that p-coumaric acid turns on not only P450 genes, but representatives of every other type of detoxification gene in the genome. This signal can also turn on honey bee immunity genes that code for antimicrobial proteins.

According to Berenbaum, three other honey constituents were effective inducers of these detoxification enzymes. These components probably originate in the tree resins that bees use to make propolis, the “bee glue” which lines all of the cells and seals cracks within a hive.

“Propolis turns on immunity genes — it’s not just an antimicrobial caulk or glue. It may be medicinal, and in fact, people use it medicinally, too,” Berenbaum said.

Many commercial beekeepers use honey substitutes such as high-fructose corn syrup or sugar water to feed their colonies. Berenbaum believes the new research shows that honey is “a rich source of biologically active materials that truly matter to a bee.”

She hopes that future testing and development will yield honey substitutes that contain p-coumaric acid so beekeepers can enhance their bees’ ability to withstand pathogens and pesticides.

Although she doesn’t recommend that beekeepers “rush out and dump p-coumaric acid into their high fructose corn syrup,” she hopes that her team’s research can be used as the basis of future work aimed at improving bee health.

“If I were a beekeeper, I would at least try to give them some honey year-round,” Berenbaum said, “because if you look at the evolutionary history of Apis mellifera, this species did not evolve with high fructose corn syrup. It is clear that honey bees are highly adapted to consuming honey as part of their diet.”

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