WASHINGTON, DC—December 16, 2014—Using mathematical modeling, researchers at New York and Vanderbilt universities have shown that commensal bacteria that cause problems later in life most likely played a key role in stabilizing early human populations. The finding, published in mBio®, the online open-access journal of the American Society for Microbiology, offers an explanation as to why humans co-evolved with microbes that can cause or contribute to cancer, inflammation, and degenerative diseases of aging.
The work sprung from a fundamental question in biology about senescence, or aging past the point of reproduction. “Nature has a central problem—it must have a way to remove old individuals, whether fish or trees or people,” says Martin Blaser, microbiologist at New York University Langone Medical Center in New York City. “Resources are always limited. And young guys are ultimately competing with older ones.”
In most species, individuals die shortly after the reproductive phase. But humans are weird—we have an extra long senescence phase. Blaser began to think about the problem from the symbiotic microbe’s point of view and he came up with a hypothesis: “The great symbionts keep us alive when we are young, then after reproductive age, they start to kill us.” They are part of the biological clock of aging.
In other words, he hypothesized that evolution selected for microbes that keep the whole community of hosts healthy, even if that comes with a cost to an individual host’s health.
Modeling of early human population dynamics could tell him if he was on the right track. Blaser worked together with his collaborator Glenn Webb, professor of mathematics at Vanderbilt University in Nashville, to define a mathematical model of an early human population, giving it characteristics similar to a time 500-100,000 years ago, when the human population consisted of sparse, isolated communities.
Webb came up with a non-linear differential equation to describe the variables involved, their rates of change over time, and the relationship between those rates. “It can reveal something that’s not quite appreciated or intuitive, because it sorts out relationships changing in time,” even with many variables, such as age-dependent fertility rates and mortality rates, changing simultaneously, explains Webb.
Using this baseline model, the team could tweak the conditions to see what happened to the population dynamics. For example, they increased the fertility rate from roughly six children per female to a dozen, proposing that this might be one way for populations to overcome the burden of senescence, by boosting juvenile numbers. Instead, they were surprised to see that this created wild oscillations in total population size over time—an unstable scenario.
“You could imagine if something bad happens during a low point, like a drought, then the population crashes or might be extinguished,” says Blaser. Over time, the increased fertility rate adds to the pressure that a larger population of older people puts on the juveniles due to limited resources. Likewise, when Blaser and Webb plugged parameters into the model that greatly increased mortality from a microbial infection akin to Shigella, which primarily kills children, the population crashed to zero.
Next they set juvenile mortality to a constant, low level and senescent mortality risk was set to increase each year with age—a condition that mimics certain symbiotic bacteria such as Helicobacter pylori that can become harmful in old age. This model exhibited a stable population equilibrium.
“By preferentially knocking off older individuals, you get a robust population, and this is what Nature is doing,” says Blaser. Now, though, the legacy of co-evolving with such microbes has become a burden as longevity stretches out, because some of these microbes contribute to inflammatory and degenerative diseases. Recognizing that our own once-beneficial microbes might be the agents of mortality in later life, could lead to better preventives or treatments for diseases of aging.
WASHINGTON, DC – December 9, 2014 – Seasonal flu vaccines may protect individuals not only against the strains of flu they contain but also against many additional types, according to a study published this week in mBio®, the online open-access journal of the American Society for Microbiology.
The work, directed by researchers at St. Jude Children’s Research Hospital in Memphis, Tenn., found that some study participants who reported receiving flu vaccines had a strong immune response not only against the seasonal H3N2 flu strain from 2010, when blood samples were collected for analysis, but also against flu subtypes never included in any vaccine formulation.
The finding is exciting “because it suggests that the seasonal flu vaccine boosts antibody responses and may provide some measure of protection against a new pandemic strain that could emerge from the avian population,” said senior study author Paul G. Thomas, PhD, an Associate Member in the Department of Immunology at St. Jude. “There might be a broader extent of reactions than we expected in the normal human population to some of these rare viral variants.”
Because avian influenza viruses have an important role in emerging infections, Thomas and colleagues tested whether exposure to different types of birds can elicit immune responses to avian influenza viruses in humans. They studied blood samples taken from 95 bird scientists attending the 2010 annual meeting of the American Ornithologist Union. They exposed plasma from the samples to purified proteins of avian influenza virus H3, H4, H5, H6, H7, H8 and H12 subtypes using two laboratory tests to see how many different viruses participants reacted to, and how strongly. The first test, ELISA, measures if any antibodies -- proteins produced by the body that are used by the immune system to identify and neutralize foreign objects such as bacteria and viruses – combine in any way to a protein called HA on the surface of the virus. The second, HAI, measures if antibodies can bind to HA and interrupt its association with a substance viruses use to get inside human cells.
In the ELISA tests, 77 percent of participants had detectable antibodies against avian influenza proteins. Most individuals tested had a strong antibody response to the seasonal H3N2 human virus-derived H3 subtype, part of that year’s vaccine (2009-2010), but many also had strong measurable antibody responses to group 1 HA (avian H5, H6, H8, H12) and group 2 HA (avian H4, human H7) subtypes. Sixty-six percent of participants had some level of detectable antibodies against four or more HA proteins, and a few had responses to all subtypes tested, most of which have not previously been detected in the human population.
In additional experiments, the scientists found that participants who had significant antibody responses did not necessarily also have significant immune system T cell responses to avian viruses, indicating that these two arms of immunity can be independently boosted after vaccination or infection; that individuals who reported receiving seasonal influenza vaccination had significantly higher antibodies to the avian H4, H5, H6, and H8 subtypes; and that participants with exposure to poultry had significantly higher antibody responses to the H7 subtype, but to none of the other subtypes tested. Exposure to other types of birds did not play a role in immunity.
A person’s immune response on the ELISA test did not necessarily predict response on the HAI test, and vice versa. As HAI antibodies only target the “head” of the HA while ELISA antibodies can be against the head or the relatively conserved “stalk” domain, this result indicated that some individuals were more likely to target the conserved stalk region (i.e. show greater reactivity in ELISA than in HAI).
The work has opened up a lot of questions in figuring out why people mount different types of responses, and potentially how the seasonal vaccine may play a role in boosting these responses, Thomas said. He has started additional studies in other groups of people with varied vaccination and infection histories to tease apart what exposures boost immunity against avian influenza viruses.
The study was supported by the National Institutes of Health Centers of Excellence for Influenza Research and Surveillance (St. Jude CEIRS, contract HHSN272201400006C) and the American Lebanese Syrian Associated Charities (ALSAC), a fund-raising organization for the hospital. The article can be found online at http://bit.ly/mbiodec9.
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mBio® is an open access online journal published by the American Society for Microbiology to make microbiology research broadly accessible. The focus of the journal is on rapid publication of cutting-edge research spanning the entire spectrum of microbiology and related fields. It can be found online at http://mbio.asm.org.
The American Society for Microbiology is the largest single life science society, composed of over 39,000 scientists and health professionals. ASM's mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.
WASHINGTON, DC – December 3, 2014 - Nancy A. Sansalone, MPA has been named Interim Executive Director of the American Society for Microbiology (ASM) effective January 1, 2015. She steps in for Michael Goldberg, who is retiring at the end of 2014 after 30 years of stellar leadership. She has been asked by the ASM Officers to lead the staff, to steward the operations and finances and to prepare the organization for change while the Society conducts an international search for a permanent Executive Director/CEO. The search is expected to begin in January 2015.
Sansalone joined ASM in 2010 as the Deputy Executive Director. In this role, she provides leadership and management expertise to the board leadership and staff to ensure the fulfillment of the Society’s mission and strategic plan and provides leadership direction for the Society’s operational, programmatic and business activities.
Sansalone has spent her entire career in association management and higher education administration. Prior to joining ASM, she served as the CFO and Chief Operating Officer at the Special Libraries Association (SLA) and Vice President and CFO of the American Association for Higher Education (AAHE). Previously, Sansalone worked for 10 years with the Council of Graduate Schools (CGS), serving as Vice President for Finance and Administration and Treasurer for the Council’s Board of Directors.
She also has served as a volunteer leader on numerous non-profit boards such as the National Association for Women in Education where she served as the elected President, the Washington Higher Education Secretariat Metropolitan Employer Trust as an Advisory Board member, Capital Association for Women in Education as President, National Conference for College Women Student leaders as Chair, National Center for Higher Education Meeting Professionals as Chair, American Society for Association Executives as a member of the Finance and Administration Advisory Board and as a member of the ERIC Clearing House on Higher Education Coordinating Board. She also has held administrative posts at both Harvard University working with international programs at the Kennedy School of Government and Northeastern University in the Cooperative Education Division.
Sansalone is a graduate of Northeastern University with a Master’s Degree in Public Administration and a Bachelors of Science Degree in Political Science and Public Administration. She completed work at Harvard University in their advanced graduate study in management program.
She lives in Arlington, Virginia with her spouse Jim and their four dogs.
WASHINGTON, DC – December 1, 2014 -- Microbial succession in a sterilized restroom begins with bacteria from the gut and the vagina, and is followed shortly by microbes from the skin. Restrooms are dominated by a stable community structure of skin and outdoor associated bacteria, with few pathogenic bacteria making them similar to other built environments such as your home. The research is published ahead of print in Applied and Environmental Microbiology.
In the study, the investigators characterized the structure, function, and abundance of the microbial community, on floors, toilet seats, and soap dispensers, following decontamination of each surface. They analyzed the surfaces hourly at first, and then daily, for up to eight weeks. “We hypothesized that while enteric bacteria would be dispersed rapidly due to toilet flushing, they would not survive long, as most are not good competitors in cold, dry, oxygen-rich environments,” says corresponding author Jack A. Gilbert of San Diego State University. “As such, we expected the skin microbes to take over—which is exactly what we found.”
“Reproduceable successional ecology is remarkable,” says Gilbert, who has conducted similar studies of the home (www.homemicrobiome.com), and the hospital (www.hospitalmicrobiome.com). “Most systems have the potential to have multiple outcomes. The restroom surfaces, though, were remarkably stable, always ending up at the same endpoint.”
Indeed, the communities associated with each surface became more similar in species and abundance within five hours following initial sterilization, and the resulting late-successional surface community structure remained stable for the remainder of the 8 weeks’ sampling. Floor communities showed a rapid reduction in abundance of Firmicutes and Bacteroidetes, while the relative abundance of Proteobacteria, Cyanobacteria, and Actinobacteria declined over the course of a day. Cyanobacteria are likely derived from dietary plant biomass or from plant material tracked in from outdoors.
Toilet seat samples, alone, clustered according to restroom gender, with Lactobacillus and Anaerococcus—vaginal flora—dominating ladies’ room toilet seats, while the gut-associated Roseburia and Blautia, were more copious on toilet seats in men’s rooms.
Ultimately, skin and outdoor-associated taxa comprised 68-98 percent of cultured communities, with fecal taxa representing just 0-15 percent of these. And out-door-associated taxa predominated in restrooms prior to sterilization, as well as in long-term post-sterilization communities, suggesting that over the long term, human-associated bacteria need to be dispersed in restrooms in order to be maintained there.
Overall, the research suggests that the restroom is no more healthy or unhealthy than your home, says Gilbert.”A key criterion of of healthy or unhealthy might be the presence or relative abundance of pathogens. While we found cassettes associated with methicillin-resistant Staphylococcus aureus (MRSA) the predominant Staph organisms didn’t harbor those genes, so MRSA may be there but it is very rare.” Restrooms, he says, are not necessarily unhealthy, but classifying them as healthy would not necessarily be accurate.
The research, he says, is very important for understanding the environmental ecology of the built environment, and will likely help in building restrooms and buildings generally that are healthier for humans.
Journal of Virology is a publication of the American Society for Microbiology (ASM). The ASM is the largest single life science society, composed of over 39,000 scientists and health professionals. Its mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.
WASHINGTON, DC - November 13, 2014 -- The strains of enterotoxigenic Escherichia coli (ETEC) that infect adults and children in Asia, Africa, and the Americas, have notably similar toxins and virulence factors, according to research published ahead of print in the Journal of Bacteriology. That bodes well for vaccine development, says corresponding author Åsa Sjöling, now of the Karolinska Institutet, Stockholm, Sweden. ETEC infects 400 million people annually, or 5.3 percent of the world's population, killing 400,000.
In the study, Sjöling et al. set out to determine whether the heat labile toxin (LT) had become more toxic over time, and whether the bacterium had evolved to secrete more of it. LT causes the "travelers' diarrhea" that so frequently afflicts Americans abroad, and that plagues residents of many low and middle income countries. But they found that over the 30 year period from which they had isolates, the two most potent toxin types, LT1 and LT2, had changed little but had spread globally.
"When new ETEC strains acquire either LT1 or LT2 they seem to have a much better chance to persist and spread," says Sjöling. Colonization factors, the compounds the bacterium uses to adhere to the lining of the human got, also remained conserved over time, and the most common colonization factors identified globally were often associated with LT1 and LT2.
The research results from a collaboration between the University of Gothenburg (where Sjöling did this research), which has the world's largest collection of ETEC strains, and sequencing experts at the Sanger Institute, Cambridge, UK. "We soon saw that strains with similar toxin variants and colonization factor profiles often remained closely related despite having been isolated on different continents, with time spans between those isolations ranging up to 30 years," says Sjöling.
The paper is published concurrently with a paper in Nature Genetics by many of the same authors. In that paper, investigators developed whole-genome sequence data for 362 ETEC strains over 30 years, in 20 countries. "This research strengthens our belief that it is possible to target a broad range of ETEC groups with one vaccine," says Gordon Dougan of the Sanger Institute, a coauthor of both papers.
"We believe that the vaccine developed at the University of Gothenburg will be protective and useful globally since this vaccine is based on the toxin types and colonization factors we found to be most successful worldwide," says Sjöling.
While ETEC was believed to vary widely from place to place, the Nature Genetics investigators traced many of the 21 lineages to an individual bacterium that acquired the genetic information needed to infect humans between 51 and 174 years ago, and then spread. That, in turn, suggests that the bacterium is stable, and that it is unlikely to become vaccine-resistant, and that the vaccine will be effective worldwide in both children and adults, says Sjöling.
Journal of Bacteriology is a publication of the American Society for Microbiology (ASM). The ASM is the largest single life science society, composed of over 39,000 scientists and health professionals. Its mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.
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