‘Villain’ gut bacteria may help control diabetes

BLACKSBURG, Va., Feb. 8, 2013 – A stomach bacterium believed to cause health problems such as gastritis, ulcers, and gastric cancer may play a dual role by balancing the stomach’s ecosystem and controlling body weight and glucose tolerance, according to immunologists at the Virginia Bioinformatics Institute of Virginia Tech.

Usually the villain in studies of gastric cancer and peptic ulcers, Helicobacter pylori infect about half of the world’s population although most infected individuals don’t get sick. The bacterium’s dwindling numbers coincide with the epidemic of obesity and diabetes in developed countries.

“H. pylori is the dominant member of the gastric microbiota and infects about half of the world population. While H. pylori infection can be associated with severe disease, it helps control chronic inflammatory, allergic, or autoimmune diseases,” said Josep Bassaganya-Riera, director of the Nutritional Immunology and Molecular Medicine Laboratory (NIMML, www.nimml.org) and the Center for Modeling Immunity to Enteric Pathogens (MIEP, www.modelingimmunity.org) at Virginia Tech. “We demonstrated for the first time that gastric colonization with H. pylori exerts beneficial effects in mouse models of obesity and diabetes.”

During the past 20 years, obesity in the United States has increased dramatically, according to the Centers for Disease Control and Prevention. About 36 percent of U.S. adults and approximately 17 percent of young people aged 2 to 19 years are obese. Obesity is the leading risk factor for type 2 diabetes and the rates of diabetes have increased in parallel with the rates of obesity.

Mice infected with H. pylori showed less insulin resistance than uninfected mice or other mice infected with a more virulent strain of H. pylori, according to the study. Researchers believe that whether the infection is harmful or beneficial depends on the interaction between the genetic makeup of H. pylori and host’s immune response.

H. pylori carrying cytotoxin-associated gene pathogenicity island were harmful. But the bacteria without or with an atypical island may be integral parts of human stomach microbiota. Indeed, studies show that humans have been colonized by H. pylori for about 116,000 years.

“The role of H. pylori as a pathogen does not provide an explanation as to why it has colonized the stomach of humans thousands of years. Our new findings suggest that H. pylori may provide important metabolic traits required to ameliorate diabetes that humans have not evolved on their own,” Bassaganya-Riera said. “This suggests that the overuse of antibiotics for everything from misdiagnosed infections in humans to supplementary livestock feed may destroy beneficial bacteria and contribute directly to diseases such as obesity, allergies, inflammatory bowel disease, and asthma. It may be time for humans to reconsider how we can better co-exist with H. pylori and other microbes as a means of promoting health.”

“This novel findings underscore the complex relationship between H. pylori and humans, with effects not limited to the stomach, but more broadly affecting systemic inflammation and metabolism,” said Martin Blaser, Frederick H. King Professor of Internal Medicine and Chairman of the Department of Medicine; Professor of Microbiology at New York University School of Medicine.

“To better understand the complex relationship between H. pylori and the human host and to better predict health outcomes the Center for Modeling Immunity to Enteric Pathogens has developed computer models of the mechanisms by which H. pylori interacts with the host and new tools for investigating such interactions,” Bassaganya-Riera said.

To see more about tracing the evolutionary history of H. pylori, please see: Here.

To learn more about the role of antibiotics and gut bacteria in obesity, please see: Here.

Read related papers:

¹Bassaganya-Riera J MG Dominguez-Bello B. Kronsteiner A. Carbo M. Viladomiu M. Pedragosa P. Lu X. Zhang B.W. Sobral S. Mane S.K. Mohapatra W.T. Horne A.G. Guri M. Groeschl G. Lopez-Velasco and R. Hontecillas (2012). Helicobacter pylori colonization ameliorates glucose homeostasis in mice through a PPAR gamma-dependent mechanism. Plos One, 7(11): e50069.

²Mane SP, Dominguez-Bello MG, Blaser MJ, Sobral BW, Hontecillas R, Skoneczka J, Mohapatra SK, Crasta OR, Evans C, Modise T, Shallom S, Shukla M, Varon C, Mégraud F, Maldonado-Contreras AL, Williams KP, Bassaganya-Riera J. (2010) Host-Interactive Genes in Amerindian Helicobacter pylori Diverge From Their Old World Homologs and Mediate Inflammatory Responses. Journal of Bacteriology 192(12): 3078-3092.

Please visit the MIEP Web Portal at www.modelingimmunity.org.

MIEP is funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, under Contract No. HHSN272201000056C. PI: Josep Bassaganya-Riera.

About NIMML

The NIMML Institute is a 501 (c) (3) non-profit public charity foundation focused on a transdisciplinary, team-science approach to precision medicine at the interface of immunology, inflammation, and metabolism. The NIMML Institute team has led numerous large-scale transdisciplinary projects and is dedicated to solving important societal problems by combining the expertise of immunologists, computational biologists, toxicologists, modelers, translational researchers, and molecular biologists. The Institute is headquartered in Blacksburg, VA. For more information, please visit www.nimml.org or contact [email protected].