Martin J. Blaser
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Martin J. Blaser is the Muriel G. and George W. Singer Professor of Translational Medicine, Director of the NYU Human Microbiome Program, former Chair of the Department of Medicine, and Professor of Microbiology at New York University School of Medicine. In 2013 he was elected to the American Academy of Arts and Sciences. He is an established researcher in microbiology and infectious diseases. Blaser's work has focused on Helicobacter pylori, Campylobacter species, Bacillus anthracis, and more recently on the human microbiome.
Blaser obtained his undergraduate education from the University of Pennsylvania in 1969, graduated from the New York University School of Medicine in 1973, and did his post-graduate training at the University of Colorado School of Medicine from 1973 to 1979. Blaser then was an Epidemic Intelligence Service Officer at the Centers for Disease Control and Prevention from 1979 to 1981.
In 1998, Blaser established the Foundation for Bacteria.
In 2005, Blaser was elected the President of the Infectious Diseases Society of America. He has served the National Institutes of Health on the Board of Scientific Counselors of the National Cancer Institute (2005–2010; Chair 2009–2010), and on the Advisory Board for Clinical Research (2009–2013). In 2011, he was elected into the Institute of Medicine, in recognition of professional achievement and commitment to service in medicine and health.
Blaser is best known for his studies of Helicobacter pylori and its relationship with human diseases. His work helped establish the role of H. pylori in the causation of gastric cancer, the second leading cause of cancer death in the world. Studies of the diversity of H. pylori lead him to identify the CagA protein and its gene in 1989, which broadened understanding of H. pylori interactions with humans. His team found that cagA+ strains induced enhanced host responses, development of atrophic gastritis, gastric cancer, and peptic ulcer disease, compared to cagA− strains, and that cagA+ strains signal human gastric cells differently from cagA− strains, and affect gastric physiology in markedly different ways than in the absence of H. pylori. This work led to a general model for the persistence of co-evolved organisms, based on the presence of a Nash equilibrium, and also for the relationship of persisting microbes to cancer.
Beginning in 1996, he hypothesized that H. pylori strains might have benefit to humans as well as costs. Despite considerable and ongoing skepticism by the community of H. pylori investigators, Blaser and his colleagues progressively developed a body of research that provided evidence that gastric colonization by this organism provided protection against the esophageal diseases of GERD (gastroesophageal reflux disease), Barrett's esophagus, and esophageal adenocarcinoma, work that has been confirmed by independent investigators. His work has suggested a benefit of H. pylori against such early life illnesses as childhood diarrhea and asthma. This work is consistent with the hypothesis that H. pylori is an ancient, universal inhabitant of the human stomach that has been disappearing as a result of 20th century changes in socio-economic status, including the use of antibiotics.
In 1998, Blaser created the term acagia, to indicate a susceptibility for esophageal diseases in persons not carrying cagA+ H. pylori strains. Since then, acagia has come to reflect the rise in other diseases associated with the loss of cagA+ H. pylori, and may become a metaphor for the disappearance of members of the human microbiome that have symbiotic roles. In 2009, with Stanley Falkow, he hypothesized that human microecology is rapidly changing with potentially substantial consequences. He envisioned a step-wise (generational) change to explain the epidemic rise of such diseases as childhood-onset asthma and obesity. Blaser has proposed that greater understanding of our indigenous (and sometimes disappearing) microbiota can lead to improvements in human health.
He has proposed that the routine use (and overuse) of antibiotics in young children may be causing collateral damage, with extinctions of our ancient microbiota at critical stages of early life. This scenario may be contributing to the risk of epidemic metabolic, immunologic, and developmental disorders.
- Blaser MJ. The bacteria behind ulcers. Scientific American February, 1996; 274:104–109.
- Atherton JC, Blaser MJ. Co-adaptation of Helicobacter pylori and humans: ancient history, modern implications. Journal of Clinical Investigation 2009; 119:2475–87.
- Nomura A, Stemmerman GN, Chyou P-H, Kato I, Pérez-Pérez GI, Blaser MJ. Helicobacter pylori infection and gastric carcinoma in a population of Japanese-Americans in Hawaii. New England Journal of Medicine 1991; 325:1132–1136.
- Blaser MJ, Pérez-Pérez GI, Kleanthous H, Cover TL, Peek RM, Chyou PH, Stemmermann GN, Nomura A. Infection with Helicobacter pylori strains possessing cagA associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Research 1995; 55:2111–2115.
- Blaser MJ, Kirschner D. The equilibria that permit bacterial persistence in human hosts. Nature 2007; 449:843–849.
- Blaser MJ. Understanding microbe-induced cancers. Cancer Prevention Research 2008; 1:15–20.
- Blaser MJ. An endangered species in the stomach. Scientific American, February 2005; 292:38–45.
- Blaser MJ. Disappearing microbiota: Helicobacter pylori protection against esophageal adenocarcinoma. Cancer Prevention Research 2008; 1:308–311.
- Blaser MJ. Who are we? Indigenous microbes and the ecology of human diseases. EMBO Reports 2006; 7:956–960.
- Blaser MJ, Falkow S. What are the consequences of the disappearing human microbiota? Nature Reviews Microbiology 2009; 7:887–894.
- Blaser MJ. Harnessing the power of the human microbiome. Proceedings of the National Academy of Sciences, USA. 2010; 107:6125–6126.
- Blaser MJ. Antibiotic overuse: Stop the killing of beneficial bacteria. Nature 2011; 476:393–394.
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