Martin J. Blaser

Last updated
Martin J. Blaser
Martin Blaser working in his lab at the NYU Langone Medical Center.jpg
Blaser in his lab with Xuesong Zhang
Born (1948-12-03) December 3, 1948 (age 74)
Alma mater
Spouses
Scientific career
Institutions Robert Wood Johnson Medical School

Martin J. Blaser (born 1948) [1] is the director of the Center for Advanced Biotechnology and Medicine at Rutgers (NJ) Biomedical and Health Sciences and the Henry Rutgers Chair of the Human Microbiome and Professor of Medicine and Pathology and Laboratory Medicine at the Rutgers Robert Wood Johnson Medical School in New Jersey. [2]

Contents

In 2013, Blaser was elected to the American Academy of Arts and Sciences. He is a researcher in microbiology and infectious diseases. Blaser's work has focused on Helicobacter pylori , Campylobacter species, Salmonella , Bacillus anthracis , and on the human microbiome. [3] [4]

Education, early work, recent service

Blaser obtained his undergraduate education (bachelor's of arts degree in economics) from the University of Pennsylvania in 1969, graduated with an M.D. degree from the New York University School of Medicine in 1973, and did his post-graduate residency and fellowship at the University of Colorado School of Medicine from 1973 to 1979 in Internal Medicine and Infectious Diseases. [5]

Since 2013, Blaser has been married to fellow microbiome researcher and colleague Maria Gloria Dominguez-Bello. [6] [7] Two prior marriages, first to the artist Susan J. Walp [8] and later to the writer and editor Ronna Wineberg[ citation needed ] ended in divorce.

Blaser was an Epidemic Intelligence Service Officer at the Centers for Disease Control and Prevention from 1979 to 1981. [9]

In 1998, Blaser established the Foundation for Bacteria, which started the Virtual Museum of Bacteria. [10]

Blaser was elected as an officer of the Infectious Diseases Society of America, serving from 2004-2008, including a one-year term as president in 2006-2007. [11] He has served the National Institutes of Health (NIH) 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; Chair 2012-2013). In 2011, he was elected into the National Academy of Medicine (formerly Institute of Medicine), in recognition of professional achievement and commitment to service in medicine and health. [9] In 2013, he was elected to the American Academy of Arts and Sciences.

In 2014, he was the Kinyoun Lecturer at the National Institute for Allergy and Infectious Diseases (NIAID) at NIH, and received the Alexander Fleming Award for lifetime achievement from the Infectious Diseases Society of America. He received the Cura Personalis award from Georgetown University in 2015. His scientific papers have been cited more than 140,000 times (Google Scholar). He is one of three editors of Principles and Practice of Infectious Diseases (also known as Mandell), the 'bible' of textbooks in the field of Infectious Diseases, with >300 chapters; 10th edition is now being written.

In 2015, he was selected to be on the list of the TIME 100 Most Influential People in the world, [12] He served on the Advisory Council of the National Center for Complementary and Integrative Health (NCCIH) of the National Institutes of Health from 2015-2019. He was appointed by President Obama as the Chair of the President's Advisory Council on Combating Antibiotic-Resistant Bacteria (PACCARB) for a term from 2015–2022, serving in the Obama, Trump, and Biden administrations. In 2019, he founded the Rutgers University Microbiome Program (RUMP), which is a university-wide project to develop microbiome science, and examine its impact on health, agriculture, the environment, and human culture. He now co-leads RUMP with Rutgers professors Maria Gloria Dominguez Bello and Liping Zhao.

Blaser sits on scientific advisory boards for Elysium Health, [13] [14] Procter & Gamble, Dupont, and several biotechnology start-up companies. In June 2018, Blaser joined the Scientific Advisory Board of the newly founded Seed. [15] In December 2020, he became the chair of start-up Micronoma's scientific advisory board. [16] [17] He serves as Co-Chair of the Advisory Board of Humans and Microbiome program off the Canadian Institute for Advanced Research (CIFAR) a In 2019 he received the Robert-Koch-Medal in Gold, and the Karl August Mobius Fellowship from Kiel Life Sciences. [18] In 2021, he received the Prize Medal from the Microbiology Society (UK), for his studies of the human microbiome including Helicobacter pylori as an agent of disease in humans. [19] In 2022, he received an honorary doctoral degree from the University of Bordeaux (Docteur honoris causa) [20]

Research

Blaser is best known [21] for his studies of Helicobacter pylori and its relationship with human diseases. [22] [23] Initially dismissive and skeptical of Nobel laureate Barry Marshall's findings of H. Pylori's relationship to gastric and peptic ulcers, which Blaser described as "the most preposterous thing I’d ever heard; I thought, this guy is a madman,” [24] [25] Blaser's work nonetheless later helped establish the role of H. pylori in the causation of gastric cancer, the second leading cause of cancer death in the world. [26] 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. [27] 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. [23] This work led to a general model for the persistence of co-evolved organisms, based on the presence of a Nash equilibrium, [28] and also for the relationship of persisting microbes to cancer, [29] and age-related mortality. [30]

Beginning in 1996, he hypothesized that H. pylori strains might have benefit to humans as well as costs. [31] 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 gastroesophageal reflux disease (GERD), Barrett's esophagus, and esophageal adenocarcinoma, work that has since been confirmed by independent investigators. [32] 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 [33] that has been disappearing as a result of 20th century changes in socio-economic status, including the use of antibiotics and that this loss has health consequences, not only good (less gastric cancer), but bad as well (more esophageal disease and cancer, and more childhood-onset allergic asthma and hay fever).

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. [29] [32] In 2009, with Stanley Falkow, he hypothesized that human microecology is rapidly changing with potentially substantial consequences. [34] He envisioned a step-wise (generational) diminution in microbial diversity, especially in early life to explain the epidemic rise of such diseases as childhood-onset asthma and obesity. Blaser has proposed that greater understanding of our indigenous (and progressively disappearing) microbiota can lead to improvements in human health. [35]

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. [36] This scenario may be contributing to the risk of epidemic metabolic, immunologic, and neurodevelopmental disorders. [36] Studies in mice have contributed strong support to these hypotheses., [37] [38] [39] and on-going work in children with reference to many diseases, [40] including asthma, [41] [42] [43] show the importance of early life microbiome perturbation in increasing risk. [44] Recent studies with colleagues at the Mayo Clinic have shown a strong association of antibiotic exposure before the age of two and the development of multiple condition in later childhood, including asthma, eczema, overweight and obesity, ADHD, and learning disability, [45] providing further support for his hypothesis. His studies in mice provide evidence that the effects of antibiotic perturbation on the microbiota can be transmitted via the mother to the next generation, affecting both intestinal micro-ecology and disease manifestations. [46] [47] In recent studies, he has shown that antibiotic-induced microbiota perturbation leading to disease (Type 1 diabetes) in an experimental mouse model can be interdicted by subsequent exposure of young animals maternal cecal contents; this work provides evidence and a proof-of-principle that the antibiotic-induced dysbiosis can be limited by restorative practices. [48]

Missing Microbes

Blaser is the author of a book for general audiences, Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues, about the degradation of internal microbial ecosystems of humans as a result of modern medical practices. Professional science writer Sandra Blakeslee helped write Missing Microbes [49] , which was published by Henry Holt and Co. in April 2014, and has been translated into 20 languages. [50] [51] [52] [53] The book was a finalist for the 2015 LA Times Book Prize in Science, and won the National Library of China's 2017 Wenjin Book Award. Under the leadership of his wife, Dr. Maria Gloria Dominguez Bello, a group of scientists have formed the Microbiota Vault, Inc. (www.microbiotavault.org ), a not-for-profit non-governmental organization (NGO) public charity in the United States; Blaser serves as a member of the Board of Directors and an officer of the Foundation. Modeled after the Seed Vault in Svalbard, Norway, the Microbiota Vault has the purpose of creating a repository for the preservation of the human microbiota for future generations before it disappears, and fostering research and education about the human microbiota in developing countries. [54] A documentary film with focus on the work of Blaser and Dominguez Bello entitled "The Invisible Extinction" [55] was created by film makers Steven Lawrence and Sarah Schenk. Its World premiere was at the Copenhagen documentary film festival (CPH:DOX) in March 2022.

Related Research Articles

Peptic ulcer disease (PUD) is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

<i>Helicobacter pylori</i> Species of bacteria

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, and are less effective. Its helical or spiral body is thought to have evolved in order to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren.

<span class="mw-page-title-main">Human microbiome</span> Microorganisms in or on human skin and biofluids

The human microbiome is the aggregate of all microbiota that reside on or within human tissues and biofluids along with the corresponding anatomical sites in which they reside, including the skin, mammary glands, seminal fluid, uterus, ovarian follicles, lung, saliva, oral mucosa, conjunctiva, biliary tract, and gastrointestinal tract. Types of human microbiota include bacteria, archaea, fungi, protists, and viruses. Though micro-animals can also live on the human body, they are typically excluded from this definition. In the context of genomics, the term human microbiome is sometimes used to refer to the collective genomes of resident microorganisms; however, the term human metagenome has the same meaning.

<i>Helicobacter</i> Genus of bacteria

Helicobacter is a genus of gram-negative bacteria possessing a characteristic helical shape. They were initially considered to be members of the genus Campylobacter, but in 1989, Goodwin et al. published sufficient reasons to justify the new genus name Helicobacter. The genus Helicobacter contains about 35 species.

In medicine, the hygiene hypothesis states that early childhood exposure to particular microorganisms protects against allergies by strengthening the immune system. In particular, a lack of such exposure is thought to lead to poor immune tolerance. The time period for exposure begins before birth and ends at school age.

<span class="mw-page-title-main">Gut microbiota</span> Community of microorganisms in the gut

Gut microbiota, gut microbiome, or gut flora, are the microorganisms, including bacteria, archaea, fungi, and viruses, that live in the digestive tracts of animals. The gastrointestinal metagenome is the aggregate of all the genomes of the gut microbiota. The gut is the main location of the human microbiome. The gut microbiota has broad impacts, including effects on colonization, resistance to pathogens, maintaining the intestinal epithelium, metabolizing dietary and pharmaceutical compounds, controlling immune function, and even behavior through the gut–brain axis.

Dysbiosis is characterized by a disruption to the microbiome resulting in an imbalance in the microbiota, changes in their functional composition and metabolic activities, or a shift in their local distribution. For example, a part of the human microbiota such as the skin flora, gut flora, or vaginal flora, can become deranged, with normally dominating species underrepresented and normally outcompeted or contained species increasing to fill the void. Dysbiosis is most commonly reported as a condition in the gastrointestinal tract.

Timeline of peptic ulcer disease and <i>Helicobacter pylori</i>

This is a timeline of the events relating to the discovery that peptic ulcer disease and some cancers are caused by H. pylori. In 2005, Barry Marshall and Robin Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery that peptic ulcer disease (PUD) was primarily caused by Helicobacter pylori, a bacterium with affinity for acidic environments, such as the stomach. As a result, PUD that is associated with H. pylori is currently treated with antibiotics used to eradicate the infection. For decades prior to their discovery, it was widely believed that PUD was caused by excess acid in the stomach. During this time, acid control was the primary method of treatment for PUD, to only partial success. Among other effects, it is now known that acid suppression alters the stomach milieu to make it less amenable to H. pylori infection.

<span class="mw-page-title-main">Skin flora</span> Microbiota that reside on the skin

Skin flora, also called skin microbiota, refers to microbiota that reside on the skin, typically human skin.

<span class="mw-page-title-main">Carcinogenic bacteria</span>

Cancer bacteria are bacteria infectious organisms that are known or suspected to cause cancer. While cancer-associated bacteria have long been considered to be opportunistic, there is some evidence that bacteria may be directly carcinogenic. The strongest evidence to date involves the bacterium H. pylori and its role in gastric cancer.

<span class="mw-page-title-main">Microbiota</span> Community of microorganisms

Microbiota are the range of microorganisms that may be commensal, mutualistic, or pathogenic found in and on all multicellular organisms, including plants. Microbiota include bacteria, archaea, protists, fungi, and viruses, and have been found to be crucial for immunologic, hormonal, and metabolic homeostasis of their host.

<span class="mw-page-title-main">Infectious causes of cancer</span>

Estimates place the worldwide risk of cancers from infectious causes at 16.1%. Viral infections are risk factors for cervical cancer, 80% of liver cancers, and 15–20% of the other cancers. This proportion varies in different regions of the world from a high of 32.7% in Sub-Saharan Africa to 3.3% in Australia and New Zealand.

Helicobacter pylori virulence factor CagA is a 120–145kDa protein encoded on the 40kb cag pathogenicity island (PAI). H. pylori strains can be divided into CagA positive or negative strains. Approximately 60% of H. pylori strains isolated in Western countries carry cag PAI, whereas almost all of the East Asian isolates are cag PAI-positive.

Helicobacter felis is a bacterial species in the Helicobacteraceae family, Campylobacterales order, Helicobacter genus. This bacterium is Gram-negative, microaerophilic, urease-positive, and spiral-shaped. Its type strain is CS1T. It can be pathogenic.

Helicobacter salomonis is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases, although its role in the development of many of these other diseases requires further study. Humans infected with H. salomonis may develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter suis, Helicobacter felis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. salomonis are often group together and termed Helicobacter heilmannii sensu lato.

Helicobacter heilmannii sensu lato refers to a group of bacterial species within the Helicobacter genus. The Helicobacter genus consists of at least 40 species of spiral-shaped flagellated, Gram-negative bacteria of which the by far most prominent and well-known species is Helicobacter pylori. H. pylori is associated with the development of gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and various subtypes of extranodal marginal zone lymphomas, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori has also been associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study.

Helicobacter bizzozeronii is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species, primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. bizzozeronii are prone to develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter felis, Helicobacter salomonis, Helicobacter suis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. bizzozeronii are often grouped together and termed Helicobacter heilmannii sensu lato.

Helicobacter suis is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species, primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. suis may develop some of the same gastrointestinal diseases - stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter salomonis, Helicobacter felis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. suis are often group together and termed Helicobacter heilmannii sensu lato.

Helicobacter heilmannii s.s. is a species within the Helicobacter genus of Gram negative bacteria. Helicobacter pylori is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the non-lymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. heilmannii s.s. may develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter suis, Helicobacter felis, and Helicobacter salomonis. Because of their disease associations, these four Helicobacter species plus H. heilmannii s.s. are often group together and termed Helicobacter heilmannii sensu lato.

<span class="mw-page-title-main">Maria Gloria Dominguez-Bello</span> American microbial ecologist

Maria Gloria Dominguez-Bello is a Venezuelan-American microbial ecologist that has worked on adaptations of gut fermentation organs in animals, gastric colonization by bacteria, assembly of the microbiota in early life, effect of practices that reduce microbiota transmission and colonization in humans, and effect of urbanization. She is the Henry Rutgers Professor of Microbiome and Health at Rutgers University, New Brunswick. Her lab at collaborates in multidisciplinary science, integrating microbiology, immunology, pediatrics, nutrition, anthropology, environmental engineering and architecture/urban studies, and microbial ecology.

References

  1. "Annette & Irwin Eskind Biomedical Library". library.vanderbilt.edu. Archived from the original on September 21, 2017. Retrieved June 2, 2021.
  2. "Rutgers Names New Director for Center for Advanced Biotechnology and Medicine". Rutgers Today. 2018-12-10. Retrieved 2018-12-23.
  3. "NYU Faculty Bibliography, 2000-: Martin Jack Blaser". NYU Health Sciences Libraries. Retrieved 2017-09-22.
  4. "NYU Blaser Lab Website".
  5. Blaser, Martin J. (1979-08-01). "Campylobacter Enteritis: Clinical and Epidemiologic Features". Annals of Internal Medicine. 91 (2): 179–185. doi:10.7326/0003-4819-91-2-179. ISSN   0003-4819. PMID   380433.
  6. Pollan, Michael (2013-05-15). "Some of My Best Friends Are Germs". The New York Times. ISSN   0362-4331 . Retrieved 2020-01-14.
  7. "Rutgers Love Stories: Groundbreaking Researchers of the Microbiome Have Great Chemistry". www.rutgers.edu. February 12, 2020. Retrieved 2020-03-23.
  8. "Martin Blaser, Medical Student, Marries Miss Susan J. Walp". The New York Times. 1972-07-10. ISSN   0362-4331 . Retrieved 2020-01-13.
  9. 1 2 CDC (2021-06-01). "CDC Works 24/7". Centers for Disease Control and Prevention. Retrieved 2021-06-02.
  10. "Bacteria Museum". www.bacteriamuseum.org.
  11. "IDSA Presidents". www.idsociety.org. Retrieved 2020-05-09.
  12. "Martin Blaser". Time.
  13. "Scientific Advisory Board - Pioneers in Science, Medicine & Aging". Elysium Health. Retrieved 2018-09-18.
  14. "Scientific Advisory Board - Martin J. Blaser, PhD". Elysium Health. Retrieved 2018-09-18.
  15. "We : Seed". seed.com. Retrieved 2018-09-18.
  16. "Micronoma Establishes Scientific Advisory Board". BioSpace. Retrieved 2021-01-10.
  17. "Micronoma | Saving patient lives with early cancer screening test" . Retrieved 2021-01-10.
  18. "Home". Robert-Koch-Stiftung.
  19. "Microbiology Society Prize Medal". Nov 26, 2020 via Wikipedia.
  20. "Présentation of the Honorary Doctorate Insigna". Bordeaux Institute of Oncology. Retrieved 2022-06-27.
  21. Specter, Michael. "Germs Are Us". The New Yorker. Retrieved 2021-06-02.
  22. Blaser MJ. "The bacteria behind ulcers. Scientific American February, 1996; 274:104–109.
  23. 1 2 Atherton, JC; Blaser, MJ (2009). "Co-adaptation of Helicobacter pylori and humans: ancient history, modern implications". Journal of Clinical Investigation. 119 (9): 2475–87. doi: 10.1172/jci38605 . PMC   2735910 . PMID   19729845.
  24. Thagard, Paul (March 1998). "Ulcers and bacteria I: discovery and acceptance". Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences. 29 (1): 107–136. doi:10.1016/s1369-8486(98)00006-5. ISSN   1369-8486.
  25. "Ulcers.and.Bacteria". cogprints.org. Retrieved 2021-01-10.
  26. Nomura, Abraham; Stemmermann, Grant N.; Chyou, Po-Huang; Kato, Ikuko; Perez-Perez, Guillermo I.; Blaser, Martin J. (1991-10-17). "Helicobacter pylori Infection and Gastric Carcinoma among Japanese Americans in Hawaii". New England Journal of Medicine. 325 (16): 1132–1136. doi: 10.1056/NEJM199110173251604 . ISSN   0028-4793. PMID   1891021.
  27. Blaser, M. J.; Perez-Perez, G. I.; Kleanthous, H.; Cover, T. L.; Peek, R. M.; Chyou, P. H.; Stemmermann, G. N.; Nomura, A. (1995-05-15). "Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach". Cancer Research. 55 (10): 2111–2115. ISSN   0008-5472. PMID   7743510.
  28. Blaser, MJ; Kirschner, D (2007). "The equilibria that permit bacterial persistence in human hosts". Nature. 449 (7164): 843–849. doi:10.1038/nature06198. hdl: 2027.42/62883 . PMID   17943121. S2CID   3166518.
  29. 1 2 Blaser MJ. Understanding microbe-induced cancers. Cancer Prevention Research 2008; 1:15–20.
  30. Blaser, MJ; Webb, GF (2014). "Host demise as a beneficial function of indigenous microbiota in human hosts". mBio. 5 (6): 1–9. doi: 10.1128/mBio.02262-14 . PMC   4271553 . PMID   25516618.
  31. Blaser MJ. "An endangered species in the stomach. Scientific American, February 2005; 292:38–45.
  32. 1 2 Blaser, MJ (2008). "Disappearing microbiota: Helicobacter pylori protection against esophageal adenocarcinoma". Cancer Prevention Research. 1 (5): 308–311. doi: 10.1158/1940-6207.capr-08-0170 . PMID   19138974.
  33. Blaser, MJ (2006). "Who are we? Indigenous microbes and the ecology of human diseases". EMBO Reports. 7 (10): 956–960. doi:10.1038/sj.embor.7400812. PMC   1618379 . PMID   17016449.
  34. Blaser, Martin J.; Falkow, Stanley (December 2009). "What are the consequences of the disappearing human microbiota?". Nature Reviews. Microbiology. 7 (12): 887–894. doi:10.1038/nrmicro2245. ISSN   1740-1534. PMC   9354563 . PMID   19898491. S2CID   8502776.
  35. Blaser, MJ (2010). "Harnessing the power of the human microbiome". Proceedings of the National Academy of Sciences USA. 107 (14): 6125–6126. Bibcode:2010PNAS..107.6125B. doi: 10.1073/pnas.1002112107 . PMC   2851969 . PMID   20360554.
  36. 1 2 Blaser, Martin (2011-08-24). "Antibiotic overuse: Stop the killing of beneficial bacteria". Nature. 476 (7361): 393–394. Bibcode:2011Natur.476..393B. doi: 10.1038/476393a . ISSN   1476-4687. PMID   21866137. S2CID   205066874.
  37. Cho, I; Yamanishi, S; Cox, L; Methé, BA; Zavadil, J; Li, K; Gao, Z; Mahana, D; Raju, K; Teitler, I; Li, H; Alekseyenko, AV; Blaser, MJ (2012). "Antibiotics in early life alter the murine colonic microbiome and adiposity". Nature. 488 (7413): 621–6. Bibcode:2012Natur.488..621C. doi:10.1038/nature11400. PMC   3553221 . PMID   22914093.
  38. Cox, LM; et al. (Aug 2014). "Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences". Cell. 158 (4): 705–21. doi:10.1016/j.cell.2014.05.052. PMC   4134513 . PMID   25126780.
  39. Nobel, Y; et al. (2015). "Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment". Nature Communications. 6: 7486. Bibcode:2015NatCo...6.7486N. doi: 10.1038/ncomms8486 . PMC   4491183 . PMID   26123276.
  40. Trasande, L; Blustein, J; Liu, M; Corwin, E; Cox, LM; Blaser, MJ (2013). "Infant antibiotic exposures and early life body mass". International Journal of Obesity. 37 (1): 16–23. doi: 10.1038/ijo.2012.132 . PMC   3798029 . PMID   22907693.
  41. Arrieta, Marie-Claire; Stiemsma, Leah T.; Dimitriu, Pedro A.; Thorson, Lisa; Russell, Shannon; Yurist-Doutsch, Sophie; Kuzeljevic, Boris; Gold, Matthew J.; Britton, Heidi M.; Lefebvre, Diana L.; Subbarao, Padmaja (2015-09-30). "Early infancy microbial and metabolic alterations affect risk of childhood asthma". Science Translational Medicine. 7 (307): 307ra152. doi: 10.1126/scitranslmed.aab2271 . ISSN   1946-6242. PMID   26424567. S2CID   206687974.
  42. Stokholm, Jakob; Blaser, Martin J.; Thorsen, Jonathan; Rasmussen, Morten A.; Waage, Johannes; Vinding, Rebecca K.; Schoos, Ann-Marie M.; Kunøe, Asja; Fink, Nadia R.; Chawes, Bo L.; Bønnelykke, Klaus (December 2018). "Maturation of the gut microbiome and risk of asthma in childhood". Nature Communications. 9 (1): 141. Bibcode:2018NatCo...9..141S. doi:10.1038/s41467-017-02573-2. ISSN   2041-1723. PMC   5762761 . PMID   29321519.
  43. Borbet, Timothy C.; Zhang, Xiaozhou; Müller, Anne; Blaser, Martin J. (December 2019). "The role of the changing human microbiome in the asthma pandemic". Journal of Allergy and Clinical Immunology. 144 (6): 1457–1466. doi:10.1016/j.jaci.2019.10.022. PMC   6905199 . PMID   31812180.
  44. Dominguez-Bello MG, Blaser MJ. "Asthma: Undoing millions of years of co-evolution in early life? Science Translational Medicine 2015; 7:307fs39.
  45. Aversa, Zaira; Atkinson, Elizabeth J.; Schafer, Marissa J.; Theiler, Regan N.; Rocca, Walter A.; Blaser, Martin J.; LeBrasseur, Nathan K. (January 2021). "Association of Infant Antibiotic Exposure With Childhood Health Outcomes". Mayo Clinic Proceedings. 96 (1): 66–77. doi:10.1016/j.mayocp.2020.07.019. PMC   7796951 . PMID   33208243.
  46. Schulfer, Anjelique F.; Battaglia, Thomas; Alvarez, Yelina; Bijnens, Luc; Ruiz, Victoria E.; Ho, Melody; Robinson, Serina; Ward, Tonya; Cox, Laura M. (2017-11-27). "Intergenerational transfer of antibiotic-perturbed microbiota enhances colitis in susceptible mice". Nature Microbiology. 3 (2): 234–242. doi:10.1038/s41564-017-0075-5. ISSN   2058-5276. PMC   5780248 . PMID   29180726.
  47. Blaser, Martin J. (March 2018). "The Past and Future Biology of the Human Microbiome in an Age of Extinctions". Cell. 172 (6): 1173–1177. doi: 10.1016/j.cell.2018.02.040 . ISSN   0092-8674. PMID   29522739.
  48. Zhang, Xue-Song; Yin, Yue Sandra; Wang, Jincheng; Battaglia, Thomas; Krautkramer, Kimberly; Li, Wei Vivian; Li, Jackie; Brown, Mark; Zhang, Meifan; Badri, Michelle H.; Armstrong, Abigail J.S. (October 2021). "Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice". Cell Host & Microbe. 29 (8): 1249–1265.e9. doi:10.1016/j.chom.2021.06.014. PMC   8370265 . PMID   34289377.
  49. "Sandra Blakeslee : Science Writer". www.sandrablakeslee.com. Retrieved 2016-12-12.
  50. McKenna, Maryn (April 2014). "Drugs: Gut response". Nature. 508 (7495): 182–183. Bibcode:2014Natur.508..182M. doi: 10.1038/508182a . ISSN   1476-4687.
  51. Mather, A. E. (2014-05-02). "Antibiotics and Collateral Damage". Science. 344 (6183): 472–473. Bibcode:2014Sci...344..472M. doi:10.1126/science.1252914. ISSN   0036-8075. S2CID   51602149.
  52. torrent 2019, Alien 303 vst. "Alien 303 Vst Torrent". Alien 303 Vst Torrent. Retrieved 2021-06-02.
  53. Brody, Jane E. (2014-07-14). "We Are Our Bacteria". Well. Retrieved 2021-06-02.
  54. Dominguez Bello, Maria Gloria (5 October 2018). "Preserving human microbial diversity: Microbiota from humans of all cultures are needed to ensure the health of future generations". Science. 362 (6410): 33–34. doi:10.1126/science.aau8816. PMID   30287652. S2CID   52919917.
  55. https://www.theinvisibleextinction.com/