Martin J. Blaser | |
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Born | December 3, 1948 |
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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]
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]
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]
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]
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.
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.
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.
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.
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.
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.
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.
Skin flora, also called skin microbiota, refers to microbiota that reside on the skin, typically human skin.
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.
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.
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.
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.