Gastrointestinal Mucosal Pathobiology [GMPB]

[GMPB Roster]

The Gastrointestinal Mucosal Pathobiology [GMPB] Study Section reviews applications involving gastrointestinal immunology, host-microbial interactions, intestinal infections and inflammation including chronic inflammatory bowel disease. The intestinal epithelium is the interface between the intestinal immune system and the microbiota; thus epithelial cell biology as it relates to mucosal defense or repair is also included.

Specific areas covered by GMPB:

  • Gastrointestinal mucosal immunology including but not limited to studies on gut associated lymphoid tissue (GALT), intraepithelial lymphocytes (IEL), lamina propria lymphocytes (LPL), and draining mesenteric lymph nodes.
  • Gastrointestinal responses to bacterial and dietary antigens including active immunity or tolerance, and the role of mucosal adjuvants in triggering either pathway.
  • Mechanisms of innate immunity in host defense in the gastrointestinal system, including cryptins, defensins, lysozyme, mucins, and natural IgA decoy receptors.
  • Mucosal immune and inflammatory responses to H. pylori infection.
  • Mucosal receptors for pathogens (including toxin) and for molecular pattern recognition (toll-receptors, and like receptors, NOD2).
  • Mechanisms of acute and chronic intestinal inflammation in experimental models including studies on genetic susceptibility as they relate to pathogenesis.
  • Basic and clinical studies in human inflammatory bowel disease, gluten sensitive enteropathy, auto-immune gastritis, and other types of immune-mediated gastrointestinal diseases.
  • Identification of microbes/microbial products that drive chronic intestinal inflammation.
  • Mechanisms of tissue injury and repair in intestinal inflammation.
  • Interactions between the microbiota and intestinal mucosa including the effects of probiotics.
  • Gastrointestinal cell biology and barrier function including cytokine and chemokine production in response to pathogens, toxins or chemical injury.
  • Intestinal responses to enteric pathogens including enterocyte and immune responses.
  • Host cell responses (including inflammatory mechanisms) to invasion by microbial pathogens in the gastrointestinal system.
  • Gastrointestinal responses to food-borne infections, including toxin-mediated and invasive pathogens, and agents likely to be employed in bioterrorism
  • Oxidant-induced injury including ischemia-reperfusion injury, neutrophil activation and endothelial cell responses
  • Studies of GI tract related to dysplasia and pre-neoplasia as a consequence of chronic GI infection or inflammation, including familial adenomatous polyposis (FAP), and mechanisms of hereditary syndromes.
  • NSAID-induced gastrointestinal injury and inflammation.
  • Effects of alcohol or other toxicants on the gastrointestinal immune system.

GMPB has the following shared interests within the DIG IRG:

There are shared interests in signal transduction, oxidative stress epithelial biology and barrier, and genetic basis of disease with other study sections in the IRG. Assignments to GMPB will be based on a central focus on immunity, infection or inflammation of the gastrointestinal tract.

  • With Gastrointestinal Cell and Molecular Biology [GCMB]:  Applications with a focus on transcription factors such as NF-kappaB in animal models or humans with inflammation or infection could be assigned to GMPB, while studies of transcription factors and gene regulation without such a focus will be assigned to GCMB.  Studies on dysplasia and pre-neoplasia as a consequence of chronic gastrointestinal infection or inflammation will be assigned to GMPB. All other studies in this area will be assigned to GCMB. Molecular and genetic studies of Barrett's esophagus would be assigned to GCMB.
  • With Hepatobilary Biology and Pathobiology [HBPP]: Studies regarding hepatic infection, inflammation or immune responses are appropriate for assignment to HBPP. 
  • With Clinical and Integrative Gastrointestinal Pathobiology [CIGP]: CIGP will be assigned studies regarding genetic susceptibility to IBD in humans.  Studies involving functional analysis of genes associated with the pathogenesis of IBD or other gastrointestinal inflammatory states will be assigned to GMPB.  Patient oriented GI research would be assigned to CIGP.  Studies on pancreatitis will be assigned to CIGP.

GMPB has the following shared interests outside the DIG IRG:

  • With the Risk, Prevention and Health Behavior [RPHB] IRG: Applications that focus on physiologic or biologic processes of gastrointestinal disorders could be referred to GMPB; applications with the primary focus on psychological, behavioral or social-risk factors as well as clinical trials of behavioral medicine and lifestyle-based gastrointestinal prevention strategies and therapies could be referred to RPHB.
  • With the Immunology [IMM] IRG: There are several shared interests between GMPB and the IMM IRG in the area of mucosal immunology and inflammation. Typically, studies of general mucosal immunology, where the focus is on the immune system, would be assigned to the Immunology IRG.   Similarly, studies on inflammatory bowel disease, gluten sensitive enteropathy, and other types of immune-mediated gastrointestinal diseases, where the focus is on the gastrointestinal system or liver, would be assigned to GMPB.
  • With the Infectious Diseases and Microbiology [IDM] IRG:  Assignment to GMPB may be appropriate for applications where the focus is on the mucosal-based inflammatory responses to pathogenic microbes and their products. Assignment to the IDM IRG may be appropriate for studies where the focus is the pathogen, or antibiotic therapy.
  • With the Oncological Sciences [ONC] IRG: In general, studies of GI dysplasia, and pre-neoplastic conditions of the GI system or liver would be assigned to GCMB.  Studies of familial adenomatous polyosis (FAP) as well as the pathology and treatment of polyps in the GI system would be assigned to GMPB.  Studies that focus on GI or liver cancers would be assigned to the ONC IRG.


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Last updated: February 20, 2008

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