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Bacteria--Mast Cell Interactions in Inflammatory Disease.
Ravi Malaviya1, Teruo Ikeda, Elaine A. Ross
1Department of Pathology, Jewish Hospital of St. Louis, St. Louis, USA.
American Journal of Therapeutics
|October 1, 1995
Summary
Type 1 fimbriated E. coli adhere to and are killed by intestinal mast cells. This interaction triggers mast cell degranulation, releasing inflammatory mediators and impacting gastrointestinal inflammatory diseases.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Chronic gastrointestinal inflammatory diseases involve mast cell proliferation and mediator secretion.
- The specific factors stimulating mast cells in the gut mucosa remain unidentified.
Purpose of the Study:
- To investigate the interaction between intestinal mast cells and type 1 fimbriated Escherichia coli.
- To determine the role of fimbriae in E. coli adherence to mast cells and subsequent mast cell responses.
Main Methods:
- Co-culture of rat mast cells with type 1 fimbriated E. coli, a fimH mutant, and nonfimbriated E. coli.
- Assessment of bacterial adherence, phagocytosis, and mast cell degranulation.
- Measurement of mast cell bactericidal activity, including superoxide anion generation and phagosome acidification.
Main Results:
- Type 1 fimbriated E. coli, but not the fimH mutant or nonfimbriated E. coli, adhered strongly to mast cells.
- Mast cells phagocytosed and killed adherent type 1 fimbriated E. coli via superoxide generation and vacuole acidification.
- Mast cell degranulation occurred, leading to the release of inflammatory mediators like histamine.
Conclusions:
- Type 1 fimbriated E. coli interact with and are eliminated by intestinal mast cells.
- This interaction contributes to mast cell activation and mediator release, with implications for gastrointestinal inflammation.
- Understanding this host-pathogen interaction is crucial for both normal immune defense and inflammatory disease pathogenesis.