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Mast cell degranulation induced by type 1 fimbriated Escherichia coli in mice
R Malaviya1, E Ross, B A Jakschik
1Department of Pathology, Jewish Hospital of St. Louis, Missouri 63110.
Abstract:
The strategic location of mast cells at the host-environment interface and their ability to release potent mediators of inflammation have suggested that these cells may play a pivotal role in host defense against bacterial infection. The ability of the opportunistic pathogen, Escherichia coli, to induce degranulation of mast cells obtained from the mouse peritoneum was investigated. We determined that unlike a mutant derivative deficient in the FimH subunit of the fimbriae or nonfimbriated E. coli, type 1 fimbriated E. coli induced mast cell degranulation in vitro. The magnitude of mast cell degranulation was directly proportional to the number of adherent bacteria on the cell surface in the initial period of the interaction. Using a mouse model of bacterial peritonitis, we demonstrated mast cell degranulation and histamine release by type 1 fimbriated bacteria in vivo. Furthermore, beads coated with FimH but not with FimA, the major subunit of type 1 fimbriae, evoked mast cell release of histamine in vivo in amounts comparable to that elicited by type 1 fimbriated E. coli. These studies reveal that mast cells can be degranulated by interaction with type 1 fimbriated E. coli and that FimH, the mannose-binding component of the fimbriae, is a potent mast cell stimulant.
Insights
Type 1 fimbriated Escherichia coli trigger mast cell degranulation. The FimH protein on these bacteria is identified as a key stimulant for mast cell activation and histamine release, crucial in host defense.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Mast cells, strategically positioned at host-environment interfaces, are implicated in host defense against bacterial infections due to their inflammatory mediator release.
- Escherichia coli, an opportunistic pathogen, possesses fimbriae, which are crucial for bacterial adhesion and virulence.
Purpose of the Study:
- To investigate the capacity of Escherichia coli to induce mast cell degranulation.
- To identify the specific bacterial components responsible for mast cell activation.
Main Methods:
- In vitro degranulation assays using mouse peritoneal mast cells and various strains of Escherichia coli (type 1 fimbriated, FimH-deficient mutant, nonfimbriated).
- In vivo studies using a mouse model of bacterial peritonitis to assess mast cell degranulation and histamine release.
- Experiments using FimH-coated beads to evaluate the role of FimH in histamine release.
Main Results:
- Type 1 fimbriated Escherichia coli, but not FimH-deficient or nonfimbriated strains, induced significant mast cell degranulation in vitro.
- Mast cell degranulation magnitude correlated with bacterial adherence.
- In vivo, type 1 fimbriated bacteria induced mast cell degranulation and histamine release.
- FimH-coated beads mimicked the histamine-releasing effect of fimbriated E. coli in vivo.
Conclusions:
- Mast cells are activated and degranulated by interaction with type 1 fimbriated Escherichia coli.
- The FimH protein, a mannose-binding component of type 1 fimbriae, is identified as a potent stimulant for mast cell degranulation and histamine release.
- FimH plays a critical role in initiating mast cell responses during bacterial peritonitis.
