Mast Cells Play a Crucial Role in Staphylococcus aureus Peptidoglycan-Induced Diarrhea

Feng, Bai–Sui; He, Shaoheng; Zheng, Peng‐Yuan; Wu, Linda; Yang, Ping‐Chang

doi:10.2353/ajpath.2007.061274

Cited by 61 publications

(57 citation statements)

References 46 publications

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“…Oral intake of histamine-rich foods induces gastrointestinal symptoms in humans, such as diarrhea and flatulence (36). Activated, subsequently degranulated intestinal mast cells, which are increased in a mouse model of diarrhea induced by oral ingestion of Staphylococcus aureus peptidoglycan and histamine, are involved in the induction of diarrhea (37). Accordingly, mast cell activation by ASP-produced C5a, represented by histamine-dependent VL (Fig.…”

Section: Discussionmentioning

confidence: 99%

Production of C5a by ASP, a Serine Protease Released from Aeromonas sobria

Nitta¹,

Imamura²,

Wada

et al. 2008

The Journal of Immunology

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Aeromonas sobria causes pus and edema at sites of infection. However, the mechanisms underlying these effects have not been elucidated. C5a, the amino-terminal fragment of the complement 5th component (C5), mimics these events. To investigate the involvement of C5a in the pathophysiology of A. sobria infection, we examined release of C5a from human C5 by a serine protease (ASP), a putative virulence factor secreted by this bacterium. C5 incubated with enzymatically active ASP induced neutrophil migration in a dose-dependent manner from an ASP concentration of 3 nM and in an incubation time-dependent manner in as little as 7 min, with neutrophil accumulation in guinea pigs at intradermal injection sites and neutrophil superoxide release. These effects on neutrophils were inhibited by a C5a-receptor antagonist. The ASP incubation mixture with C5 but not C3 elicited vascular leakage in a dose- and incubation time-dependent manner, which was inhibited by a histamine H1-receptor antagonist. Together with these C5a-like activities, ASP cleaved C5 to release only one C5a Ag, the m.w. of which was similar to that of C5a. Immunoblotting using an anti-C5a Ab revealed generation of a C5a-like fragment from human plasma incubated with ASP. These results suggest that ASP-elicited neutrophil migration and vascular leakage via C5a production from C5 could occur in vivo, which was supported by that ASP did not affect functions of C5a and neutrophil C5a receptor. Through C5a generation, ASP could be associated with the induction of pus and edema caused by infection with this bacterium.

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Section: Discussionmentioning

confidence: 99%

Production of C5a by ASP, a Serine Protease Released from Aeromonas sobria

Nitta¹,

Imamura²,

Wada

et al. 2008

The Journal of Immunology

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“…20 One previous report indicated that TLR5 recognizes flagellin. 21,22 We thus took another approach to elucidate if flagellin activated mast cell via acting on TLR5 to elicit the release of inflammatory mediators that might contribute to the initiation of mucosal inflammation.…”

Section: Flagellin-specific Immune Response Induces Momcs To Release mentioning

confidence: 99%

“…20 Cultured mast cells (Ͼ95% purity) were injected to W/W v mice via the tail vein at a dose of 50,000 cells/mouse in 0.25 saline; the transfer was executed once more, 1 month later. The mice were used for flagellin sensitization experiments 2 months after the first mast cell reconstitution.…”

Section: Reconstitution Of Mast Cell In W/w V Micementioning

confidence: 99%

Fc Gamma Receptor Signaling in Mast Cells Links Microbial Stimulation to Mucosal Immune Inflammation in the Intestine

Chen

Feng

Zheng

et al. 2008

The American Journal of Pathology

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Microbes and microbial products are closely associated with the pathogenesis of inflammatory bowel disease (IBD); however, the mechanisms behind this connection remain unclear. It has been previously reported that flagellin-specific antibodies are increased in IBD patient sera. As mastocytosis is one of the pathological features of IBD, we hypothesized that flagellin-specific immune responses might activate mast cells that then contribute to the initiation and maintenance of intestinal inflammation. Thirtytwo colonic biopsy samples were collected from IBD patients. A flagellin/flagellin-specific IgG/Fc gamma receptor I complex was identified on biopsied mast cells using both immunohistochemistry and co-immunoprecipitation experiments; this complex was shown to co-localize on the surfaces of mast cells in the colonic mucosa of patients with IBD. In addition, an ex vivo study showed flagellin-IgG was able to bind to human mast cells. These cells were found to be sensitized to flagellin-specific IgG; re-exposure to

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“…Activation of MCs with NOD agonists results in the release of pro-inflammatory cytokines and inflammation in the intestine. 15 MC activation via NOD receptors has been linked to the development of inflammation during Crohn's disease and NOD2 expressing MCs are found in high numbers in the intestines of inflammatory bowel disease patients. 16 Interestingly, it has been shown that NOD ligands are not only derived from microbial pathogens but also from parasitic helminths and that these ligands help to drive Th2 immunity.…”

Section: How Do Mast Cells Contribute To Enhanced Tissue-derivedmentioning

confidence: 99%