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Microbial Metabolite Butyrate Suppresses Murine Mast Cell Activation
Author(s) -
Zhang Hanying,
Du Min,
Xue Yansong,
Yang Qiyuan,
Zhu Meijun
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.607.4
Subject(s) - degranulation , sodium butyrate , apoptosis , acetylation , cell growth , mast cell , microbiology and biotechnology , cytokine , butyrate , histone deacetylase , chemistry , histone , biology , immunology , biochemistry , receptor , fermentation , gene
Background Mast cell is known for its roles in mediating food allergy and regulating gut inflammation. Butyrate, a major short chain fatty acid produced by gut microbiota, exerts beneficial effects on intestinal homeostasis. However, its role in modulating mast cell function remain undefined. Methods: Murine mastocytoma P815 cells (P815) or murine bone marrow derived mast cells (BMMC) were treated with sodium butyrate (NaB). The proliferation, cell cycle, apoptosis, degranulation and cytokine secretion were assessed. Results In P815 cells, NaB inhibited cell proliferation, increased acetylation of both histone 3 and α‐tubulin. The growth inhibition effect of NaB is probably through reducing c‐kit expression and inducing cell cycle arrest and apoptosis, which is indicated by enhanced annexin V/PI staining, caspase‐3 and PARP cleavage. In BMMC, NaB treatment dramatically suppressed FcεRI dependent TNFα and IL‐6 release without affecting degranulation. Furthermore, NaB enhanced histone 3 acetylation but diminished mRNA expression of Tnf ‐α and Il‐6 , possibly through inhibiting the transcription initiation as revealed by reduced RNA polymerase II binding to the promoters of Tnf‐α and Il‐6 . Conclusions NaB modulates murine mast cell function possibly through enhancing histone acetylation, which is of importance in developing therapeutics for diseases involving mast cells (NIH R15HD073864).