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Butyrate protects against disruption of the blood‐milk barrier and moderates inflammatory responses in a model of mastitis induced by lipopolysaccharide
Author(s) -
Wang JingJing,
Wei ZhengKai,
Zhang Xu,
Wang YaNan,
Fu Yunhe,
Yang ZhengTao
Publication year - 2017
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.13976
Subject(s) - lipopolysaccharide , occludin , barrier function , inflammation , mastitis , butyrate , chemistry , immunology , intestinal permeability , sodium butyrate , pharmacology , tight junction , medicine , biology , microbiology and biotechnology , biochemistry , fermentation , gene
Background and Purpose Short‐chain fatty acids are fermentation end products produced by gut bacteria, which have been shown to ameliorate inflammatory bowel diseases and allergic asthma. However, the mechanism involved remains largely unknown. Here, we investigate the protective effects and mechanisms of sodium butyrate (SB) on LPS‐induced mastitis model. Experimental Approach Effects of increasing doses of SB on blood‐milk barrier function and inflammation are studied in BALB/c mice with LPS‐induced mastitis. The underlying mechanisms of anti‐inflammatory effects of SB were further investigated in LPS‐stimulated mouse mammary epithelial cells (mMECs). Key Results The results show that SB decreased LPS‐induced disruption in mammary tissues, infiltration of inflammatory cells and the levels of TNF‐α, IL‐6 and IL‐1β. SB up‐regulated the tight junction proteins occludin and claudin‐3 and reduced blood‐milk barrier permeability in LPS‐induced mastitis. Studies in vitro revealed that SB inhibited LPS‐induced inflammatory response by inhibition of the NF‐κB signalling pathway and histone deacetylases in LPS‐stimulated mMECs. Conclusions and Implications In our model, SB protected against LPS‐induced mastitis by preserving blood‐milk barrier function and depressing pro‐inflammatory responses, suggesting the potential use of SB as a prophylactic agent to protect blood‐milk barrier function in mastitis.