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Palmitic acid activates murine mast cells via Toll like receptor 4 (TLR4)
Author(s) -
Zhang Hanying,
Zhao Junxing,
Wang Hui,
Du Min,
Zhu Mei-Jun
Publication year - 2012
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.26.1_supplement.877.13
Subject(s) - degranulation , tryptase , tlr4 , mast cell , interleukin 33 , toll like receptor , inflammation , innate immune system , microbiology and biotechnology , receptor , immune system , tlr7 , cytokine , immunology , biology , biochemistry , interleukin
Obesity has been closely correlated with aberrant immune status and increasing risk for associated inflammatory diseases. Free fatty acid, which increases in obese condition, is demonstrated to be ligands for Toll like receptor (TLR) 4. Mast cells are critical mediators of innate immunity. Objective To explore the role of TLR4 in mast cell activation under obese conditions. Methods P815 mast cells and primary bone marrow mast cells (BMMC) isolated from wild‐type and TLR4 knockout (KO) mice were treated with palmitic acid (PA), and mast cell degranulation, proliferation and associated signaling were analyzed. Results PA treatment increased tryptase release and inflammatory cytokine expression in P815 cells; TLR4 inhibitor TAK‐242 blocked this activation but didn't affect their proliferation and apoptosis. Consistently, BMMC separated from TLR4 KO mice failed to be activated by PA despite activation of wild‐type BMMC. Conclusion TLR4 plays important roles in mediating PA induced mast cell activation. Due to the importance of mast cells in inflammation and innate immunity, our data demonstrate that PA induces activation of mast cells via TLR4, which may provide a novel mechanism explaining low‐grade inflammation induced by obesity ( RR016474 ; USDA‐NRI 2008‐35203‐19084; 2009‐65203‐05716).