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Eps8 facilitates phagocytosis by increasing TLR4‐MYD88 interaction in LPS‐stimulated macrophages
Author(s) -
Leu Tzeng-Horng,
Chen Yen-Jen,
Maa Ming-Chei
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.lb157
Subject(s) - phagocytosis , tlr4 , phagosome , microbiology and biotechnology , macrophage , chemistry , colocalization , innate immune system , receptor , biology , signal transduction , biochemistry , in vitro
Toll‐like receptors (TLRs) are crucial in macrophage phagocytosis, which is pivotal in host innate immune response. However, the detailed mechanism is not fully defined. Here, we demonstrated the induction of Src and Eps8 in LPS‐treated macrophages was TLR4‐ and MyD88‐dependent, and their attenuation reduced LPS‐promoted phagocytosis. Confocal microscopy indicated the colocalization of Eps8 and TLR4 in the cytosol and at the phagosome. Consistently, both Eps8 and TLR4 were present in the same immunocomplex regardless of LPS stimulation. Inhibition of this complex formation by eps8 siRNA or overexpression of PH‐truncated Eps8 (i.e. 261‐p97 Eps8 ) decreased LPS‐induced TLR4‐MyD88 interaction and the following activation of Src, FAK, and p38 MAPK. Importantly, attenuation of Eps8 impaired bacterium killing ability of macrophages. Thus, Eps8 is a key regulator of the LPS‐stimulated TLR4‐MyD88 interaction and contributes to macrophage phagocytosis. This work was supported by the National Science Council (NSC100‐2325‐B‐006‐011‐)