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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Rep 2015 ; 13 (9): 1909-21 Nephropedia Template TP
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Dectin-1 Regulates Hepatic Fibrosis and Hepatocarcinogenesis by Suppressing TLR4 Signaling Pathways #MMPMID26655905
Seifert L; Deutsch M; Alothman S; Alqunaibit D; Werba G; Pansari M; Pergamo M; Ochi A; Torres-Hernandez A; Levie E; Tippens D; Greco SH; Tiwari S; Ly NNG; Eisenthal A; van Heerden E; Avanzi A; Barilla R; Zambirinis CP; Rendon M; Daley D; Pachter HL; Hajdu C; Miller G
Cell Rep 2015[Dec]; 13 (9): 1909-21 PMID26655905show ga
Dectin-1 is a C-type lectin receptor critical in anti-fungal immunity but Dectin-1 has not been linked to regulation of sterile inflammation or oncogenesis. We found that Dectin-1 expression is upregulated in hepatic fibrosis and liver cancer. However, Dectin-1 deletion exacerbates liver fibro-inflammatory disease and accelerates hepatocarcinogenesis. Mechanistically, we found that Dectin-1 protects against chronic liver disease by suppressing TLR4 signaling in hepatic inflammatory and stellate cells. Accordingly, Dectin-1?/? mice exhibited augmented cytokine production and reduced survival in LPS-mediated sepsis whereas Dectin-1 activation was protective. We showed that Dectin-1 inhibits TLR4 signaling by mitigating TLR4 and CD14 expression which are regulated by Dectin-1-dependent M-CSF expression. Our study suggests that Dectin-1 is an attractive target for experimental therapeutics in hepatic fibrosis and neoplastic transformation. More broadly, our work deciphers critical cross-talk between pattern recognition receptors and implicates a role for Dectin-1 in suppression of sterile inflammation, inflammation-induced oncogenesis, and LPS-mediated sepsis.