G.-Mendes, B. (Beatriz)

Filtering

20211

Settings

Author search.filters.isAuthorOfPublication.7d239ab0-7cfd-4740-97a3-ea110d688af0

Search Results

Now showing 1 - 1 of 1
  • Thumbnail Image
    CRIg on liver macrophages clears pathobionts and protects against alcoholic liver disease
    (Nature Publishing Group, 2021) Duan, Y. (Yi); Chu, H. (Huikuan); Brandl, K. (Katharina); Jiang, L. (Lu); Zeng, S. (Suling); Meshgin, N. (Nairika); Papachristoforou, E. (Eleni); Argemí, J. (Josepmaria); G.-Mendes, B. (Beatriz); Wang, Y. (Yanhan); Su, H. (Hua); Sun, W. (Weizhong); Castilla-Llorente, C. (Cristina); Hendrikx, T. (Tim); Liu, X. (Xiao); Hosseini, M. (Mojgan); Kisseleva, T. (Tatiana); Brenner, D.A. (D. A.); Bataller, R. (Ramón); Ramachandran, P. (Prakash); Karin, M. (Michael); Fu, W. (Wenxian); Schnabl, B. (Bernd)
    Complement receptor of immunoglobulin superfamily (CRIg) is expressed on liver macrophages and directly binds complement component C3b or Gram-positive bacteria to mediate phagocytosis. CRIg plays important roles in several immune-mediated diseases, but it is not clear how its pathogen recognition and phagocytic functions maintain homeostasis and prevent disease. We previously associated cytolysin-positive Enterococcus faecalis with severity of alcohol-related liver disease. Here, we demonstrate that CRIg is reduced in liver tissues from patients with alcohol-related liver disease. CRIg-deficient mice developed more severe ethanol-induced liver disease than wild-type mice; disease severity was reduced with loss of toll-like receptor 2. CRIg-deficient mice were less efficient than wild-type mice at clearing Gram-positive bacteria such as Enterococcus faecalis that had translocated from gut to liver. Administration of the soluble extracellular domain CRIg-Ig protein protected mice from ethanol-induced steatohepatitis. Our findings indicate that ethanol impairs hepatic clearance of translocated pathobionts, via decreased hepatic CRIg, which facilitates progression of liver disease.