title: Liver myofibroblasts up-regulate monocyte CD163 expression via PGE2 during hepatitis B induced liver failure.
abstract: BACKGROUND
  Although patients with liver failure exhibit a generalized inflammatory-imbalance status, substantial evidence indicates that this immunosuppressive or anti-inflammatory state may be deleterious. Increased expression of CD163 (known to be involved in several anti-inflammatory functions of the immune system) in patients with liver failure is significantly correlated with a fatal outcome. However, little is known of the regulatory mechanisms that influence the expression of CD163.
  
  
  METHODS
  We assessed the expression of CD163 on monocytes from both circulating cells and the liver tissues of patients with hepatitis B induced liver failure using flow cytometry and isolated the myofibroblasts from diseased livers. The ability of human liver myofibroblasts to regulate CD163 expression on monocytes was studied in vitro.
  
  
  RESULTS
  We showed that CD163⁺ monocytes were enriched primarily in diseased livers and that they were associated with liver myofibroblasts in the same area. Accordingly, liver myofibroblasts were significantly superior to normal skin fibroblasts in inducing the expression of CD163 on monocytes in vitro. Moreover, we found that liver myofibroblasts triggered the activation of monocytes by secreting PGE2. Inhibition of PGE2 production in liver myofibroblasts using NS-398 markedly reduced CD163 expression in vitro.
  
  
  CONCLUSIONS
  These results suggest that liver myofibroblasts play a direct role in regulating the expression of CD163 on monocytes in human liver tissues and thereby may regulate monocyte function during hepatitis B induced liver failure.
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Yinong
authors.initials: Y
authors.lastname: Ye
authors.forename: Fenglan
authors.initials: F
authors.lastname: Wang
authors.forename: Jianyun
authors.initials: J
authors.lastname: Zhu
authors.forename: Qiyi
authors.initials: Q
authors.lastname: Zhao
authors.forename: Yubao
authors.initials: Y
authors.lastname: Zheng
authors.forename: Yurong
authors.initials: Y
authors.lastname: Gu
authors.forename: Chan
authors.initials: C
authors.lastname: Xie
authors.forename: Zhanlian
authors.initials: Z
authors.lastname: Huang
authors.forename: Qiang
authors.initials: Q
authors.lastname: Tai
authors.affiliation: Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-sen University, No 600 Tianhe Road, Guangzhou 510630, Guangdong Province, People's Republic of China. ytchong2005@126.com.
authors.forename: Yutian
authors.initials: Y
authors.lastname: Chong
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Gao
mesh_terms: D015703:Antigens, CD / Q000378:metabolism*; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism*; D002452:Cell Count; D002469:Cell Separation; D015232:Dinoprostone / Q000378:metabolism*; D006509:Hepatitis B / Q000150:complications* / Q000473:pathology; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D017093:Liver Failure / Q000209:etiology* / Q000473:pathology / Q000821:virology; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D058628:Myofibroblasts / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D009578:Nitrobenzenes / Q000494:pharmacology; D010641:Phenotype; D011956:Receptors, Cell Surface / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D009578:Nitrobenzenes; D011956:Receptors, Cell Surface; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D015232:Dinoprostone