C5a/C5aR pathway is essential for the pathogenesis of murine viral fulminant hepatitis by way of potentiating Fgl2/fibroleukin expression

• Published in: Hepatology (Baltimore, Md.) Vol. 60; no. 1; pp. 114 - 124
• Main Authors: Xu, Gui‐lian, Chen, Jian, Yang, Fei, Li, Gui‐qing, Zheng, Li‐xin, Wu, Yu‐zhang
• Format: Journal Article
• Language: English
• Published: United States Wolters Kluwer Health, Inc 01.07.2014
• Subjects: Acute Disease; Animals; Complement C5a - immunology; Complement C5a - metabolism; Female; Fibrinogen - immunology; Fibrinogen - metabolism; Hepatitis; Hepatitis, Viral, Animal - immunology; Hepatitis, Viral, Animal - metabolism; Hepatology; Humans; Liver Failure, Acute - immunology; Liver Failure, Acute - metabolism; MAP Kinase Signaling System - immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Mortality; Murine hepatitis virus - immunology; Murine hepatitis virus - metabolism; Pathogenesis; Receptor, Anaphylatoxin C5a - genetics; Receptor, Anaphylatoxin C5a - immunology; Receptor, Anaphylatoxin C5a - metabolism; Severity of Illness Index; Up-Regulation - immunology; Viral infections

Viral fulminant hepatitis (FH) remains a serious clinical problem with very high mortality. Lacking understanding of FH pathogenesis has in essence hindered efficient clinical treatment. Inferring from a correlation observed between the genetic differences in the complement component 5 (C5) and the...