Different from AFLD, except for the deposition of triglycerides in hepatocytes, AH is also characterized by the infiltration of inflammatory cells, elevated inflammatory cytokine levels, increased serum transaminase levels, and liver injury. Previous studies have shown that inflammatory cytokines play an important role in the occurrence and development of ALD [33,34]. In AH, inflammatory cytokine levels were elevated, leading to liver cell dysfunction and continued tissue damage [35]. The complement system is also associated with the pathogenesis of AH. Cohen et al. [36] reported that C1q deficiency abolishes the activation of the CP, reduces the expression of inflammatory cytokines, and attenuates liver tissue injury. These results were further confirmed in a study of an alcoholic liver model in mice by Smathers et al. [34]. Moreover, in AH patients, C1q and C5 levels were significantly increased, and the expression of C5aR was also upregulated in the Mallory-Denk body forming cells, which are the major features of ongoing inflammation in AH [37,38]. These studies showed that complement activation is involved in the occurrence of AH and the impairment of liver function. The
