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 underlying mechanism may be that there is a crosstalk between toll-like receptors (TLRs) and C3aR and C5aR in AH [21,37,39,40]. TLRs belong to the pattern recognition receptor family, which can bind to damage-associated molecular patterns or pathogen-associated molecular patterns (PAMPs). PAMPs mainly refer to bacterial metabolites, including bacterial lipopolysaccharide, peptidoglycan, RNA, and DNA, which can reach the liver upon alcohol-induced intestinal microecology imbalance, subsequently initiating the innate immune response and inducing the expression of inflammatory cytokines (such as TNF-α and interleukin-6). In addition, PAMPs increase lipid deposition and inflammatory infiltration in hepatocytes. McCullough et al. [41] found that complement FD promotes the clearance of apoptotic cells and maintains tissue homeostasis in AH and suggested that inappropriate complement activation likely delays the clearance of apoptotic cells and impairs healing/recovery in ALD. Fan et al. [42] found that complement activation is expected to be a diagnostic and prognostic indicator for patients with AH. However, the detailed mechanisms of complement function in AH
