In our studies, pathway analysis using DAVID [41] and GO Consortium [42, 43] platforms identified 5 KEGG pathways enriched in the 312 Alc-DE group, with phagosome being one of highest including transcripts for Atp6ap1, C3, Calr, Cd300lf, Coro1a, Ctss, Cyba, Fcgr1a, Itgb5, Mfge8, Ncf1, Psap, Pycard, RT1-A1, RT1-CE14, RT1-N3, RT1-S3, Sirpa, Slc11a1, and Tlr2. Many of these genes regulate the processes of phagocytosis and degradation (Table 1). In addition, we found that alcohol increased levels of several complement transcripts, including C1qa,b, and c; C3; and C3aR1, and moreover that the C1q variants were not increased by TII alone. This is consistent with studies showing that alcohol increases complement proteins, including C1q, C3a, C5a, C3aR, and C5aR, in liver [65, 66] and adipose tissue [67]. Since microglial complement activation can cause neuronal damage [68], these findings suggest that C1q induction in the brain could contribute to alcohol-induced neuropathology. While this may be mediated through activation of the complement pathways, observations that several complement proteins, including C1q and C3b promote phagocytosis [69, 70] and that CR3 regulates amyloid clearance [71–74], suggests that
