SAA1 and infection: In the early/moderate stage of infection, activation of hepatocellular GR will induce CXCL2 and APPs such as SAA1 and moderately inhibit the TNF-stimulated expression/secretion of most inflammatory cytokines/chemokines, with the exception of CXCL10, which can directly kill both Gram-positive and Gram-negative bacterial pathogens in vitro [116].