Interaction(s) among adipose-fatty acid-binding protein (A-FABP), Toll-like receptor (TLR), cytokines, free radicals, unsaturated fatty acids, and their products and inflammation and resolution of inflammation. Infections, injuries (including surgery), and high-fat diet activate macrophages and TLRs, leading to secretion of increased amounts of pro-inflammatory cytokines that, in turn, produce an excess of free radicals. Pro-inflammatory cytokines, TLRs, and free radicals activate A-FABP and cyclooxygenase 2 (COX-2), leading to increased production of pro-inflammatory prostaglandins (PGs), leukotrienes (LTs), and thromboxanes (TXs) from unsaturated fatty acids and decreases in the synthesis and release of anti-inflammatory lipoxins (LXs), resolvins (RSVs), and protectins (PRTs). Blocking the expression of A-FABP and TLRs will suppress inflammation. Unsaturated fatty acids and LXs, RSVs, and PRTs are expected to suppress macrophage activation and expression of A-FABP and TLRs and inhibit inflammation. Increased expression of A-FABP also occurs in obesity, type 2 diabetes mellitus (DM), and coronary heart disease (CHD). Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), macrophage activation, increased expression of A-FABP, and increased production of PGs, LTs, TXs, and free radicals enhance insulin resistance in infections and sepsis. AA, arachidonic acid; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; HMGB1, high-mobility group box 1; LPS, lipopolysaccharide; NL, nitrolipid; NO, nitric oxide; ROS, reactive oxygen species.