Fig. 1.
Role of acute local inflammation in HF. From acute to chronic inflammation. There is an interplay of both the innate and adaptive immune system in the development of inflammatory cardiovascular disease and its contribution to HF. The initial effect of PAMPs and DAMPs to TLRs pathways promotes the synthesis of inflammatory cytokines through NFκB. In a 2nd phase, NLRP3 activation promotes the maturation and secretion of IL-1β and IL-18. TLR and NLRP3 activation on cardiomyocytes contributes to pro-inflammatory cytokine production that is enhanced by APCs, such as DCs, macrophages, and B cells. This mechanism, if unchecked, can contribute to secondary tissue damage by humoral and cellular mechanisms by B and T cell driving mechanisms of chronic inflammation, leading to pervasive cell phenotype skewing, antibody production, and eventual fibrosis and cell contractile dysfunction. APC, antigen presenting cell. DAMPS, damage-associated molecular patterns. IL, interleukin. IFN, interferon, PAMPs pathogen-associated molecular patterns. TLR, toll-like receptors. TH, T-helper cell. Tregs, regulatory T cell. TNF, tumor necrosis factor. ROS, reactive oxygen species. ATP, adenosine triphosphate. DSRNA, double-stranded RNA. SSRNA, single-strand RNA, TH, T-helper cell