Lipid Bodies: Inflammatory Organelles Implicated in Host-Trypanosoma cruzi Interplay during Innate Immune Responses

Figure 1

Activation of heart inflammatory macrophages during the acute infection with Trypanosoma cruzi. In response to acute infections, a cascade of events recruits cells derived from monocytic lineage from the peripheral blood into heart. This cascade culminates in a strong activation of macrophages. Classical activation of macrophages involves the key cytokine interferon gamma (IFN-γ) and T. cruzi components (GPI anchors and CpG-rich DNA). These parasite products are recognized at the macrophage surface by Toll-like receptors (TLRs)-2 and 9, respectively. These receptors are a class of pattern recognition receptors (PRRs), which initiate an immune response and directly activates macrophages. Additionally, TLR-2 can heterodimerizate either TLR1 or TLR6 to recognize T. cruzi GPI anchors [33]. TNF-α is one of the most efficient activators of macrophages to a trypanocidal function. PAMPS, pathogen-associated molecular patterns; GPI, glycosyl phosphatidy linositol; TNF-α, tumor necrosis factor-alpha; MIP-1α, macrophage inflammatory protein α; MCP-1/CCL-2, monocyte chemoattractant protein-1; IP-10, inducible protein 10.