Platelets, Macrophages, and Thromboinflammation in Chagas Disease

J Inflamm Res. 2022 Oct 4;15:5689-5706. doi: 10.2147/JIR.S380896. eCollection 2022.ABSTRACTChagas disease (CD) is a major health problem in the Americas and an emerging health problem in Europe and other nonendemic countries. Several studies have documented persistence of the protozoan parasite Trypanosoma cruzi, and oxidative and inflammatory stress are major pathogenic factor. Mural and cardiac thrombi, cardiac arrhythmias, and cardiomyopathy are major clinical features of CD. During T. cruzi infection, parasite-released factors induce endothelial dysfunction along with platelet (PLT) and immune-cell activation. PLTs have a fundamental role in maintaining hemostasis and preventing bleeding after vascular injury. Excessive activation of PLTs and coagulation cascade can result in thrombosis and thromboembolic events, which are recognized to occur in seropositive individuals in early stages of CD when clinically symptomatic heart disease is not apparent. Several host and parasite factors have been identified to signal hypercoagulability and increase the risk of ischemic stroke in early phases of CD. Further, PLT interaction with immune cells and their role in host defense against pathogens and inflammatory processes have only recently been recognized and evolving. In the context of parasitic diseases, PLTs function in directly responding to T. cruzi infection, and PLT interactions with immune cells in shaping the proinflammatory or immunoregulatory function of monocytes, macro...
Source: Cell Research - Category: Cytology Authors: Source Type: research