ArticleRevista da Sociedade Brasileira de Medicina Tropical2026
Effects of MK-886, an inhibitor of the 5-lipoxygenase-activating protein, on peripheral blood mononuclear cells from patients with Chagas' heart disease.
Article in Revista da Sociedade Brasileira de Medicina Tropical, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChagas disease, caused by Trypanosoma cruzi, remains a major public health challenge in Latin America. Lipid mediators, including leukotrienes, play a key role in modulating the immune response during infection. 5-Lipoxygenase deficiency has been associated with cardioprotective effects in mouse models. Accordingly, this study evaluated the effects of MK-886, a 5-lipoxygenase-activating protein inhibitor, on the immune response of cells from patients with Chagas heart disease.
methodsPeripheral blood mononuclear cells (PBMCs) from patients with chronic Chagas disease were stimulated with T. cruzi antigen in the presence or absence of MK-886. Cytokine production (interferon [IFN]-γ, interleukin [IL]-13, IL-17, IL-10, and tumor necrosis factor [TNF]-α), apoptosis, necrosis, and cell proliferation were assessed.
resultsT. cruzi antigen significantly increased cytokine production, cell death, and proliferation in PBMCs from patients with chronic Chagas disease. MK-886 significantly reduced IFN-γ, IL-13, and IL-17 production without altering IL-10 or TNF-α production. Additionally, MK-886 treatment markedly reduced apoptosis, necrosis, and proliferation in T. cruzi-stimulated PBMCs from patients with chronic Chagas disease.
conclusionsMK-886 has the potential to reduce tissue-damaging inflammation and fibrosis associated with Th1, Th2, and Th17 responses without inducing immunosuppression, while IL-10 and TNF-α production remained unchanged in PBMCs from patients with chronic Chagas disease. Accordingly, targeting the leukotriene pathway may delay the progression of cardiac damage in Chagas disease.
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