Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages
Figure 1
Aspirin (ASA) impairs Trypanosoma cruzi internalization by peritoneal macrophages. (a) Internalization index of the interaction process between macrophages treated for 30 minutes with increasing concentrations of ASA (0.625, 1.25, and 2.5 mM) and exposed to T. cruzi (Y strain). After treatment with ASA, peritoneal macrophages interacted with 5 : 1 trypomastigotes for 2 hours, after which they are washed, fixed with Bouin’s fixative, and stained with Giemsa. Quantification was carried out under a light microscope where the number of intracellular parasites was counted in a total of at least 500 cells. MTT assay to measure cell viability in macrophages after treatment with ASA at 0.625 to 2.5 mM concentrations. H2O2 (1000 μM) was used as negative control (insert). Values are the means ± standard error of mean of 10 experiments or two experiments (MTT assay). for a comparison with infected cells cultured in medium alone. (b) The combined effect of celecoxib and aspirin on the entry of T. cruzi into phagocytic cells. Macrophages were treated for 30 minutes with celecoxib (0.625 mM) and ASA (0.625 mM) exposed to T. cruzi as describe above. Results are the mean ± standard error for triplicate determinations and are representative of three independent experiments. , for a comparison with infected cells cultured in medium alone. (c) Light microscopy observations confirm T. cruzi inhibition invasion of ASA treated cells. Observation after Giemsa staining by light microscopy of the interaction process between peritoneal macrophages treated (or not) with different concentration of ASA and exposed to trypomastigotes forms of T. cruzi. The black arrows indicate internalized parasites. Bars = 10 μm.
