Non-canonical NLRP3 inflammasome activation and IL-1β signaling are necessary to L. amazonensis control mediated by P2X7 receptor and leukotriene B4
Fig 2
L. amazonensis control via LTB4 was dependent on the NLRP3 inflammasome and IL-1R signaling.
Peritoneal macrophages from C57BL/6 (A-C), NLRP3-/- (D-F), ASC-/- (G-I), Casp-1/11-/- (J-L), and IL-1R-/- (M-O) mice were infected with L. amazonensis promastigotes at a ratio of 10:1 (Leishmania:macrophage). After 4 hours, the free parasites were washed and after 24 hours, infected cells were treated (B, E, H, K, and N) or not (A, D, G, J, and M) with 100 nM of LTB4. Twenty-four hours later, cells were stained with May-Grunwald-Giemsa and the infection index was determined by direct counting under light microscopy. Normalized values represent means ± SEM of 3–4 independent experiments performed in triplicate. Arrows correspond to vacuoles with L. amazonensis and asterisks represent empty vacuoles. (*P < 0.05) compared to the control group (without treatment).