Skip to main content

Advertisement

Fig. 3 | Parasites & Vectors

Fig. 3

From: Role of the lipoxin A4 receptor in the development of neutrophil extracellular traps in Leishmania infantum infection

Fig. 3

H3Cit formation in neutrophil-like HL-60 cells with/without lipoxin A4 receptor silencing after stimulation by L. infantum promastigotes for 5 h. HL-60 cells induced to differentiate into neutrophil-like cells (with 1.25% DMSO) with or without lipoxin A4 receptor gene silencing were exposed to L. infantum promastigotes or left untreated for 5 h at 37 °C. H3Cit formation was quantified by flow cytometric assay. a Isotype of H3Cit. b Percentage of H3Cit-positive differentiated HL-60 cells in experimental group Neu; c Percentage of H3Cit-positive differentiated HL-60 cells in experimental group siRNA+Leish; d Percentage of H3Cit-positive differentiated HL-60 cells in experimental group Neu+Leish; e Comparison of the H3Cit-positive neutrophil percentages among experimental groups. The differences were analyzed by one-way ANOVA, then LSD was applied in the following two groups’ comparison; f HL-60 cells were transfected with control siRNA or lipoxin A4 receptor-specific siRNA. Lipoxin A4 receptor transcripts were quantified relative to GAPDH mRNA, using qRT-PCR. Differences were analyzed by Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001. Abbreviations: Neu, differentiated HL-60 cells without treatment; siRNA+Leish, differentiated HL-60 cells in lipoxin A4 receptor-silenced HL-60 cells exposed to L. infantum promastigotes; Neu+Leish, differentiated HL-60 cells stimulated by L. infantum promastigotes

Back to article page