Fig. 11

Schematic summary of results. a 0 h p.i.: macrophages were infected with L. m. promastigotes. b 10 min p.i.: promastigotes attached to macrophages and were phagocytosed by the cells. c 1 h p.i. (early infection phase): promastigotes differentiated intracellularly into amastigotes. At this point, the differentiation was not complete. Hyperphosphorylation of MTOR and RPS6 suggested autophagy inhibition. d 24 h p.i. (late infection phase): amastigote differentiation was completed. ATG5, BNIP3, CTSE, MIF, UB, and miRNAs mmu-miR-155-5p and mmu-miR-210-5p, were overexpressed. Expression of miRNAs mmu-miR-101c and mmu-miR-129-5p was downregulated. The LC3B-II/LC3B-I ratio was elevated and suggested an increased autophagic flux. Glycolytic genes were upregulated. Overexpressed MIF might have attracted new uninfected host macrophages. Putative regulatory mechanisms at the RNA level were identified, which were summarized in LISA and MONA-of-LISA. Additionally, inflammatory functions (e.g., the immune response and chemokine signaling pathway) were upregulated, which indicates L. m.-infected BMDM had an inflammatory phenotype. e 48 h p.i.: amastigotes were autophagically digested, which resulted in a decline in the infection rate. p.i. = post infection