The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions.

摘要: Urinary tract infections (UTI) are among the most common in humans. Uropathogenic Escherichia coli (UPEC) can invade and replicate within bladder epithelial cells, some UPEC strains also survive macrophages. To understand transcriptional programme associated with intramacrophage survival, we performed host-pathogen co-transcriptome analyses using RNA sequencing. Mouse bone marrow-derived macrophages (BMMs) were challenged over a 24h time course two reference that possess contrasting phenotypes: UTI89, which survives BMMs, 83972, is killed by BMMs. Neither of these caused significant BMM cell death at low multiplicity infection was used this study. We developed an effective computational framework simultaneously separated, annotated quantified mammalian bacterial transcriptomes. Bone responded to broadly similar gene expression programme. In contrast, responses diverged markedly from each other. identified UTI89 genes up-regulated post-infection, hypothesized may contribute survival. Indeed, showed deletion one such (pspA) significantly reduced survival Our study provides technological for capturing global changes level co-cultures, has generated new insights into mechanisms use persist environment.