AI Article Synopsis
- AIEC (Adherent-invasive Escherichia coli) is linked to Crohn's disease by triggering inflammation through high cytokine production in infected macrophages.
- AIEC can replicate within macrophages, and this study found that their replication relies on bacterial glycolysis, suggesting a metabolic dependency.
- The macrophage response to AIEC infection is similar to that of a non-replicating glycolysis mutant and a harmless strain of E. coli, indicating that AIEC does not disrupt the typical macrophage response during infection.
Article Abstract
Adherent-invasive Escherichia coli (AIEC) have been implicated in the aetiology of Crohn's disease (CD), a chronic inflammatory bowel condition. It has been proposed that AIEC-infected macrophages produce high levels of pro-inflammatory cytokines thus contributing to the inflammation observed in CD. AIEC can replicate in macrophages and we wanted to determine if bacterial replication was linked to the high level of cytokine production associated with AIEC-infected macrophages. Therefore, we undertook a genetic analysis of the metabolic requirements for AIEC replication in the macrophage and we show that AIEC replication in this niche is dependent on bacterial glycolysis. In addition, our analyses indicate that AIEC have access to a wide range of nutrients in the macrophage, although the levels of purines and pyrimidines do appear to be limiting. Finally, we show that the macrophage response to AIEC infection is indistinguishable from the response to the non-replicating glycolysis mutant (ΔpfkAB) and a non-pathogenic strain of E. coli, MG1655. Therefore, AIEC does not appear to subvert the normal macrophage response to E. coli during infection.
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