| Summary: | Colibactin is a complex secondary metabolite that leads to genotoxicity that interferes with the eukaryotic cell cycle. It plays an important role in many diseases, including neonatal mouse sepsis and meningitis. Avian pathogenic <i>Escherichia coli</i> (APEC) is responsible for several diseases in the poultry industry and may threaten human health due to its potential zoonosis. In this study, we confirmed that <i>c</i><i>lbG</i> was necessary for the APEC XM strain to produce colibactin. The deletion of <i>clbG</i> on APEC XM contributed to lowered γH2AX expression, no megalocytosis, and no cell cycle arrest in vitro. None of the 4-week Institute of Cancer Research mice infected with the APEC XM Δ<i>clbG</i> contracted meningitis or displayed weakened clinical symptoms. Fewer histopathological lesions were observed in the APEC XM Δ<i>clbG</i> group. The bacterial colonization of tissues and the relative expression of cytokines (<i>IL-1β</i>, <i>IL-6</i>, and <i>TNF-α</i>) in the brains decreased significantly in the APEC XM Δ<i>clbG</i> group compared to those in the APEC XM group. The tight junction proteins (claudin-5, occludin, and ZO-1) were not significantly destroyed in APEC XM Δ<i>clbG</i> group in vivo and in vitro. In conclusion, <i>clbG</i> is necessary for the synthesis of the genotoxin colibactin and affects the development of APEC meningitis in mice.
|
|---|
