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Escherichia coli K1 is the most common Gram-negative bacterium that causes neonatal meningitis; thus, a better understanding of its pathogenic molecular mechanisms is critical. However, the mechanisms by which E. coli K1 senses the signals of the host and expresses toxins for survival are poorly understood. As an extracytoplasmic function sigma factor, RpoE controls a wide range of pathogenesis-associated pathways in response to environmental stress. We found that the ΔrpoE mutant strain reduced the binding and invasion rate in human brain microvascular endothelial cells (HBMECs) in vitro, level of bacteremia, and percentage of meningitis in vivo. To confirm the direct targets of RpoE in vivo, we performed qRT-PCR and ChIP-qPCR on known toxic genes. RpoE was found to regulate pathogenic target genes, namely, ompA, cnf1, fimB, ibeA, kpsM, and kpsF directly and fimA, aslA, and traJ indirectly. The expression of these genes was upregulated when E. coli K1 was cultured with antibacterial peptides, whereas remained unchanged in the presence of the ΔrpoE mutant strain. Moreover, RpoE reduced IL-6 and IL-8 levels in E. coli K1-infected HBMECs. Altogether, these findings demonstrate that RpoE mediates the host adaptation capacity of E. coli K1 via a regulatory mechanism on virulence factors.

RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of Escherichia coli K1