Abstract
Escherichia coli K1 is the leading cause of meningitis in newborns. Understanding the molecular basis of E. coli K1 pathogenicity will help develop treatment of meningitis and prevent neurological sequelae. E. coli K1 replicates in host blood and forms a high level of bacteremia to cause meningitis in human. However, the mechanisms that E. coli K1 employs to sense niche signals for survival in host blood are poorly understood. We identified one intergenic region in E. coli K1 genome that encodes a novel small RNA, sRNA-17. The expression of sRNA-17 was downregulated by ArcA in microaerophilic blood. The ΔsRNA-17 strain grew better in blood than did the wild-type strain and enhanced invasion frequency in human brain microvascular endothelial cells. Transcriptome analyses revealed that sRNA-17 regulates tens of differentially expressed genes. These data indicate that ArcA downregulates the sRNA-17 expression to benefit bacterial survival in blood and penetration of the blood–brain barrier. Our findings reveal a signaling mechanism in E. coli K1 for host adaptation.
Highlights
Invasion of the central nervous system (CNS) by pathogenic bacteria causes meningitis, which results in 170,000 deaths worldwide per year (World Health Organization [WHO], 2018)
We found that 42 intergenic sequences above 1 kb contain potential ArcA-binding site
We found that one intergenic region may express a non-coding small RNA
Summary
Invasion of the central nervous system (CNS) by pathogenic bacteria causes meningitis, which results in 170,000 deaths worldwide per year (World Health Organization [WHO], 2018). High mortality and morbidity are associated with bacterial meningitis. Escherichia coli K1 is the most common gram-negative bacterium that causes meningitis in newborns (Kim, 2010; Ouchenir et al, 2017). To cross the blood–brain barrier (BBB) and invade CNS, E. coli K1 has to escape host defense system, survive and replicate in the blood, and form a high level of bacteremia (Doran et al, 2016). E. coli NlpI and OmpA contribute to bacteremia
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