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Our previous studies have shown that meningitic  Escherichia coli  can colonize the brain and cause neuroinflammation. Controlling the balance of inflammatory responses in the host central nervous system is particularly vital. Emerging evidence has shown the important regulatory roles of long non-coding RNAs (lncRNAs) in a wide range of biological and pathological processes. However, whether lncRNAs participate in the regulation of meningitic  E. coli -mediated neuroinflammation remains unknown. In the present study, we characterized a cytoplasm-enriched antisense lncRNA  DDIT4-AS1 , which showed similar concordant expression patterns with its parental mRNA  DDIT4  upon  E. coli  infection.  DDIT4-AS1  modulated  DDIT4  expression at both mRNA and protein levels. Mechanistically,  DDIT4-AS1  promoted the stability of  DDIT4  mRNA through RNA duplex formation.  DDIT4-AS1  knockdown and  DDIT4  knockout both attenuated  E. coli -induced NF-κB signaling as well as pro-inflammatory cytokines expression, and  DDIT4-AS1  regulated the inflammatory response by targeting  DDIT4 . In summary, our results show that  DDIT4-AS1  promotes  E. coli -induced neuroinflammatory responses by enhancing the stability of  DDIT4  mRNA through RNA duplex formation, providing potential nucleic acid targets for new therapeutic interventions in the treatment of bacterial meningitis.

Long Non-coding Antisense RNA DDIT4-AS1 Regulates Meningitic Escherichia coli-Induced Neuroinflammation by Promoting DDIT4 mRNA Stability