We found that the cytoplasm-enriched antisense lncRNA DDIT4-AS1 showed concordant expression patterns with DDIT4 upon E. coli infection, and DDIT4-AS1 modulated DDIT4 expression by enhancing the stability of DDIT4 mRNA through RNA duplex formation, thereby promoting NF-κB activation and pro-inflammatory gene expression. The gene discussed is NFKB1; the disease is escherichia coli infection.