Moreover, the overexpression of DDIT4-AS1 augmented E. coli-induced IL-1β and TNF-α expression; however, the pro-inflammatory effect of DDIT4-AS1 vanished in DDIT4 KO cells (Fig. 7f), which revealed that DDIT4-AS1 functions are mediated by DDIT4. Collectively, these data indicate that DDIT4-AS1 plays a pro-inflammatory role in the progress of E. coli infection by promoting DDIT4 mRNA stability. Here, TNF is linked to escherichia coli infection.