The E. coli HPI Suppresses PI3K/Akt/mTOR to Trigger Autophagy Failing to Prevent Injury but Autophagy Enhancement Reduces Damage

This dataset provides the raw experimental data supporting the findings of our study on the E. coli high‑pathogenicity island (HPI) and its role in host autophagy and inflammation. Using a ΔHPI mutant generated by CRISPR/Cas9, we compared the effects of HPI‑positive (HPI⁺) and HPI‑deficient (E. coli ΔHPI) strains in both murine intestinal tissues and RAW264.7 macrophages. The data include in vivo mouse model analyses (intestinal M cells, secretory IgA, histopathology, and cytokine profiles) and in vitro macrophage assays (autophagic flux via LC3‑II, p62, Beclin‑1, PI3K/Akt/mTOR signaling, TEM, immunofluorescence, and CQ flux experiments). Pharmacological modulators of autophagy (rapamycin, 3‑MA, CQ) and genetic knockdown (Beclin‑1 siRNA) were employed to investigate the functional role of autophagy. The data demonstrate that HPI triggers a protective autophagic response that is insufficient to counteract HPI’s own pro‑inflammatory damage, whereas pharmacological enhancement of autophagy (e.g., rapamycin) rescues the host and reduces tissue injury. These data support the central conclusion that boosting autophagy may be a promising therapeutic strategy against HPI‑bearing pathogenic E. coli infections.