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. Author manuscript; available in PMC: 2022 Oct 11.
Published in final edited form as: Cell Rep. 2022 Sep 27;40(13):111409. doi: 10.1016/j.celrep.2022.111409

Figure 6. HIF signaling is essential for in vivo control of STm by xenophagy.

Figure 6.

(A) Intragastric infection of ODD-Luc mice with STm increases HIF stabilization (luciferase activity) in the cecum. Quantification of cecal radiance shown in plot below images (n = 4 per group, p < 0.01). Scale bar: 1 cm.

(B) Hif1bΔIEC mice demonstrate defects in autophagy in the intestinal epithelium by LC3 and p62 by western blot analysis of intestinal scrapings.

(C) Hif1bΔIEC mice show reduced intestinal levels of the HIF targets Pgk1 and Ckb, as well as the HIF-driven autophagy protein Atg9, by qPCR analysis. *p < 0.05 by t test.

(D) Deletion of intestinal epithelial HIF-1β (Hif1bΔIEC) in vivo does not change levels of colonization following infection with STm in the ileum, cecum, or colon. Results are normalized to wild-type (+/+) controls. N = 5 mice per group.

(E) Deletion of intestinal HIF-1β (Hif1bΔIEC) in vivo increases dissemination of STm to liver and spleen following intragastric infection and provokes increased intestinal inflammation as measured by shortened colon length. Results are normalized to wild-type (+/+) controls. N = 5 mice per group, where *p < 0.025 by t test.