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. 2022 Mar 3;12:829682. doi: 10.3389/fcimb.2022.829682

Figure 2.

Figure 2

The contribution of autophagy signaling in C. jejuni invasion step. (A) HeLa cells were treated with 200 nM Bafilomicin-A1 (Baf) or 50 μM Chloroquine (CQ) for 3 h. The number of intracellular C. jejuni was measured by gentamicin protection assay at 1 h p. i., and decided by counting of Colony Forming Unit (CFU). (B) The number of intracellular C. jejuni in HeLa cells, which treated by 1 μM Torin 1 (Torin) or 200 nM Rapamycin (Rapa) for 3 h, were measured by gentamicin protection assay at 1 h p. i. (C) HeLa cells which stably express pEGFP or pEGFP-LC3B vector were infected with C. jejuni for 1 h, and the number of invaded bacteria was estimated by gentamicin protection assay. (D) siRNA against autophagy-related genes were transfected to HeLa cells, and intracellular bacterial number at 1 h p. i. was measured by gentamicin protection assay. (E) The expression of ULK1 complex components, ULK1, FIP200, and ATG13, were attenuated by shRNA-mediated knockdown in HeLa cells, and the invaded bacterial number was measured by gentamicin protection assay at 1 h p. i. All data are expressed as means ± standard deviations from 3 independent experiments. Differences were evaluated with Two-tailed Student’s t-test. *p < 0.05, **p < 0.001.