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. 2023 Oct 19;14:1249436. doi: 10.3389/fimmu.2023.1249436

Figure 6.

Figure 6

A lysosome pathway is involved in intestinal defense via PMK-1/p38. (A, B) PA14 survival assays of the intestine-specific RNAi strain VP303 fed on vector control, hlh-30 (A), lipl-1 (B) RNAi bacteria, prior PA14 exposure. (C, D) Survival assays of wild-type and inx-14(ag17) mutant animals fed on vector control, hlh-30 (C), or lipl-1 (D) RNAi bacteria, prior to PA14 exposure. (E, F) Survival assays of wild-type and glp-1(e2141) mutants fed on vector control, hlh-30 (E), or lipl-1 (F) RNAi bacteria, prior to PA14 exposure. (G, H) Survival assays of wild-type and pmk-1(km25) mutants fed on vector control, hlh-30 (G), or lipl-1 (H) RNAi bacteria, prior to PA14 exposure. (I, J) qRT-PCR analyses of the expression levels of six PMK-1/p38-dependent genes in wild-type animals fed on vector control, hlh-30 (I), or lipl-1 (J) RNAi bacteria, prior to OP50 or PA14 exposure. All experiments were repeated at least three times. Column data with plots are presented as mean ± SEM. Statistical significance was determined by log-rank test for survival assay or Kruskal–Wallis with Dunn’s multiple comparison test for (I, J). *P < 0.05; **P < 0.01; ***P < 0.001; n.s., not significant.