The type III secretion system effector EseJ plays a regulatory role inside bacteria. It suppresses the adherence of Edwardsiella piscicida (E. piscicida ) to host epithelial cells by down regulating type 1 fimbriae. In this study, we observed that more macrophages infected with ΔeseJ strain of E. piscicida detached as compared with those infected with the wild‐type (WT) strain. Terminal deoxynucleotidyl transferase dUTP nick‐end labelling (TUNEL) staining and cleaved caspase‐3 examination revealed that the detachment is due to increased apoptosis, suggesting that EseJ suppresses macrophage apoptosis. However, apoptosis inhibition by EseJ is not relative to a type III secretion system (T3SS) and is not related to EseJ's translocation. Since EseJ negatively regulates type 1 fimbriae, murine J774A.1 cells were infected with ΔeseJ ΔfimA or ΔeseJ ΔfimH strains. It was demonstrated that ΔeseJ stimulates macrophage apoptosis through type 1 fimbriae. Moreover, we found that infecting J774A.1 cells with the ΔeseJ strain increased levels of cleaved caspase‐8, caspase‐9, and caspase‐3, demonstrating that EseJ inhibits apoptosis through either an extrinsic or a combination of extrinsic and intrinsic pathways. Pre‐treatment of macrophages with caspase‐8 inhibitor prior to infection with the ΔeseJ strain decreased the levels of cleaved caspase‐8, caspase‐9, and caspase‐3, indicating that the ΔeseJ strain stimulates apoptosis, mainly through an extrinsic pathway by up regulating type 1 fimbriae. Zebrafish larvae or blue gourami fish infected with the ΔeseJ strain consistently exhibited higher apoptosis than those infected with the E. piscicida WT strain or ΔeseJ ΔfimA strain. Taken together, we revealed that the T3SS protein EseJ of E. piscicida inhibits host apoptosis, mainly through an extrinsic pathway by down regulating type 1 fimbriae.

中文翻译：

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Edwardsiella piscicida III型蛋白EseJ通过下调1型菌毛来抑制细胞凋亡，从而刺激caspase-8的裂解。

III型分泌系统效应子EseJ在细菌内部起调节作用。它通过下调1型菌毛来抑制爱德华氏菌（E. piscicida）粘附于宿主上皮细胞。在这项研究中，我们观察到更多的巨噬细胞被piscicida的ΔeseJ株感染与感染野生型（WT）菌株的患者相比，它们分离。末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色和裂解的caspase-3检查显示该脱离是由于凋亡增加所致，表明EseJ抑制了巨噬细胞凋亡。但是，EseJ的凋亡抑制与III型分泌系统（T3SS）无关，并且与EseJ的移位无关。由于EseJ负调节1型菌毛，鼠J774A.1细胞用Δ eseJ Δ FIMA或Δ eseJ Δ fimH菌株。已证明ΔeseJ通过1型菌毛刺激巨噬细胞凋亡。此外，我们发现用Δ感染J774A.1细胞eseJ菌株增加了裂解的caspase-8，caspase-9和caspase-3的水平，表明EseJ通过外在或内在和内在途径的组合抑制凋亡。在感染ΔeseJ菌株之前用caspase-8抑制剂对巨噬细胞进行预处理可以降低裂解的caspase-8，caspase-9和caspase-3的水平，这表明ΔeseJ菌株主要通过外在途径刺激细胞凋亡。通过上调1型菌毛。感染了Δ斑马鱼或蓝色鲈鱼eseJ应变比那些感染了一致表现出更高的凋亡E. piscicida WT菌株或Δ eseJ Δ FIMA应变。总之，我们发现该蛋白T3SS的EseJ E. piscicida抑制宿主细胞凋亡，主要是通过一个外部途径通过下调1型菌毛。