Page 195 - 《水产学报》2025年第8期
P. 195

曹磊,等                                                                  水产学报, 2025, 49(8): 089416




                 Edwardsiella piscicida T3SS effector EseJ regulates PPARγ production to
                                      promote colonization in macrophages



                                                                 4
                                                 2,3
                           1,2
                   CAO Lei  ,     ZHANG Yuanxing  ,     Choi Sangho  ,     SHAO Shuai  1,2,3* ,     WANG Qiyao  1,2,3*
                                          1. State Key Laboratory of Bioreactor Engineering,
                                East China University of Science and Technology, Shanghai 200237, China;
                                 2. Shanghai Engineering Research Center of Maricultured Animal Vaccines,
                                East China University of Science and Technology, Shanghai 200237, China;
                              3. Laboratory of Aquatic Animal Diseases, Ministry of Agriculture and Rural Affairs,
                                East China University of Science and Technology, Shanghai 200237, China;
                                 4. National Research Laboratory of Molecular Microbiology and Toxicology,
                                      Seoul National University, Seoul 151-742, Republic of Korea


              Abstract: The Type III secretion system (T3SS) and its effector proteins are crucial virulence factors in the pathogenesis of
              bacterial pathogens. A dozen of T3SS effector proteins have been identified in Edwardsiella piscicida, a bacterial pathogen
              threatening the aquaculture, but the specific role of EseJ, a specific effector with large molecular weight (1 358 aa and 146 kDa)
              essential for infection processes, remains unclear. This study revealed that PPARγ expression was upregulated during the infec-
              tion of J774A.1 macrophages by E. piscicida, whereas the T3SS-deficient mutant (ΔT3SS) did not alter PPARγ expression.
              Screening of several deletion mutants of T3SS effectors further validated that EseJ promotes PPARγ expression in J774A.1
              cells. During E. piscicida infection, EseJ-induced PPARγ expression suppressed the secretion of pro-inflammatory cytokines,
              enhanced the production of anti-inflammatory cytokines, reduced the release of mitochondrial reactive oxygen species (ROS),
              and  alleviated  mitochondrial  damages.  The  upregulation  of  PPARγ  contributed  to  E.  piscicida  colonization  within  J774A.1
              cells. Additionally, pull-down assays highlighted 77 host proteins potentially interacting with EseJ and bacterial two-hybrid
              assays confirmed the direct interaction between EseJ and the ubiquinone oxidoreductase subunit 7 (NDUFA7). In conclusion,
              our study provides new insights into the role of T3SS effector EseJ in the pathogenesis of E. piscicida, providing potential tar-
              gets for the prevention and control of E. piscicida infections.
              Key words: Edwardsiella piscicida; host-pathogen interaction; peroxisome proliferator-activated receptor γ (PPARγ); effector
              protein
              Corresponding authors: SHAO Shuai. E-mail: shaoscott@ecust.edu.cn;
                                 WANG Qiyao. E-mail: oaiwqiyao@ecust.edu.cn
              Funding projects: National Key Research and Development Program of China (2022YFE0101200); National Natural Science
              Foundation of China (32130108); National Modern Agricultural Industry Technology System Project (CARS-47)



















              中国水产学会主办  sponsored by China Society of Fisheries                          https://www.china-fishery.cn
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