Abstract：To study the effect of SopE, a type III secretory system effector encoded by Salmonella enterica serovar Typhi, on SCV induced by S. Typhi after invasion of macrophages. S.Typhi GIFU1007was used as the wild type (WT) strain to construct the sopE mutant (ΔsopE) by homologous recombination using the suicide plasmid pGMB151. The ΔsopE complementary strain (C-ΔsopE) was constructed with the plasmid complementary method by using pBAD33.The recombinant plasmid pET28-SFGFP was introduced into the WT, ΔsopE and C-ΔsopE , respectively, to yield WT/pBAD33::pET28-SFGFP, ΔsopE/pBAD33::pET28-SFGFP and C-ΔsopE/pET28-SFGFP. The effect of SopE on the intracellular viability of S. Typhi was studied by THP-1 intracellular viability assay of macrophages. The effect of SopE on the stability of late SCV was investigated by immunofluorescence and real-time quantitative PCR (qRT-PCR). The relationship between SopE and autophagy was further investigated by qRT-PCR and Western blot. The intracellular viability of THP-1 macrophages with ΔsopE/pBAD33::PET28-SFGFP was significantly lower than that of WT/pBAD33::PET28-SFGFP and C-ΔsopE/PET28-SFGFP. The immunofluorescence assay and qRT-PCR results showed that deletion of sopE decreased the stability of late SCV. The qRT-PCR and Western blot results showed that SopE inhibited the expression of autophagy related genes. The data presented here showed that SopE regulated the stability of late SCV by affecting autophagy.
Jennings E, Thurston TLM, Holden DW.Salmonella SPI-2 Type III Secretion System Effectors: Molecular Mechanisms And Physiological Consequences[J].Cell Host Microbe, 2017, 22(2):217-231
[3]
Cemma M, Brumell JH.Interactions of pathogenic bacteria with autophagy systems[J].Curr Biol, 2012, 22(13):R540-5
[4]
Owen KA, Casanova JE.Salmonella Manipulates Autophagy to "Serve and Protect"[J].Cell Host Microbe, 2015, 18(5):517-9
[5]
Schlumberger MC, Hardt WD.Triggered phagocytosis by Salmonella: bacterial molecular mimicry of RhoGTPase activation/deactivation[J].Curr Top Microbiol Immunol, 2005, 291:29-42
[6]
Lim JS, Shin M, Kim HJ, Kim KS, Choy HE, Cho KA.Caveolin-1 mediates Salmonella invasion via the regulation of SopE-dependent Rac1 activation and actin reorganization[J].J Infect Dis, 2014, 210(5):793-802
[7]
Bishop AL, Hall A.Rho GTPases and their effector proteins[J].Biochem J, 2000, 348(Pt 2):241-255
[8]
Agbor TA, McCormick BA.Salmonella effectors: important players modulating host cell function during infection[J].Cell Microbiol, 2011, 13(12):1858-69
[9]
Fattinger SA, B?ck D, Di Martino ML, Deuring S, Samperio VP, Ek V, Furter M, Kreibich S, Bosia F, Müller-Hauser AA, Nguyen BD, Rohde M, Pilhofer M, Hardt WD, Sellin ME.Salmonella Typhimurium discreet-invasion of the murine gut absorptive epithelium[J].PLoS Pathog, 2020, 16(5):e1008503-
[10]
Verlhac P, Vire C, Faure M.Dual function of CALCOCO2NDP52 during xenophagy[J].Autophagy, 2015, 11(6):965-966
[11]
R?der J, Hensel M.Presence of SopE and mode of infection result in increased Salmonella-containing vacuole damage and cytosolic release during host cell infection by Salmonella enterica[J].Cell Microbiol, 2020, 22(5):e13155-
[12]
Sindhwani A, Arya SB, Kaur H, Jagga D, Tuli A, Sharma M.Salmonella exploits the host endolysosomal tethering factor HOPS complex to promote its intravacuolar replication[J].PLoS Pathog, 2017, 13(10):e1006700-
[13]
Meunier E, Dick MS, Dreier RF, Schürmann N, Kenzelmann Broz D, Warming S, Roose-Girma M, Bumann D, Kayagaki N, Takeda K, Yamamoto M, Broz P.Caspase-11 activation requires lysis of pathogen-containing vacuoles by IFN-induced GTPases[J].Nature, 2014, 509(7500):366-370
[14]
Vonaesch P, Sellin ME, Cardini S, Singh V, Barthel M, Hardt WD.The Salmonella Typhimurium effector protein SopE transiently localizes to the early SCV and contributes to intracellular replication[J].Cell Microbiol, 2014, 16(12):1723-1735
[15]
Jennings E, Thurston TLM, Holden DW.Salmonella SPI-2 Type III Secretion System Effectors: Molecular Mechanisms And Physiological Consequences[J].Cell Host Microbe, 2017, 22(2):217-231
[16]
Knuff K, Finlay BB.What the SIF Is Happening-The Role of Intracellular Salmonella-Induced Filaments[J].Front Cell Infect Microbiol, 2017, 7:335-
[17]
Marsman M, Jordens I, Kuijl C, Janssen L, Neefjes J.Dynein-mediated vesicle transport controls intracellular Salmonella replication[J].Mol Biol Cell, 2004, 15(6):2954-2964
[18]
LaRock DL, Chaudhary A, Miller SI.Salmonellae interactions with host processes[J].Nat Rev Microbiol, 2015, 13(4):191-205
[19]
Bernal-Bayard J, Ramos-Morales F.Molecular Mechanisms Used by to Evade the Immune System[J].Curr Issues Mol Biol, 2018, 25:133-168
[20]
Wang L, Yan J, Niu H, Huang R, Wu S.Autophagy and Ubiquitination in Infection and the Related Inflammatory Responses[J].Front Cell Infect Microbiol, 2018, 8:78-
[21]
Steele-Mortimer O.The Salmonella-containing vacuole: moving with the times[J].Curr Opin Microbiol, 2008, 11(1):38-45
[22]
Teo WX, Kerr MC, Teasdale RD.MTMR4 Is Required for the Stability of the Salmonella-Containing Vacuole[J].Front Cell Infect Microbiol, 2016, 6:91-
Wen Xin, Klionsky DJ.How bacteria can block xenophagy: an insight from[J].Autophagy, 2020, 16(2):193-194
[25]
Xu Y, Zhou P, Cheng S, Lu Q, Nowak K, Hopp AK, Li L, Shi X, Zhou Z, Gao W, Li D, He H, Liu X, Ding J, Hottiger MO, Shao F.A Bacterial Effector Reveals the V-ATPase-ATG16L1 Axis that Initiates Xenophagy[J].Cell, 2019, 178(3):552-566
