禽沙门菌诱导宿主免疫应答的特性
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摘要
沙门菌病(Salmonellosis)是全世界最普遍的食源性疾病之一,不仅对养殖业造成经济损失,还对人类安全构成威胁。禽沙门菌感染肠道后,可诱导肠上皮细胞表达多种TLRs和炎症反应的发生,在分泌的趋化因子作用下免疫效应细胞迁移到感染部位。细菌通过肠上皮细胞屏障后被巨噬细胞或树突状细胞吞噬,其中巨噬细胞是沙门菌的主要定殖场所。天然免疫系统将抗原递呈给淋巴细胞后,机体能够在2–3周内通过以Th1为主的免疫应答清除在肠道和深层组织中的沙门菌。而宿主特异性血清型鸡白痢沙门菌从肠道侵入后,在肝脾和其他器官中定殖,进而引发全身感染。早期感染阶段不会引起肠道炎症反应,主要诱导以Th2为主的免疫应答,而Th1型应答相对较弱,有利于鸡白痢沙门菌在机体内的持续存在和感染。本文围绕禽沙门菌的致病机理和免疫应答特性进行阐述,尤其对鸡白痢沙门菌免疫逃逸和持续载菌的特性进行深入分析,为禽沙门菌病的防控提供新靶标和新见解。
Salmonellosis is one of the most widespread food-borne diseases throughout the world, not only causes economic losses to the breeding industry, but also poses a threat to human health. Avian Salmonella enters the small intestine where infection can be established, inducing intestinal epithelial cells express a number of TLRs and inflammation. These lead to the expression of chemokines that attract immune effector cells to the sites of infection.Following translocation across the intestinal epithelial barrier, bacteria are phagocytosed by cells such as macrophages and DCs, macrophages are its preferred cell type. The adaptive immune response is stimulated by the innate immune system through antigen presentation to lymphocytes. Adaptive immunity can clear infection within 2–3 weeks following infection by a Th1 dominated response in the gut and deeper tissues. In contrast, avian systemic salmonellosis caused by the host-adapted serovar S. Pullorum is characterized by invasion from the intestine with multiplication in the spleen, liver and other organs. The stage of infection resulted in little inflammation in vivo or in vitro. S. Pullorum tends to induce an immune response that more closely resembled the Th2 response in mammals and would allow S. Pullorum to establish an intracellular carriage evading Th1-mediated clearance. This review compared the pathogenesis and immune response characteristics of Salmonella, especially the mechanisms by which S. Pullorum evades host immunity and produces the persistent carrier state. Finally, it will be helpful to provide new targets and new opinions for the prevention and control of avian salmonellosis.
Salmonellosis is one of the most widespread food-borne diseases throughout the world, not only causes economic losses to the breeding industry, but also poses a threat to human health. Avian Salmonella enters the small intestine where infection can be established, inducing intestinal epithelial cells express a number of TLRs and inflammation. These lead to the expression of chemokines that attract immune effector cells to the sites of infection.Following translocation across the intestinal epithelial barrier, bacteria are phagocytosed by cells such as macrophages and DCs, macrophages are its preferred cell type. The adaptive immune response is stimulated by the innate immune system through antigen presentation to lymphocytes. Adaptive immunity can clear infection within 2–3 weeks following infection by a Th1 dominated response in the gut and deeper tissues. In contrast, avian systemic salmonellosis caused by the host-adapted serovar S. Pullorum is characterized by invasion from the intestine with multiplication in the spleen, liver and other organs. The stage of infection resulted in little inflammation in vivo or in vitro. S. Pullorum tends to induce an immune response that more closely resembled the Th2 response in mammals and would allow S. Pullorum to establish an intracellular carriage evading Th1-mediated clearance. This review compared the pathogenesis and immune response characteristics of Salmonella, especially the mechanisms by which S. Pullorum evades host immunity and produces the persistent carrier state. Finally, it will be helpful to provide new targets and new opinions for the prevention and control of avian salmonellosis.
引文
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[26]Matthews TD,Schmieder R,Silva GGZ,Busch J,Cassman N,Dutilh BE,Green D,Matlock B,Heffernan B,Olsen GJ,Hanna LF,Schifferli DM,Maloy S,Dinsdale EA,Edwards RA.Genomic comparison of the closely-related Salmonella enterica serovars Enteritidis,Dublin and Gallinarum.PLoSONE,2015,10(6):e0126883.
[27]Li QC,Xu YH,Jiao XA.Identification of Salmonella Pullorum genomic sequences using suppression subtractive hybridization.Journal of Microbiology and Biotechnology,2009,19(9):898-903.
[28]Yin JL,Chen Y,Xie XL,Xia J,Li QC,Geng SZ,Jiao XA.Influence of Salmonella enterica serovar Pullorum pathogenicity island 2 on type III secretion system effector gene expression in chicken macrophage hd11 cells.Avian Pathology,2017,46(2):209-214.
[29]Tao Z,Zhu C,Song W,Xu W,Zhang S,Liu H,Li H.Inductive expression of the NOD1 signalling pathway in chickens infected with Salmonella Pullorum.British Poultry Science,2017,58(3):242-250.
[30]Qiu LL,Ma T,Chang GB,Liu XP,Guo XM,Xu L,Zhang Y,Zhao WM,Xu Q,Chen GH.Expression patterns of NLRC5and key genes in the stat1 pathway following infection with Salmonella Pullorum.Gene,2017,597:23-29.
[31]Ma T,Xu L,Wang H,Guo X,Li Z,Wan F,Chen J,Liu L,Liu X,Chang G,Chen G.Identification of the crucial genes in the elimination and survival process of Salmonella enterica ser.Pullorum in the chicken spleen.Animal Genetics,2017,48(3):303-314.
[32]Liu XQ,Wang F,Jin J,Zhou YG,Ran JS,Feng ZQ,Wang Y,Liu YP.MyD88 polymorphisms and association with susceptibility to Salmonella Pullorum.Biomed Research International,2015,2015:692973.
[33]van der Heijden J,Reynolds LA,Deng WY,Mills A,Scholz R,Imami K,Foster LJ,Duong F,Finlay BB.Salmonella rapidly regulates membrane permeability to survive oxidative stress.mBio,2016,7(4):e01238-16.
[34]Mambu J,Virlogeux-Payant I,Holbert S,Grepinet O,Velge P,Wiedemann A.An updated view on the rck invasin of Salmonella:still much to discover.Frontiers in Cellular and Infection Microbiology,2017,7:500.
[35]Ferrer-Navarro M,Ballesté-Delpierre C,Vila J,Fàbrega A.Characterization of the outer membrane subproteome of the virulent strain Salmonella Typhimurium SL1344.Journal of Proteomics,2016,146:141-147.
[36]Setta AM,Barrow PA,Kaiser P,Jones MA.Early immune dynamics following infection with Salmonella enterica serovars Enteritidis,Infantis,Pullorum and Gallinarum:cytokine and chemokine gene expression profile and cellular changes of chicken cecal tonsils.Comparative Immunology,Microbiology and Infectious Diseases,2012,35(5):397-410.
[37]Berndt A,Pieper J,Methner U.CirculatingγδT cells in response to Salmonella enterica serovar Enteritidis exposure in chickens.Infection and Immunity,2006,74(7):3967-3978.
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[39]Cheeseman JH,Levy NA,Kaiser P,Lillehoj HS,Lamont SJ.Salmonella Enteritidis-induced alteration of inflammatory CXCL chemokine messenger-RNA expression and histologic changes in the ceca of infected chicks.Avian Diseases,2008,52(2):229-234.
[40]Matulova M,Varmuzova K,Sisak F,Havlickova H,Babak V,Stejskal K,Zdrahal Z,Rychlik I.Chicken innate immune response to oral infection with Salmonella enterica serovar Enteritidis.Veterinary Research,2013,44:37.
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[2]Brown NF,Finlay BB.Potential origins and horizontal transfer of type III secretion systems and effectors.Mobile Genetic Elements,2011,1(2):118-121.
[3]Jiao XA,Li QC.The research progress of pathogenic bacteria omics.China Poultry,2011,33(19):37-40,43.(in Chinese)焦新安,李求春.病原细菌组学的研究进展.中国家禽,2011,33(19):37-40,43.
[4]Barrow PA,Neto OCF.Pullorum disease and fowl typhoid-new thoughts on old diseases:a review.Avian Pathology,2011,40(1):1-13.
[5]FAO/WHO.Salmonella and Campylobacter in chicken meat:microbiological risk assessment series 19.World Health Organization,2009.
[6]Barrow PA.Salmonella infections:immune and non-immune protection with vaccines.Avian Pathology,2007,36(1):1-13.
[7]Chappell L,Kaiser P,Barrow P,Jones MA,Johnston C,Wigley P.The immunobiology of avian systemic salmonellosis.Veterinary Immunology and Immunopathology,2009,128(1/3):53-59.
[8]Guo AZ,Lasaro MA,Sirard JC,Kraehenbühl JP,Schifferli DM.Adhesin-dependent binding and uptake of Salmonella enterica serovar Typhimurium by dendritic cells.Microbiology,2007,153:1059-1069.
[9]Clayton DJ,Bowen AJ,Hulme SD,Buckley AM,Deacon VL,Thomson NR,Barrow PA,Morgan E,Jones MA,Watson M,Stevens MP.Analysis of the role of 13 major fimbrial subunits in colonisation of the chicken intestines by Salmonella enterica serovar Enteritidis reveals a role for a novel locus.BMC Microbiology,2008,8:228.
[10]Xiong D,Song L,Hu MZ,Pan ZM,Jiao XA.Progress on application of immune evasion mechanisms by Salmonella.Progress in Veterinary Medicine,2015,36(4):96-99,100.(in Chinese)熊丹,宋丽,胡茂志,潘志明,焦新安.沙门菌免疫逃逸机制及其应用研究进展.动物医学进展,2015,36(4):96-99,100.
[11]Kaiser P,Rothwell L,Galyov EE,Barrow PA,Burnside J,Wigley P.Differential cytokine expression in avian cells in response to invasion by Salmonella Typhimurium,Salmonella Enteritidis and Salmonella Gallinarum.Microbiology,2000,146 Pt 12:3217-3226.
[12]Sijben JWC,Klasing KC,Schrama JW,Parmentier HK,van der poel JJ,Savelkoul HFJ,Kaiser P.Early in vivo cytokine genes expression in chickens after challenge with Salmonella Typhimurium lipopolysaccharide and modulation by dietary n-3 polyunsaturated fatty acids.Developmental&Comparative Immunology,2003,27(6/7):611-619.
[13]Setta A,Barrow PA,Kaiser P,Jones MA.Immune dynamics following infection of avian macrophages and epithelial cells with typhoidal and non-typhoidal Salmonella enterica serovars;bacterial invasion and persistence,nitric oxide and oxygen production,differential host gene expression,NF-κBsignalling and cell cytotoxicity.Veterinary Immunology and Immunopathology,2012,146(3/4):212-224.
[14]Monack DM,Bouley DM,Falkow S.Salmonella Typhimurium persists within macrophages in the mesenteric lymph nodes of chronically infected Nramp1+/+mice and can be reactivated by IFNγneutralization.Journal of Experimental Medicine,2004,199(2):231-241.
[15]Vazquez-Torres A,Xu YS,Jones-Carson J,Holden DW,Lucia SM,Dinauer MC,Mastroeni P,Fang FC.Salmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase.Science,2000,287(5458):1655-1658.
[16]Batista DFA,Freitas Neto OC,Barrow PA,de Oliveira MT,Almeida AM,Ferraudo AS,Berchieri A Jr.Identification and characterization of regions of difference between the Salmonella Gallinarum biovar Gallinarum and the Salmonella Gallinarum biovar Pullorum genomes.Infection,Genetics and Evolution,2015,30:74-81.
[17]Chakravortty D,Hansen-Wester I,Hensel M.Salmonella pathogenicity island 2 mediates protection of intracellular Salmonella from reactive nitrogen intermediates.Journal of Experimental Medicine,2002,195(9):1155-1166.
[18]Hulme SD,Barrow PA,Foster N.Inhibited production of iNOS by murine J774 macrophages occurs via a pho P-regulated differential expression of NFκB and AP-1.Interdisciplinary Perspectives on Infectious Diseases,2012,2012:483170.
[19]Xu ZC,Qin Y,Wang YQ,Li XQ,Cao H,Zheng SJ.A critical role of bacterioferritin in Salmonella Pullorum-induced IFN-βexpression in DF-1 cells.Frontiers in Microbiology,2016,7:20.
[20]Jones MA,Wigley P,Page KL,Hulme SD,Barrow PA.Salmonella enterica serovar Gallinarum requires the Salmonella pathogenicity island 2 type III secretion system but not the Salmonella pathogenicity island 1 type IIIsecretion system for virulence in chickens.Infection and Immunity,2001,69(9):5471-5476.
[21]Jones MA,Hulme SD,Barrow PA,Wigley P.The Salmonella pathogenicity island 1 and Salmonella pathogenicity island 2type III secretion systems play a major role in pathogenesis of systemic disease and gastrointestinal tract colonization of Salmonella enterica serovar Typhimurium in the chicken.Avian Pathology,2007,36(3):199-203.
[22]Shin S,Brodsky IE.The inflammasome:learning from bacterial evasion strategies.Seminars in Immunology,2015,27(2):102-110.
[23]Sahler JM,Eade CR,Altier C,March JC.Salmonella enterica serovar Typhimurium increases functional PD-L1synergistically with gamma interferon in intestinal epithelial cells via Salmonella pathogenicity island 2.Infection and Immunity,2018,86(5):e00674-17.
[24]Blondel CJ,Yang HJ,Castro B,Chiang S,Toro CS,Zaldívar M,Contreras I,Andrews-Polymenis HL,Santiviago CA.Contribution of the type VI secretion system encoded in SPI-19 to chicken colonization by Salmonella enterica serotypes Gallinarum and Enteritidis.PLoS ONE,2010,5(7):e11724.
[25]Blondel CJ,Jiménez JC,Leiva LE,álvarez SA,Pinto BI,Contreras F,Pezoa D,Santiviago CA,Contreras I.The type VI secretion system encoded in Salmonella pathogenicity island 19 is required for Salmonella enterica serotype Gallinarum survival within infected macrophages.Infection and Immunity,2013,81(4):1207-1220.
[26]Matthews TD,Schmieder R,Silva GGZ,Busch J,Cassman N,Dutilh BE,Green D,Matlock B,Heffernan B,Olsen GJ,Hanna LF,Schifferli DM,Maloy S,Dinsdale EA,Edwards RA.Genomic comparison of the closely-related Salmonella enterica serovars Enteritidis,Dublin and Gallinarum.PLoSONE,2015,10(6):e0126883.
[27]Li QC,Xu YH,Jiao XA.Identification of Salmonella Pullorum genomic sequences using suppression subtractive hybridization.Journal of Microbiology and Biotechnology,2009,19(9):898-903.
[28]Yin JL,Chen Y,Xie XL,Xia J,Li QC,Geng SZ,Jiao XA.Influence of Salmonella enterica serovar Pullorum pathogenicity island 2 on type III secretion system effector gene expression in chicken macrophage hd11 cells.Avian Pathology,2017,46(2):209-214.
[29]Tao Z,Zhu C,Song W,Xu W,Zhang S,Liu H,Li H.Inductive expression of the NOD1 signalling pathway in chickens infected with Salmonella Pullorum.British Poultry Science,2017,58(3):242-250.
[30]Qiu LL,Ma T,Chang GB,Liu XP,Guo XM,Xu L,Zhang Y,Zhao WM,Xu Q,Chen GH.Expression patterns of NLRC5and key genes in the stat1 pathway following infection with Salmonella Pullorum.Gene,2017,597:23-29.
[31]Ma T,Xu L,Wang H,Guo X,Li Z,Wan F,Chen J,Liu L,Liu X,Chang G,Chen G.Identification of the crucial genes in the elimination and survival process of Salmonella enterica ser.Pullorum in the chicken spleen.Animal Genetics,2017,48(3):303-314.
[32]Liu XQ,Wang F,Jin J,Zhou YG,Ran JS,Feng ZQ,Wang Y,Liu YP.MyD88 polymorphisms and association with susceptibility to Salmonella Pullorum.Biomed Research International,2015,2015:692973.
[33]van der Heijden J,Reynolds LA,Deng WY,Mills A,Scholz R,Imami K,Foster LJ,Duong F,Finlay BB.Salmonella rapidly regulates membrane permeability to survive oxidative stress.mBio,2016,7(4):e01238-16.
[34]Mambu J,Virlogeux-Payant I,Holbert S,Grepinet O,Velge P,Wiedemann A.An updated view on the rck invasin of Salmonella:still much to discover.Frontiers in Cellular and Infection Microbiology,2017,7:500.
[35]Ferrer-Navarro M,Ballesté-Delpierre C,Vila J,Fàbrega A.Characterization of the outer membrane subproteome of the virulent strain Salmonella Typhimurium SL1344.Journal of Proteomics,2016,146:141-147.
[36]Setta AM,Barrow PA,Kaiser P,Jones MA.Early immune dynamics following infection with Salmonella enterica serovars Enteritidis,Infantis,Pullorum and Gallinarum:cytokine and chemokine gene expression profile and cellular changes of chicken cecal tonsils.Comparative Immunology,Microbiology and Infectious Diseases,2012,35(5):397-410.
[37]Berndt A,Pieper J,Methner U.CirculatingγδT cells in response to Salmonella enterica serovar Enteritidis exposure in chickens.Infection and Immunity,2006,74(7):3967-3978.
[38]Fasina YO,Holt PS,Moran ET,Moore RW,Conner DE,McKee SR.Intestinal cytokine response of commercial source broiler chicks to Salmonella Typhimurium infection.Poultry Science,2008,87(7):1335-1346.
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