布鲁菌感染早期抗免疫机制研究进展
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摘要
布鲁菌引起的布鲁菌病在我国被列为二类动物疫病之首。虽然宿主本身具有复杂的免疫机制,用以抵御病原体,并保持宿主抗性和布鲁菌毒力之间的平衡,但布鲁菌作为一种成功的细胞内病原体,已经进化出多种策略来逃避免疫应答并在宿主内建立持续感染和繁殖。论文将从布鲁菌的毒力因子、布鲁菌在先天性免疫和适应性免疫系统中隐身策略,以及布鲁菌调控并抑制细胞凋亡、布鲁菌微小RNA(mircoRNA)在宿主免疫应答中的研究进展等方面进行综述,为了解布鲁菌病发病机理、开发新型疫苗和治疗布鲁菌病提供参考。
Brucellosis caused by Brucellais currently ranked as the top of the class B infectious disease in China.Although the host itself has a complex immune mechanism to defend against pathogens and maintain a balance between host resistance and the virulence of Brucella.However,as a successful intracellular pathogen,Brucella has evolved a variety of strategies to evade the immune response and establish a persistent infection and replication within the host.In this overview we reviewed Brucella's virulence factors,Brucella's stealth strategies in innate immunity and adaptive immune systems,as well as the inhibition of apoptosis and the study of it's microRNAs against immune mechanisms,to provide a basis for understanding the pathogenesis of brucellosis,developing new vaccines and treating brucellosis.
Brucellosis caused by Brucellais currently ranked as the top of the class B infectious disease in China.Although the host itself has a complex immune mechanism to defend against pathogens and maintain a balance between host resistance and the virulence of Brucella.However,as a successful intracellular pathogen,Brucella has evolved a variety of strategies to evade the immune response and establish a persistent infection and replication within the host.In this overview we reviewed Brucella's virulence factors,Brucella's stealth strategies in innate immunity and adaptive immune systems,as well as the inhibition of apoptosis and the study of it's microRNAs against immune mechanisms,to provide a basis for understanding the pathogenesis of brucellosis,developing new vaccines and treating brucellosis.
引文
[1] Xavier M N,Paixo T A,Hartigh A B D,et al.Pathogenesis of Brucellaspp.[J].Open Vet Sci J,2010,4(1):109-118.
[2] Gopalakrishnan A,Dimri U,Saminathan M,et al.Virulence factors,intracellular survivability and mechanism of evasion from host immune response by Brucella:An overview[J].J Anim Plant Sci,2016,26(6):1542-1555.
[3]彭永,张阁,冯宇,等.动物布鲁氏菌Rev.1疫苗研究进展[J].中国兽药杂志,2017,51(6):64-68.
[4] Sidhu-Mu1oz R S,Sancho P,Vizcaíno N.Brucella ovis PA mutants for outer membrane proteins Omp10,Omp19,SP41,and BepC are not altered in their virulence and outer membrane properties[J].Vet Microbiol,2016,186:59-66.
[5] Pathak P,Kumar A,Sarangi P P,et al.Cloning,expression and purification of virB10protein of Brucella melitensis and to evaluate its role as a serological marker for Brucellainfection in experimental and natural hosts[J].Protein Exp Purificat,2018,145:53-58.
[6] Guzmán-Verri C,Manterola L,Sola-Landa A,et al.The twocomponent system BvrR/BvrS essential for Brucella abortus virulence regulates the expression of outer membrane proteins with counterparts in members of the Rhizobiaceae[J].Proceed Nat Acad Sci USA,2002,99(19):12375-12380.
[7] Zhao Y,Hanniffy S,Arce-Gorvel V,et al.Immunomodulatory properties of Brucella melitensis lipopolysaccharide determinants on mouse dendritic cells in vitro and in vivo[J].Virulence,2017,9:465-479.
[8] Turse J E,Pei J,Ficht T A.Lipopolysaccharide-deficient Brucella variants arise spontaneously during infection[J].Front Microbiol,2011,2(54):54.
[9] Chavesolarte E,Weiss D S,Rucavado A,et al.Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection[J].PLoS One,2007,2(7):e631.
[10] Martirosyan A,Moreno E,Gorvel J P.An evolutionary strategy for a stealthy intracellular Brucella pathogen[J].Immun Revi,2011,240(1):211.
[11] Ke Y,Li W,Wang Y,et al.Inhibition of TLR4signaling by Brucella TIR-containing protein TcpB-derived decoy peptides[J].Int J Med Microbiol,2016,306(6):391.
[12] Iannino N I D,Briones G,Tolmasky M,et al.Molecular cloning and characterization of cgs,the Brucella abortus cyclicβ(1-2)glucan synthetase gene:Genetic complementation of rhizobium meliloti ndvB and agrobacterium tumefaciens chvB mutants[J].J Bacteriol,1998,180(17):4392.
[13] Campos P C,Gomes M T,Guimar2es G,et al.Brucella abortus DNA is a major bacterial agonist to activate the host innate immune system[J].Microbes Infect,2014,16(12):979-984.
[14] Alvessilva J,Tavares I P,Guimar2es E S,et al.Modulation of microtubule dynamics affects Brucella abortus intracellular survival,pathogen-containing vacuole maturation,and pro-inflammatory cytokine production in infected macrophages[J].Front Microbiol,2017,8:2217.
[15]易继海,张俊波,李爽,等.NF-κB信号通路调控布鲁氏菌胞内存活分子机制的初步研究[J].中国畜牧兽医,2016,43(3):592-600.
[16] De F P,Ficht T A,Rice-Ficht A,et al.Pathogenesis and immunobiology of brucellosis:review of Brucella-host interactions[J].Am J Pathol,2015,185(6):1505-1517.
[17] Machelart A,Khadrawi A,Demars A,et al.Chronic Brucella infection induces selective and persistent IFN-γ-dependent alterations of marginal zone macrophages in the spleen[J].Infect Immun,2017,85(11):IAI.00115-17.
[18] Richard C,Marie-Alice V,Delphine H M,et al.In situ microscopy analysis reveals local innate immune response developed around Brucellainfected cells in resistant and susceptible mice[J].PLoS Pathog,2012,8(3):e1002575.
[19] Elzer P H,Jacobson R H,Nielsen K H,et al.BALB/c mice infected with Brucella abortus express protracted polyclonal responses of both IgG2aand IgG3isotypes[J].Immunol Lett,1994,42(3):145-150.
[20] Heller M C,Watson J L,Blanchard M T,et al.Characterization of Brucella abortus infection of bovine monocyte-derived dendritic cells[J].Vet Immunol Immunopathol,2012,149(3-4):255.
[21] Spera J M,Comerci D J,Ugalde J E.Brucella alters the immune response in a prpA-dependent manner[J].Microbial Pathog,2014,S67-68(1):8-13.
[22] Elfaki M G,Al-Hokail A A.Transforming growth factor beta production correlates with depressed lymphocytes function in humans with chronic Brucellosis[J].Microbes Infect,2009,11(14-15):1089-1096.
[23] Atluri V L,Xavier M N,Jong M F D,et al.Interactions of the human pathogenic Brucellaspecies with their hosts[J].Annual Rev Microbiol,2011,65(1):523-541.
[24] Cui G,Wei P,Zhao Y,et al.Brucellainfection inhibits macrophages apoptosis via Nedd4-dependent degradation of calpain2[J].Vet Microbiol,2014,174(1-2):195-205.
[25] Wei P,Cui G,Lu Q,et al.A20promotes Brucellaintracellular growth via inhibition of macrophage cell death and activation[J].Vet Microbiol,2015,175(1):50-57.
[26] Pei J,Kahl-Mcdonagh M,Ficht T A.Brucella dissociation is essential for macrophage egress and bacterial dissemination[J].Front Cell Infect Microbiol,2014,4(2):23.
[27] Pei J,Turse J E,Ficht T A.Evidence of Brucellaabortus OPS dictating uptake and restricting NF-kappaB activation in murine macrophages[J].Microbe Infect,2008,10(6):582-590.
[28] Chen C Z,Li L,Lodish H F,et al.MicroRNAs modulate hematopoietic lineage differentiation[J].Science,2004,303(5654):83-86.
[29] Iliopoulos D,Jaeger S A,Hirsch H A,et al.STAT3activation of miR-21and miR-181b-1,via PTEN and CYLD,are part of the epigenetic switch linking inflammation to cancer[J].Molecular Cell,2010,39(4):493.
[30] Wang Y,Ke Y,Xu J,et al.Identification of a novel small noncoding RNA modulating the intracellular survival of Brucella melitensis[J].Front Microbiol,2015,6:164.
[31] Zheng K,Chen D S,Wu Y Q,et al.MicroRNA expression profile in RAW264.7cells in response to Brucella melitensis infection[J].Int J Biolog Sci,2012,8(7):1013-1022.
[2] Gopalakrishnan A,Dimri U,Saminathan M,et al.Virulence factors,intracellular survivability and mechanism of evasion from host immune response by Brucella:An overview[J].J Anim Plant Sci,2016,26(6):1542-1555.
[3]彭永,张阁,冯宇,等.动物布鲁氏菌Rev.1疫苗研究进展[J].中国兽药杂志,2017,51(6):64-68.
[4] Sidhu-Mu1oz R S,Sancho P,Vizcaíno N.Brucella ovis PA mutants for outer membrane proteins Omp10,Omp19,SP41,and BepC are not altered in their virulence and outer membrane properties[J].Vet Microbiol,2016,186:59-66.
[5] Pathak P,Kumar A,Sarangi P P,et al.Cloning,expression and purification of virB10protein of Brucella melitensis and to evaluate its role as a serological marker for Brucellainfection in experimental and natural hosts[J].Protein Exp Purificat,2018,145:53-58.
[6] Guzmán-Verri C,Manterola L,Sola-Landa A,et al.The twocomponent system BvrR/BvrS essential for Brucella abortus virulence regulates the expression of outer membrane proteins with counterparts in members of the Rhizobiaceae[J].Proceed Nat Acad Sci USA,2002,99(19):12375-12380.
[7] Zhao Y,Hanniffy S,Arce-Gorvel V,et al.Immunomodulatory properties of Brucella melitensis lipopolysaccharide determinants on mouse dendritic cells in vitro and in vivo[J].Virulence,2017,9:465-479.
[8] Turse J E,Pei J,Ficht T A.Lipopolysaccharide-deficient Brucella variants arise spontaneously during infection[J].Front Microbiol,2011,2(54):54.
[9] Chavesolarte E,Weiss D S,Rucavado A,et al.Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection[J].PLoS One,2007,2(7):e631.
[10] Martirosyan A,Moreno E,Gorvel J P.An evolutionary strategy for a stealthy intracellular Brucella pathogen[J].Immun Revi,2011,240(1):211.
[11] Ke Y,Li W,Wang Y,et al.Inhibition of TLR4signaling by Brucella TIR-containing protein TcpB-derived decoy peptides[J].Int J Med Microbiol,2016,306(6):391.
[12] Iannino N I D,Briones G,Tolmasky M,et al.Molecular cloning and characterization of cgs,the Brucella abortus cyclicβ(1-2)glucan synthetase gene:Genetic complementation of rhizobium meliloti ndvB and agrobacterium tumefaciens chvB mutants[J].J Bacteriol,1998,180(17):4392.
[13] Campos P C,Gomes M T,Guimar2es G,et al.Brucella abortus DNA is a major bacterial agonist to activate the host innate immune system[J].Microbes Infect,2014,16(12):979-984.
[14] Alvessilva J,Tavares I P,Guimar2es E S,et al.Modulation of microtubule dynamics affects Brucella abortus intracellular survival,pathogen-containing vacuole maturation,and pro-inflammatory cytokine production in infected macrophages[J].Front Microbiol,2017,8:2217.
[15]易继海,张俊波,李爽,等.NF-κB信号通路调控布鲁氏菌胞内存活分子机制的初步研究[J].中国畜牧兽医,2016,43(3):592-600.
[16] De F P,Ficht T A,Rice-Ficht A,et al.Pathogenesis and immunobiology of brucellosis:review of Brucella-host interactions[J].Am J Pathol,2015,185(6):1505-1517.
[17] Machelart A,Khadrawi A,Demars A,et al.Chronic Brucella infection induces selective and persistent IFN-γ-dependent alterations of marginal zone macrophages in the spleen[J].Infect Immun,2017,85(11):IAI.00115-17.
[18] Richard C,Marie-Alice V,Delphine H M,et al.In situ microscopy analysis reveals local innate immune response developed around Brucellainfected cells in resistant and susceptible mice[J].PLoS Pathog,2012,8(3):e1002575.
[19] Elzer P H,Jacobson R H,Nielsen K H,et al.BALB/c mice infected with Brucella abortus express protracted polyclonal responses of both IgG2aand IgG3isotypes[J].Immunol Lett,1994,42(3):145-150.
[20] Heller M C,Watson J L,Blanchard M T,et al.Characterization of Brucella abortus infection of bovine monocyte-derived dendritic cells[J].Vet Immunol Immunopathol,2012,149(3-4):255.
[21] Spera J M,Comerci D J,Ugalde J E.Brucella alters the immune response in a prpA-dependent manner[J].Microbial Pathog,2014,S67-68(1):8-13.
[22] Elfaki M G,Al-Hokail A A.Transforming growth factor beta production correlates with depressed lymphocytes function in humans with chronic Brucellosis[J].Microbes Infect,2009,11(14-15):1089-1096.
[23] Atluri V L,Xavier M N,Jong M F D,et al.Interactions of the human pathogenic Brucellaspecies with their hosts[J].Annual Rev Microbiol,2011,65(1):523-541.
[24] Cui G,Wei P,Zhao Y,et al.Brucellainfection inhibits macrophages apoptosis via Nedd4-dependent degradation of calpain2[J].Vet Microbiol,2014,174(1-2):195-205.
[25] Wei P,Cui G,Lu Q,et al.A20promotes Brucellaintracellular growth via inhibition of macrophage cell death and activation[J].Vet Microbiol,2015,175(1):50-57.
[26] Pei J,Kahl-Mcdonagh M,Ficht T A.Brucella dissociation is essential for macrophage egress and bacterial dissemination[J].Front Cell Infect Microbiol,2014,4(2):23.
[27] Pei J,Turse J E,Ficht T A.Evidence of Brucellaabortus OPS dictating uptake and restricting NF-kappaB activation in murine macrophages[J].Microbe Infect,2008,10(6):582-590.
[28] Chen C Z,Li L,Lodish H F,et al.MicroRNAs modulate hematopoietic lineage differentiation[J].Science,2004,303(5654):83-86.
[29] Iliopoulos D,Jaeger S A,Hirsch H A,et al.STAT3activation of miR-21and miR-181b-1,via PTEN and CYLD,are part of the epigenetic switch linking inflammation to cancer[J].Molecular Cell,2010,39(4):493.
[30] Wang Y,Ke Y,Xu J,et al.Identification of a novel small noncoding RNA modulating the intracellular survival of Brucella melitensis[J].Front Microbiol,2015,6:164.
[31] Zheng K,Chen D S,Wu Y Q,et al.MicroRNA expression profile in RAW264.7cells in response to Brucella melitensis infection[J].Int J Biolog Sci,2012,8(7):1013-1022.
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