衣原体与巨噬细胞相互作用研究进展
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摘要
衣原体是一类专性胞内寄生菌,在宿主细胞内生长繁殖呈现独特的双相发育周期。衣原体感染机体后,巨噬细胞参与宿主固有免疫的第一道防线,在抗衣原体感染中发挥着重要作用。同时衣原体逐渐形成多种机制免疫逃逸巨噬细胞的杀伤。现对人类常见致病的肺炎衣原体(Chlamydia pneumonia,Cpn)、沙眼衣原体(Chlamydia tracho-matis,Ct)和鹦鹉热衣原体(Chlamydia psittaci,Cps)感染巨噬细胞后的相互作用机制作一简要概述。
Chlamydia is a strict intracellular parasite with unique developmental cycle.Macrophages,as the first line of defense components in innate immunity,not only participate in inflammation induced by Chlamydia,but also play a vital role in the fight against Chlamydia infection.Meanwhile,Chlamydia has gradually formed a variety of effective mechanisms to escape from macrophage killing.A brief overview of the mechanism of interaction between C.pneumonia,C.trachomatis,C.psittaci and infecting macrophages was conducted.
Chlamydia is a strict intracellular parasite with unique developmental cycle.Macrophages,as the first line of defense components in innate immunity,not only participate in inflammation induced by Chlamydia,but also play a vital role in the fight against Chlamydia infection.Meanwhile,Chlamydia has gradually formed a variety of effective mechanisms to escape from macrophage killing.A brief overview of the mechanism of interaction between C.pneumonia,C.trachomatis,C.psittaci and infecting macrophages was conducted.
引文
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[3]REDGROVE K A,MCLAUGHLIN E A.The role of the immune response in Chlamydia trachomatis infection of the male genital tract:A double-edged sword[J].Front Immunol,2014,5:534-556.
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[10]CAO W,ZOU Y,SU S,et al.Chlamydial plasmid-encoded protein pORF5 induces production of IL-1βand IL-18 via NALP3inflammasome activation and p38 MAPK pathway[J].Int J Clin Exp Med,2015,8(11):20368-20379.
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[14]WEBSTER S J,BRODE S,ELLIS L,et al.Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection[J].PLoS Pathog,2017,13(6):e1006383-1006386.
[15]CHEN H L,DAI G Z,ZHOU A W,et al.Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammation[J].BMC Microbiol,2017,17(1):153-164.
[16]贺庆芝,曾怀才,许雪梅,等.CPSIT_p7通过激活JNK/ERK信号通路诱导宿主细胞炎症[J].免疫学杂志,2017,33(2):124-128.
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[20]BERLIOCCHI L,CHIAPPINI C,ADORNETTO A,et al.Early LC3 lipidation induced by d-limonene does not rely on m TOR inhibition,ERK activation and ROS production and it is associated with reduced clonogenic capacity of SH-SY5Y neuroblastoma cells[J].Phytomedicine,2018,40:98-105.
[21]SIQUEIRA M D S,RIBEIRO R M,TRAVASSOS L H.Autophagy and its interaction with intracellular bacterial pathogens[J].Front Immunol,2018,9:935-952.
[22]SUN H S,ENG E W,JEGANATHAN S,et al.Chlamydia trachomatis vacuole maturation in infected macrophages[J].J Leukoc Biol,2012,92(4):815-827.
[23]AL-ZEER M A,AL-YOUNES H M,LAUSTER D,et al.Autophagy restricts Chlamydia trachomatis growth in human macrophages via IFNG-inducible guanylate binding proteins[J].Autophagy,2013,9(1):50-62.
[24]FIELDS K A,MCCORMACK R,DE ARMAS L R,et al.Perforin-2 restricts growth of Chlamydia trachomatis in macrophages[J].Infect Immun,2013,81(8):3045-3054.
[25]HE X,LIANG Y,LAVALLEY M P,et al.Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflammatory activity and innate immune evasion[J].BMC Microbiol,2015,15:228-239.
[26]LI C,XU M M,WANG K,et al.Macrophage polarization and meta-inflammation[J].Transl Res,2018,191:29-44.
[27]BUZS K,MARTON A,VIZLER C,et al.Bacterial sepsis increases survival in metastatic melanoma:Chlamydophila pneumoniae induces macrophage polarization and tumor regression[J].JInvest Dermatol,2016,136(4):862-865.
[28]NADELLA V,MOHANTY A,SHARMA L,et al.Inhibitors of apoptosis protein antagonists(Smac mimetic compounds)control polarization of macrophages during microbial challenge and sterile inflammatory responses[J].Front Immunol,2017,8:1792-1813.
[29]BUCHACHER T,OHRADANOVA-REPIC A,STOCKINGERH,et al.M2 Polarization of Human macrophages favors survival of the intracellular pathogen Chlamydia pneumoniae[J].PLoSOne,2015,10(11):e0143593-143596.
[30]SHARMA M,RECUERO-CHECA M A,FAN F Y,et al.Chlamydia trachomatis regulates growth and development in response to host cell fatty acid availability in the absence of lipid droplets[J].Cell Microbiol,2018,20(2):12801-12835.
[31]TUMURKHUU G,DAGVADORJ J,PORRITT R A,et al.Chlamydia pneumoniae Hijacks a host autoregulatory IL-1βloop to drive foam cell formation and accelerate atherosclerosis[J].Cell Metab,2018,28(3):432-448.
[32]ITOH R,MURAKAMI I,CHOU B,et al.Chlamydia pneumoniae harness host NLRP3 inflammasome-mediated caspase-1 activation for optimal intracellular growth in murine macrophages[J].Biochem Biophys Res Commun,2014.452(3):689-694.
[33]SHERRID A M,HYBISKE K.Chlamydia trachomatis cellular exit alters interactions with host dendritic cells[J].Infect Immun,2017,85(5):e00046-00063.
[34]ZUCK M,ELLIS T,VENIDA A,et al.Extrusions are phagocytosed and promote Chlamydia survival within macrophages[J].Cell Microbiol,2017,19(4):e12683-12686.
[35]BEECKMAN D S,VANROMPAY D C.Biology and intracellular pathogenesis of high or low virulent Chlamydophila psittaci strains in chicken macrophages[J].Vet Microbiol,2010,141(3/4):342-353.
[36]MARQUES-DA-SILVA C,CHAVES M M,RODRIGUES J C,et al.Differential modulation of ATP-induced P2X7-associated permeabilities to cations and anions of macrophages by infection with Leishmania amazonensis[J].PLoS One,2011,6(9):e25356-25361.
[37]LI L,WANG C,WEN Y,et al.ERK1/2 and the Bcl-2 family proteins Mcl-1,t Bid,and bim are involved in inhibition of apoptosis during persistent Chlamydia psittaci infection[J].Inflammation,2018,41(4):1372-1373.
[38]吴移谋,李忠玉,陈超群,等.衣原体[M].北京:人民卫生出版社,2012:122.
[39]PALAND N,BHME L,GURUMURTHY R K,et al.Reduced display of tumor necrosis factor receptor I at the host cell surface supports infection with Chlamydia trachomatis[J].J Biol Chem,2008,283(10):6438-6448.
[40]SARKAR A,MLLER S,BHATTACHARYYA A,et al.Mechanisms of apoptosis inhibition in Chlamydia pneumoniae-infected neutrophils[J].Int J Med Microbiol,2015,305(6):493-500.
[2]ELWELL C,MIRRASHIDI K,ENGEL J.Chlamydia cell biology and pathogenesis[J].Nat Rev Microbiol,2016,14(6):385-400.
[3]REDGROVE K A,MCLAUGHLIN E A.The role of the immune response in Chlamydia trachomatis infection of the male genital tract:A double-edged sword[J].Front Immunol,2014,5:534-556.
[4]CARTER J D,HUDSON A P.Recent advances and future directions in understanding and treating Chlamydia-induced reactive arthritis[J].Expert Rev Clin Immunol,2017,13(3):197-206.
[5]NOSRATABABADI R,BAGHERI V,ZARE-BIDAKI M,et al.Toll like receptor 4:an important molecule in recognition and induction of appropriate immune responses against Chlamydia infection[J].Comp Immunol Microbiol Infect Dis,2017,51:27-33.
[6]WANG Y,LIU Q,CHEN D,et al.Chlamydial lipoproteins stimulate toll-like receptors 1/2 mediated inflammatory responses through Myd88-dependent pathway[J].Front Microbiol,2017,8:78-86.
[7]ZHOU H,HUANG Q,LI Z,et al.PORF5 plasmid protein of Chlamydia trachomatis induces MAPK-mediated pro-inflammatory cytokines via TLR2 activation in THP-1 cells[J].Sci China Life Sci,2013,56(5):460-466.
[8]SMITH-NOROWITZ T A,PERLMAN J,NOROWITZ Y M,et al.Chlamydia pneumoniae induces interleukin-12 responses in peripheral blood mononuclear cells in asthma and the role of toll like receptor 2 versus 4:a pilot study[J].Ir J Med Sci,2017,186(2):511-517.
[9]SAEKI A,SUGIYAMA M,HASEBE A,et al.Activation of NL-RP3 inflammasome in macrophages by mycoplasmal lipoproteins and lipopeptides[J].Mol Oral Microbiol,2018,33(4):300-311.
[10]CAO W,ZOU Y,SU S,et al.Chlamydial plasmid-encoded protein pORF5 induces production of IL-1βand IL-18 via NALP3inflammasome activation and p38 MAPK pathway[J].Int J Clin Exp Med,2015,8(11):20368-20379.
[11]MATSUO J,NAKAMURA S,TAKEDA S,et al.Synergistic costimulatory effect of Chlamydia pneumoniae with carbon nanoparticles on NLRP3 inflammasome-mediated interleukin-1βsecretion in macrophages[J].Infect Immun,2015,83(7):2917-2925.
[12]ABDUL-SATER A A,SAD-SADIER N,PADILLA E V,et al.Chlamydial infection of monocytes stimulates IL-1beta secretion through activation of the NLRP3 inflammasome[J].Microbes Infect,2010,12(8/9):652-661.
[13]YEUNG A T Y,HALE C,LEE A H,et al.Exploiting induced pluripotent stem cell-derived macrophages to unravel host factors influencing Chlamydia trachomatis pathogenesis[J].Nat Commun,2017,8:15013-15025.
[14]WEBSTER S J,BRODE S,ELLIS L,et al.Detection of a microbial metabolite by STING regulates inflammasome activation in response to Chlamydia trachomatis infection[J].PLoS Pathog,2017,13(6):e1006383-1006386.
[15]CHEN H L,DAI G Z,ZHOU A W,et al.Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammation[J].BMC Microbiol,2017,17(1):153-164.
[16]贺庆芝,曾怀才,许雪梅,等.CPSIT_p7通过激活JNK/ERK信号通路诱导宿主细胞炎症[J].免疫学杂志,2017,33(2):124-128.
[17]BEECKMAN D S,ROTHWELL L,KAISER P,et al.Differential cytokine expression in Chlamydophila psittaci genotype A-,B-or D-infected chicken macrophages after exposure to Escherichia coli O2:K1 LPS[J].Dev Comp Immunol,2010,34(8):812-820.
[18]PHAM O H,O'DONNELL H,AL-SHAMKHANI A,et al.T cell expression of IL-18R and DR3 is essential for non-cognate stimulation of Th1 cells and optimal clearance of intracellular bacteria[J].PLoS Pathog,2017,13(8):e1006566-1006588.
[19]SHIMA K,KAEDING N,OGUNSULIRE I M,et al.Interferon-γinterferes with host cell metabolism during intracellular Chlamydia trachomatis infection[J].Cytokine,2018,112:95-101.
[20]BERLIOCCHI L,CHIAPPINI C,ADORNETTO A,et al.Early LC3 lipidation induced by d-limonene does not rely on m TOR inhibition,ERK activation and ROS production and it is associated with reduced clonogenic capacity of SH-SY5Y neuroblastoma cells[J].Phytomedicine,2018,40:98-105.
[21]SIQUEIRA M D S,RIBEIRO R M,TRAVASSOS L H.Autophagy and its interaction with intracellular bacterial pathogens[J].Front Immunol,2018,9:935-952.
[22]SUN H S,ENG E W,JEGANATHAN S,et al.Chlamydia trachomatis vacuole maturation in infected macrophages[J].J Leukoc Biol,2012,92(4):815-827.
[23]AL-ZEER M A,AL-YOUNES H M,LAUSTER D,et al.Autophagy restricts Chlamydia trachomatis growth in human macrophages via IFNG-inducible guanylate binding proteins[J].Autophagy,2013,9(1):50-62.
[24]FIELDS K A,MCCORMACK R,DE ARMAS L R,et al.Perforin-2 restricts growth of Chlamydia trachomatis in macrophages[J].Infect Immun,2013,81(8):3045-3054.
[25]HE X,LIANG Y,LAVALLEY M P,et al.Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflammatory activity and innate immune evasion[J].BMC Microbiol,2015,15:228-239.
[26]LI C,XU M M,WANG K,et al.Macrophage polarization and meta-inflammation[J].Transl Res,2018,191:29-44.
[27]BUZS K,MARTON A,VIZLER C,et al.Bacterial sepsis increases survival in metastatic melanoma:Chlamydophila pneumoniae induces macrophage polarization and tumor regression[J].JInvest Dermatol,2016,136(4):862-865.
[28]NADELLA V,MOHANTY A,SHARMA L,et al.Inhibitors of apoptosis protein antagonists(Smac mimetic compounds)control polarization of macrophages during microbial challenge and sterile inflammatory responses[J].Front Immunol,2017,8:1792-1813.
[29]BUCHACHER T,OHRADANOVA-REPIC A,STOCKINGERH,et al.M2 Polarization of Human macrophages favors survival of the intracellular pathogen Chlamydia pneumoniae[J].PLoSOne,2015,10(11):e0143593-143596.
[30]SHARMA M,RECUERO-CHECA M A,FAN F Y,et al.Chlamydia trachomatis regulates growth and development in response to host cell fatty acid availability in the absence of lipid droplets[J].Cell Microbiol,2018,20(2):12801-12835.
[31]TUMURKHUU G,DAGVADORJ J,PORRITT R A,et al.Chlamydia pneumoniae Hijacks a host autoregulatory IL-1βloop to drive foam cell formation and accelerate atherosclerosis[J].Cell Metab,2018,28(3):432-448.
[32]ITOH R,MURAKAMI I,CHOU B,et al.Chlamydia pneumoniae harness host NLRP3 inflammasome-mediated caspase-1 activation for optimal intracellular growth in murine macrophages[J].Biochem Biophys Res Commun,2014.452(3):689-694.
[33]SHERRID A M,HYBISKE K.Chlamydia trachomatis cellular exit alters interactions with host dendritic cells[J].Infect Immun,2017,85(5):e00046-00063.
[34]ZUCK M,ELLIS T,VENIDA A,et al.Extrusions are phagocytosed and promote Chlamydia survival within macrophages[J].Cell Microbiol,2017,19(4):e12683-12686.
[35]BEECKMAN D S,VANROMPAY D C.Biology and intracellular pathogenesis of high or low virulent Chlamydophila psittaci strains in chicken macrophages[J].Vet Microbiol,2010,141(3/4):342-353.
[36]MARQUES-DA-SILVA C,CHAVES M M,RODRIGUES J C,et al.Differential modulation of ATP-induced P2X7-associated permeabilities to cations and anions of macrophages by infection with Leishmania amazonensis[J].PLoS One,2011,6(9):e25356-25361.
[37]LI L,WANG C,WEN Y,et al.ERK1/2 and the Bcl-2 family proteins Mcl-1,t Bid,and bim are involved in inhibition of apoptosis during persistent Chlamydia psittaci infection[J].Inflammation,2018,41(4):1372-1373.
[38]吴移谋,李忠玉,陈超群,等.衣原体[M].北京:人民卫生出版社,2012:122.
[39]PALAND N,BHME L,GURUMURTHY R K,et al.Reduced display of tumor necrosis factor receptor I at the host cell surface supports infection with Chlamydia trachomatis[J].J Biol Chem,2008,283(10):6438-6448.
[40]SARKAR A,MLLER S,BHATTACHARYYA A,et al.Mechanisms of apoptosis inhibition in Chlamydia pneumoniae-infected neutrophils[J].Int J Med Microbiol,2015,305(6):493-500.
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