The role of macrophages in anti-tuberculosis infection

doi:10.3969/j.issn.1000-6621.2018.02.020

Abstract

Abstract:

Macrophages play key roles in tuberculosis pathogenesis and host’s anti-tuberculosis immune defense. They represent an important component of innate immunity and are also major antigen presenting cells, functioning in both innate and acquired immunity. Tuberculosis, caused by Mycobacterium tuberculosis, is one of the main infectious diseases that are seriously harmful to human health. Mycobacterium tuberculosis can interfere with the immune response of macrophages in many ways. This review aims to elaborate the mechanisms of macrophages in various anti-tuberculosis immune responses after the infection of host by Mycobacterium tuberculosis.

Key words: Macrophages, Mycobacterium tuberculosis, Infection, Immunity, Review

Ya WANG,Chuan-you LI,Wei WANG,Shen-jie TANG. The role of macrophages in anti-tuberculosis infection[J]. Chinese Journal of Antituberculosis, 2018, 40(2): 218-221. doi: 10.3969/j.issn.1000-6621.2018.02.020

References 31

[1]	Sharma S, Raj A, Singh N , et al. Development of real-time immuno-PCR for the quantitative detection of mycobacterial PstS1 in tuberculosis patients. J Microbiol Methods, 2017,132:134-138. doi: 10.1016/j.mimet.2016.12.006 URL
[2]	Gordon S . Alternative activation of macrophages. Nat Rev Immunol, 2003,3(1):23-35. doi: 10.1038/nri978 URL
[3]	Murray PJ, Wynn TA . Obstacles and opportunities for understanding macrophage polarization. J Leukoc Biol, 2011,89(4):557-563. doi: 10.1189/jlb.0710409 URL pmid: 21248152
[4]	Lugo-Villarino G, Vérollet C, Maridonneau-Parini I , et al. Macrophage polarization: convergence point targeted by Mycobacterium tuberculosis and HIV. Front Immunol, 2011,2:43.
[5]	Marino S, Cilfone NA, Mattila JT , et al. Macrophage polarization drives granuloma outcome during Mycobacterium tuberculosis infection. Infect Immun, 2015,83(1):324-338. doi: 10.1128/IAI.02494-14 URL pmid: 25368116
[6]	Mattila JT, Ojo OO, Kepka-Lenhart D , et al. Microenvironments in tuberculous granulomas are delineated by distinct populations of macrophage subsets and expression of nitric oxide synthase and arginase isoforms. J Immunol, 2013,191(2):773-784. doi: 10.4049/jimmunol.1300113 URL
[7]	吴小娥, 陈晶, 宋淑霞 . 固有免疫细胞对结核分枝杆菌的免疫识别. 中国防痨杂志, 2015,37(2):189-193. doi: 10.3969/j.issn.1000-6621.2015.02.014 URL
[8]	Cervantes JL . MyD88 in Mycobacterium tuberculosis infection. Med Microbiol Immunol, 2017,206(3):187-193. doi: 10.1007/s00430-017-0495-0 URL pmid: 28220253
[9]	Negishi H, Yanai H, Nakajima A , et al. Cross-interference of RLR and TLR signaling pathways modulates antibacterial T cell responses. Nat Immunol, 2012,13(7):659-666. doi: 10.1038/ni.2307 URL pmid: 22610141
[10]	Kleinnijenhuis J, Oosting M, Joosten LA , et al. Innate immune recognition of Mycobacterium tuberculosis. Clin Deve Immunol, 2011,2011:405310.
[11]	Jeong YJ, Kang MJ, Lee SJ , et al. Nod2 and Rip2 contribute to innate immune responses in mouse neutrophils. Immunology, 2014,143(2):269-276. doi: 10.1016/j.cyto.2014.07.150 URL pmid: 24766550
[12]	Saxena M, Yeretssian G . NOD-like receptors: master regulators of inflammation and cancer. Front Immunol, 2014,5:327. doi: 10.3389/fimmu.2014.00327 URL pmid: 4095565
[13]	Hoving JC, Wilson GJ, Brown GD . Signalling C-type lectin receptors, microbial recognition and immunity. Cell Microbiol, 2014,16(2):185-194. doi: 10.1111/cmi.12249 URL pmid: 24330199
[14]	Ehlers S . DC-SIGN and mannosylated surface structures of Mycobacterium tuberculosis: a deceptive liaison. Eur J Cell Biol, 2010,89(1):95-101. doi: 10.1016/j.ejcb.2009.10.004 URL pmid: 19892432
[15]	Castillo EF, Dekonenko A, Arko-Mensah J , et al. Autophagy protects against active tuberculosis by suppressing bacterial burden and inflammation. Proc Natl Acad Sci U S A, 2012,109(46):E3168-E3176. doi: 10.1073/pnas.1210500109 URL
[16]	Harris J, Hope JC, Lavelle EC . Autophagy and the immune response to TB. Transbound Emerg Dis, 2009,56(6/7):248-254. doi: 10.1111/j.1865-1682.2009.01069.x URL pmid: 19389082
[17]	Gutierrez MG, Master SS, Singh SB , et al. Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages. Cell, 2004,119(6):753-766. doi: 10.1016/j.cell.2004.11.038 URL
[18]	Pahari S, Khan N, Aqdas M , et al. Infergen stimulated macro-phages restrict Mycobacterium tuberculosis growth by autophagy and release of nitric oxide. Sci Rep, 2016,6:39492. doi: 10.1038/srep39492 URL
[19]	万春辉, 杜先智 . 维生素D诱导自噬对巨噬细胞清除结核分枝杆菌的作用. 中国免疫学杂志, 2015,31(4):456-461. doi: 10.3969/j.issn.1000-484X.2015.04.005 URL
[20]	Jayaraman P, Sada-Ovalle I, Nishimura T , et al. IL-1β promotes antimicrobial immunity in macrophages by regulating TNFR signaling and caspase-3 activation. J Immunol, 2013,190(8):4196-4204. doi: 10.4049/jimmunol.1202688 URL
[21]	Yao K, Chen Q, Wu Y , et al. Unphosphorylated STAT1 represses apoptosis in macrophages during Mycobacterium tuberculosis infection. J Cell Sci, 2017,130(10):1740-1751. doi: 10.1242/jcs.200659 URL
[22]	Chen D, Li G, Fu X , et al. Wnt5a deficiency regulates inflammatory cytokine secretion, polarization, and apoptosis in Mycobacterium tuberculosis-infected macrophages. DNA Cell Biol, 2016,36(1):58-66.
[23]	Han JY, Lim YJ, Choi JA , et al. The role of prostate apoptosis response-4 (Par-4) in Mycobacterium tuberculosis infected macrophages. Sci Rep, 2016,6:32079. doi: 10.1038/srep32079 URL
[24]	Assis PA, Espíndola MS, Paula-Silva FW , et al. Mycobacterium tuberculosis expressing phospholipase C subverts PGE2 synthesis and induces necrosis in alveolar macrophages. BMC Microbiol, 2014,14:128. doi: 10.1186/1471-2180-14-128 URL
[25]	Wei M, Wang L, Wu T , et al. NLRP3 activation was regulated by DNA methylation modification during Mycobacterium tuberculosis infection. Biomed Res Int, 2016,2016:4323281.
[26]	Lupfer C, Kanneganti TD . Unsolved mysteries in NLR biology. Front Immunol, 2012,4:285. doi: 10.3389/fimmu.2013.00285 URL pmid: 24062750
[27]	Brooks MN, Rajaram MV, Azad AK , et al. NOD2 controls the nature of the inflammatory response and subsequent fate of Mycobacterium tuberculosis and M.bovis BCG in human macrophages. Cell Microbiol, 2011,13(3):402-418. doi: 10.1111/j.1462-5822.2010.01544.x URL
[28]	Mishra BB, Rathinam VA, Martens GW , et al. Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β. Nat Immunol, 2013,14(1):52-60. doi: 10.1038/ni.2474 URL
[29]	Nathan C, Shiloh MU . Reactive oxygen and nitrogen intermediates in the relationship between mammalian hosts and microbial pathogens. Proc Natl Acad Sci U S A, 2000,97(16):8841-8848. doi: 10.1073/pnas.97.16.8841 URL
[30]	Chakraborty U, Goswami A, Saha S , et al. Tumour necrosis factor-alpha and nitric oxide response in different categories of tuberculosis patients. Int J Tuberc Lung Dis, 2013,17(4):505-510. doi: 10.5588/ijtld.12.0196 URL
[31]	de Oliveira LR, Peresi E, Tavares FC , et al. DNA damage in peripheral blood mononuclear cells of patients undergoing anti-tuberculosis treatment. Mutat Res, 2012,747(1):82-85. doi: 10.1016/j.mrgentox.2012.04.003 URL