Research progress of innate immunity and adaptive immune response in diabetic patients complicated with tuberculosis infection

doi:10.19982/j.issn.1000-6621.20210686

Abstract

Abstract:

Diabetes is one of the risk factors for tuberculosis or progression to severe tuberculosis. The inflammatory environment caused by high glucose can lead to the damage of phagocytosis of innate immune cells and delayed presentation of related antigen presenting cells. Then the abnormal differentiation induced by adaptive immune response will affect the anti-Mycobacterium tuberculosis infection of CD4⁺ and CD8⁺T cells, lead to abnormal secretion of related cytokines and eventually cause immune dysfunction and accelerate the process of tuberculosis infection. Therefore, the research progress on the innate immune mechanism and adaptive immune response of diabetes to anti-tuberculosis infection were reviewed, in order to provide the basis for the anti-inflammatory treatment of diabetic patients and the formulation of reasonable immunotherapy strategies.

Key words: Tuberculosis, Diabetes mellitus, Comorbidity, Immunity, Review literature as topic

CLC Number:

LI Yu-jie, YANG Yu-ting, YANG Guo-ping. Research progress of innate immunity and adaptive immune response in diabetic patients complicated with tuberculosis infection[J]. Chinese Journal of Antituberculosis, 2022, 44(5): 512-516. doi: 10.19982/j.issn.1000-6621.20210686

References 39

[1]	World Health Organization. Latent tuberculosis infection: updated and consolidated guidelines for programmatic management. Geneva: World Health Organization, 2018.
[2]	Al-Rifai RH, Pearson F, Critchley JA, et al. Association between diabetes mellitus and active tuberculosis: A systematic review and meta-analysis. PLoS One, 2017, 12(11): e0187967. doi: 10.1371/journal.pone.0187967. doi: 10.1371/journal.pone.0187967 URL
[3]	Ferlita S, Yegiazaryan A, Noori N, et al. Type 2 Diabetes Mellitus and Altered Immune System Leading to Susceptibility to Pathogens, Especially Mycobacterium tuberculosis. J Clin Med, 2019, 8(12): 2219. doi: 10.3390/jcm8122219. doi: 10.3390/jcm8122219
[4]	毛毅, 范琳, 刘勇. 肺结核并发糖尿病的诊治研究进展. 中国防痨杂志, 2019, 41(12): 1325-1329. doi: 10.3969/j.issn.1000-6621.2019.12.015. doi: 10.3969/j.issn.1000-6621.2019.12.015
[5]	林岩, 邓国防. 糖尿病并发结核病治疗中多学科合作应注意的问题. 中国防痨杂志, 2021, 43(7): 649-652. doi: 10.3969/j.issn.1000-6621.2021.7.002. doi: 10.3969/j.issn.1000-6621.2021.7.002
[6]	Masood KI, Irfan M, Masood Q, et al. Latent M.tuberculosis infection is associated with increased inflammatory cytokine and decreased suppressor of cytokine signalling (SOCS)-3 in the diabetic host. Scand J Immunol, 2021: e13134. doi: 10.1111/sji.13134. doi: 10.1111/sji.13134
[7]	Mo J, Jin R, Yan Q, et al. Quantitative analysis of glycation and its impact on antigen binding. MAbs, 2018, 10(3): 406-415. doi: 10.1080/19420862.2018.1438796. doi: 10.1080/19420862.2018.1438796 URL
[8]	Ferlita S, Yegiazaryan A, Noori N, et al. Type 2 Diabetes Mellitus and Altered Immune System Leading to Susceptibility to Pathogens, Especially Mycobacterium tuberculosis (Review). J Clin Med, 2019, 8(12): 2219. doi: 10.3390/jcm8122219. doi: 10.3390/jcm8122219 URL
[9]	Arias L, Goig GA, Cardona P, et al. Influence of Gut Microbiota on Progression to Tuberculosis Generated by High Fat Diet-Induced Obesity in C3HeB/FeJ Mice. Front Immunol, 2019, 10: 2464. doi: 10.3389/fimmu.2019.02464. doi: 10.3389/fimmu.2019.02464 URL
[10]	Carlberg C. Vitamin D Signaling in the Context of Innate Immunity: Focus on Human Monocytes. Front Immunol, 2019, 10: 2211. doi: 10.3389/fimmu.2019.02211. doi: 10.3389/fimmu.2019.02211 pmid: 31572402
[11]	Zhao X, Yuan Y, Lin Y, et al. Vitamin D status of tuberculosis patients with diabetes mellitus in different economic areas and associated factors in China. PLoS One, 2018, 13(11): e0206372. doi: 10.1371/journal.pone.0206372. doi: 10.1371/journal.pone.0206372 URL
[12]	Kumar NP, Moideen K, Bhootra Y, et al. Elevated circulating levels of monocyte activation markers among tuberculosis patients with diabetes co-morbidity. Immunology, 2019, 156(3): 249-258. doi: 10.1111/imm.13023. doi: 10.1111/imm.13023
[13]	Torres M, Herrera MT, Fabián-San-Miguel G, et al. The Intracellular Growth of M.tuberculosis Is More Associated with High Glucose Levels Than with Impaired Responses of Monocytes from T2D Patients. J Immunol Res, 2019, 2019: 1462098. doi: 10.1155/2019/1462098. doi: 10.1155/2019/1462098
[14]	Kundu J, Verma A, Verma I, et al. Proteomic changes in Mycobacterium tuberculosis H37Rv under hyperglycemic conditions favour its growth through altered expression of Tgs3(Rv3234c) and supportive proteins (Rv0547c, AcrA1 and Mpa). Tuberculosis (Edinb), 2019, 115: 154-160. doi: 10.1016/j.tube.2019.03.006. doi: 10.1016/j.tube.2019.03.006 URL
[15]	Lopez-Lopez N, Martinez AGR, Garcia-Hernandez MH, et al. Type-2 diabetes alters the basal phenotype of human macrophages and diminishes their capacity to respond, internalise, and control Mycobacterium tuberculosis. Mem Inst Oswaldo Cruz, 2018, 113(4): e170326. doi: 10.1590/0074-02760170326. doi: 10.1590/0074-02760170326
[16]	Martinez N, Ketheesan N, West K, et al. Impaired Recognition of Mycobacterium tuberculosis by Alveolar Macrophages From Diabetic Mice. J Infect Dis, 2016, 214(11): 1629-1637. doi: 10.1093/infdis/jiw436. doi: 10.1093/infdis/jiw436 pmid: 27630197
[17]	Alim MA, Sikder S, Sathkumara H, et al. Dysregulation of key cytokines may contribute to increased susceptibility of diabetic mice to Mycobacterium bovis BCG infection. Tuberculosis (Edinb), 2019, 115: 113-120. doi: 10.1016/j.tube.2019.02.005. doi: 10.1016/j.tube.2019.02.005 URL
[18]	Vance J, Santos A, Sadofsky L, et al. Effect of High Glucose on Human Alveolar Macrophage Phenotype and Phagocytosis of Mycobacteria. Lung, 2019, 197(1): 89-94. doi: 10.1007/s00408-018-0181-z. doi: 10.1007/s00408-018-0181-z URL
[19]	Vrieling F, Wilson L, Rensen PCN, et al. Oxidized low-density lipoprotein (oxLDL) supports Mycobacterium tuberculosis survival in macrophages by inducing lysosomal dysfunction. PLoS Pathog, 2019, 15(4): e1007724. doi: 10.1371/journal.ppat.1007724. doi: 10.1371/journal.ppat.1007724 URL
[20]	Bizzell E, Sia JK, Quezada M, et al. Deletion of BCG Hip1 protease enhances dendritic cell and CD4 T cell responses. J Leukoc Biol, 2018, 103(4): 739-748. doi: 10.1002/JLB.4A0917-363RR. doi: 10.1002/JLB.4A0917-363RR URL
[21]	Kumar NP, Moideen K, Dhakshinraj SD, et al. Profiling leucocyte subsets in tuberculosis-diabetes co-morbidity. Immunology, 2015, 146(2): 243-250. doi: 10.1111/imm.12496. doi: 10.1111/imm.12496 URL
[22]	Monroy-Mérida G, Guzmán-Beltrán S, Hernández F, et al. High Glucose Concentrations Impair the Processing and Presentation of Mycobacterium tuberculosis Antigens In Vitro. Biomolecules, 2021, 11(12): 1763. doi: 10.3390/biom11121763. doi: 10.3390/biom11121763 URL
[23]	Gilardini Montani MS, Granato M, Cuomo L, et al. High glucose and hyperglycemic sera from type 2 diabetic patients impair DC differentiation by inducing ROS and activating Wnt/β-catenin and p38 MAPK. Biochim Biophys Acta, 2016, 1862(4): 805-813. doi: 10.1016/j.bbadis.2016.01.001. doi: S0925-4439(16)00002-8 pmid: 26769359
[24]	Kumar NP, Moideen K, Viswanathan V, et al. Effect of anti-tuberculosis treatment on the systemic levels of tissue inhibitors of metalloproteinases in tuberculosis-Diabetes co-morbidity. J Clin Tuberc Other Mycobact Dis, 2021, 23: 100237. doi: 10.1016/j.jctube.2021.100237. doi: 10.1016/j.jctube.2021.100237
[25]	Ayelign B, Negash M, Genetu M, et al. Immunological Impacts of Diabetes on the Susceptibility of Mycobacterium tuberculosis. J Immunol Res, 2019, 2019: 6196532. doi: 10.1155/2019/6196532. doi: 10.1155/2019/6196532
[26]	Chumburidze-Areshidze N, Kezeli T, Avaliani Z, et al. The Relationship Between Type-2 Diabetes and Tuberculosis. Georgian Med News, 2020(300): 69-74. pmid: 32383705
[27]	Cheekatla SS, Tripathi D, Venkatasubramanian S, et al. NK-CD11c⁺ Cell Crosstalk in Diabetes Enhances IL-6-Mediated Inflammation during Mycobacterium tuberculosis Infection. PLoS Pathog, 2016, 12(10): e1005972. doi: 10.1371/journal.ppat.1005972. doi: 10.1371/journal.ppat.1005972 URL
[28]	Leisching GR. PI3-Kinase δγ Catalytic Isoforms Regulate the Th-17 Response in Tuberculosis. Front Immunol, 2019, 10: 2583. doi: 10.3389/fimmu.2019.02583. doi: 10.3389/fimmu.2019.02583 pmid: 31736982
[29]	Wang X, Ma A, Han X, et al. T Cell Profile was Altered in Pulmonary Tuberculosis Patients with Type 2 Diabetes. Med Sci Monit, 2018, 24: 636-642. doi: 10.12659/msm.905651. doi: 10.12659/msm.905651 URL
[30]	Chai Q, Lu Z, Liu CH. Host defense mechanisms against Mycobacterium tuberculosis. Cell Mol Life Sci, 2020, 77(10): 1859-1878. doi: 10.1007/s00018-019-03353-5. doi: 10.1007/s00018-019-03353-5 URL
[31]	Radhakrishnan RK, Thandi RS, Tripathi D, et al. BCG vaccination reduces the mortality of Mycobacterium tuberculosis-infected type 2 diabetes mellitus mice. JCI Insight, 2020, 5(5): e133788. doi: 10.1172/jci.insight.133788. doi: 10.1172/jci.insight.133788 URL
[32]	Kathamuthu GR, Kumar NP, Moideen K, et al. Decreased Frequencies of Gamma/Delta T Cells Expressing Th1/Th17 Cytokine, Cytotoxic, and Immune Markers in Latent Tuberculosis-Diabetes/Pre-Diabetes Comorbidity. Front Cell Infect Microbiol, 2021, 11: 756854. doi: 10.3389/fcimb.2021.756854. doi: 10.3389/fcimb.2021.756854 URL
[33]	Kumar NP, Moideen K, Banurekha VV, et al. Modulation of Th1/Tc1 and Th17/Tc17 responses in pulmonary tuberculosis by IL-20 subfamily of cytokines. Cytokine, 2018, 108: 190-196. doi: 10.1016/j.cyto.2018.04.005. doi: 10.1016/j.cyto.2018.04.005 URL
[34]	Kumar NP, Moideen K, George PJ, et al. Impaired Cytokine but Enhanced Cytotoxic Marker Expression in Mycobacterium tuberculosis-Induced CD8⁺ T Cells in Individuals With Type 2 Diabetes and Latent Mycobacterium tuberculosis Infection. J Infect Dis, 2016, 213(5): 866-870. doi: 10.1093/infdis/jiv484. doi: 10.1093/infdis/jiv484 URL
[35]	Ponnana M, Sivangala R, Joshi L, et al. IL-6 and IL-18 cytokine gene variants of pulmonary tuberculosis patients with co-morbid diabetes mellitus and their household contacts in Hyderabad. Gene, 2017, 627: 298-306. doi: 10.1016/j.gene.2017.06.046. doi: 10.1016/j.gene.2017.06.046 URL
[36]	Meenakshi P, Ramya S, Lavanya J, et al. Effect of IFN-γ, IL-12 and IL-10 cytokine production and mRNA expression in tuberculosis patients with diabetes mellitus and their household contacts. Cytokine, 2016, 81: 127-136. doi: 10.1016/j.cyto.2016.03.009. doi: 10.1016/j.cyto.2016.03.009 pmid: 27002606
[37]	Bright MR, Curtis N, Messina NL. The role of antibodies in Bacille Calmette Guérin-mediated immune responses and protection against tuberculosis in humans: A systematic review. Tuberculosis (Edinb), 2021, 131: 101947. doi: 10.1016/j.tube.2020.101947. doi: 10.1016/j.tube.2020.101947 URL
[38]	SantaCruz-Calvo S, Bharath L, Pugh G, et al. Adaptive immune cells shape obesity-associated type 2 diabetes mellitus and less prominent comorbidities. Nat Rev Endocrinol, 2022, 18(1): 23-42. doi: 10.1038/s41574-021-00575-1. doi: 10.1038/s41574-021-00575-1 URL
[39]	Daryabor G, Atashzar MR, Kabelitz D, et al. The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System. Front Immunol, 2020, 11: 1582. doi: 10.3389/fimmu.2020.01582. doi: 10.3389/fimmu.2020.01582 URL