Aravindhan Vivekanandhan, Bobhate Anup, Sathishkumar Kuppan, Patil Aruna, Kumpatla Satyavani, Viswanathan Vijay
Department of Genetics, Dr. ALM PG IBMS, University of Madras, Chennai, India.
Prof. M. Viswanathan Diabetes Research Centre, Chennai, India.
Front Microbiol. 2022 Jun 27;13:884374. doi: 10.3389/fmicb.2022.884374. eCollection 2022.
The prevalence of latent tuberculosis infection (LTBI) among diabetes patients is poorly studied. In the present study, the prevalence of LTBI among pre-diabetes and diabetes patients was studied, along with immunoendocrine biomarkers ( = 804).
LTBI was screened by Quantiferon TB gold in Normal glucose tolerance [(NGT); = 170, [Pre-diabetes (PDM; = 209), Newly diagnosed diabetes (NDM; = 165) and Known diabetes (KDM; = 260) subjects. CRP, TNF-α, IL-6, IL-1β, IFN-β, IL-12, IFN-γ, IL-2, insulin, leptin, and adiponectin levels in serum and IFN-γ levels in quantiferon supernatants were quantified by ELISA. The expression of T-bet was quantified using qRT-PCR. Serum TBARS and nitrite levels were quantified by colorimetry.
The LTBI prevalence was 32% in NGT, 23% in PDM, 24% in NDM, and 32% in KDM groups, with an adjusted OR of 0.61 ( < 0.05). Downregulation of CRP, TNF-α, and nitrites and upregulation of adiponectin could be responsible for LTBI mediated protection against insulin resistance (IR), while the high levels of IL-1β, IL-12, and leptin could be responsible for IR mediated anti-TB immunity. The defective antigen-specific IFN-γ response, as seen in the KDM group, could be responsible for the low detection rate of LTBI and high probability of endogenous reactivation.
There appears to be a biphasic relationship between diabetes-latent tuberculosis: At the early stages of diabetes it is reciprocal, while at a late stage it is synergistic, this important phenomenon obviously needs further research.
糖尿病患者中潜伏性结核感染（LTBI）的患病率研究较少。在本研究中，对糖尿病前期和糖尿病患者中LTBI的患病率以及免疫内分泌生物标志物（n = 804）进行了研究。
采用结核感染T细胞检测（Quantiferon TB gold）对正常糖耐量（NGT；n = 170）、糖尿病前期（PDM；n = 209）、新诊断糖尿病（NDM；n = 165）和已知糖尿病（KDM；n = 260）受试者进行LTBI筛查。采用酶联免疫吸附测定法（ELISA）对血清中的C反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、干扰素-β（IFN-β）、白细胞介素-12（IL-12）、干扰素-γ（IFN-γ）、白细胞介素-2（IL-2）、胰岛素、瘦素和脂联素水平以及结核感染T细胞检测上清液中的IFN-γ水平进行定量。采用实时荧光定量聚合酶链反应（qRT-PCR）对T-bet的表达进行定量。采用比色法对血清中硫代巴比妥酸反应物（TBARS）和亚硝酸盐水平进行定量。
NGT组、PDM组、NDM组和KDM组的LTBI患病率分别为32%、23%、24%和32%（校正比值比为0.61，P < 0.05）。CRP、TNF-α和亚硝酸盐的下调以及脂联素的上调可能是LTBI介导的对胰岛素抵抗（IR）的保护作用的原因，而高水平的IL-1β、IL-12和瘦素可能是IR介导的抗结核免疫的原因。KDM组中出现的缺陷性抗原特异性IFN-γ反应可能是LTBI检测率低和内源性再激活可能性高的原因。
糖尿病与潜伏性结核之间似乎存在双相关系：在糖尿病早期是相互的，而在晚期是协同的，这一重要现象显然需要进一步研究。
