Unique Reciprocal Association Seen Between Latent Tuberculosis Infection and Diabetes Is Due to Immunoendocrine Modulation (DM-LTB-1)

AimThe 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 (n = 804). MethodsLTBI was screened by Quantiferon TB gold in Normal glucose tolerance [(NGT); n = 170, [Pre-diabetes (PDM; n = 209), Newly diagnosed diabetes (NDM; n = 165) and Known diabetes (KDM; n = 260) subjects. CRP, TNF-alpha, IL-6, IL-1 beta, IFN-beta, IL-12, IFN-gamma, IL-2, insulin, leptin, and adiponectin levels in serum and IFN-gamma 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. ResultsThe LTBI prevalence was 32% in NGT, 23% in PDM, 24% in NDM, and 32% in KDM groups, with an adjusted OR of 0.61 (p < 0.05). Downregulation of CRP, TNF-alpha, and nitrites and upregulation of adiponectin could be responsible for LTBI mediated protection against insulin resistance (IR), while the high levels of IL-1 beta, IL-12, and leptin could be responsible for IR mediated anti-TB immunity. The defective antigen-specific IFN-gamma response, as seen in the KDM group, could be responsible for the low detection rate of LTBI and high probability of endogenous reactivation. ConclusionThere 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.

Automated summary

This study investigated the prevalence of latent tuberculosis infection (LTBI) among diabetes patients and the relationship with immunoendocrine biomarkers.