학술논문

Systemic Levels of Pro-Inflammatory Cytokines and Post-Treatment Modulation in Tuberculous Lymphadenitis
Document Type
Academic Journal
Source
Tropical Medicine and Infectious Disease. February 2023, Vol. 8 Issue 3
Subject
Analysis
Health aspects
Interleukins -- Analysis -- Health aspects
Diseases -- Analysis -- Health aspects
Biological response modifiers -- Analysis -- Health aspects
Interferon -- Health aspects -- Analysis
Tuberculosis -- Analysis -- Health aspects
Lymphadenitis -- Health aspects -- Analysis
Language
English
ISSN
2414-6366
Abstract
Author(s): Gokul Raj Kathamuthu (corresponding author) [1,2,3,*]; Kadar Moideen [1]; Rathinam Sridhar [4]; Dhanaraj Baskaran [2]; Subash Babu [1,5] 1. Introduction Tuberculosis (TB) remains an important and key public health [...]
Pro-inflammatory cytokines are potent stimulators of inflammation and immunity and markers of infection severity and bacteriological burden in pulmonary tuberculosis (PTB). Interferons could have both host-protective and detrimental effects on tuberculosis disease. However, their role has not been studied in tuberculous lymphadenitis (TBL). Thus, we evaluated the systemic pro-inflammatory (interleukin (IL)-12, IL-23, interferon (IFN)α, and IFNβ) cytokine levels in TBL, latent tuberculosis (LTBI), and healthy control (HC) individuals. In addition, we also measured the baseline (BL) and post-treatment (PT) systemic levels in TBL individuals. We demonstrate that TBL individuals are characterized by increased pro-inflammatory (IL-12, IL-23, IFNα, IFNβ) cytokines when compared to LTBI and HC individuals. We also show that after anti-tuberculosis treatment (ATT) completion, the systemic levels of pro-inflammatory cytokines were significantly modulated in TBL individuals. A receiver operating characteristic (ROC) analysis revealed IL-23, IFNα, and IFNβ significantly discriminated TBL disease from LTBI and/or HC individuals. Hence, our study demonstrates the altered systemic levels of pro-inflammatory cytokines and their reversal after ATT, suggesting that they are markers of disease pathogenesis/severity and altered immune regulation in TBL disease.