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结核性淋巴结炎中促炎细胞因子的全身水平及治疗后调节

Systemic Levels of Pro-Inflammatory Cytokines and Post-Treatment Modulation in Tuberculous Lymphadenitis.

作者信息

Kathamuthu Gokul Raj, Moideen Kadar, Sridhar Rathinam, Baskaran Dhanaraj, Babu Subash

机构信息

National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai 600 031, India.

National Institute for Research in Tuberculosis (NIRT), Chennai 600 031, India.

出版信息

Trop Med Infect Dis. 2023 Feb 27;8(3):150. doi: 10.3390/tropicalmed8030150.

Abstract

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.

摘要

促炎细胞因子是炎症和免疫的强效刺激因子,也是肺结核(PTB)感染严重程度和细菌负荷的标志物。干扰素对结核病可能既有宿主保护作用,也有有害作用。然而,其在结核性淋巴结炎(TBL)中的作用尚未得到研究。因此,我们评估了TBL、潜伏性结核感染(LTBI)和健康对照(HC)个体的全身促炎(白细胞介素(IL)-12、IL-23、干扰素(IFN)α和IFNβ)细胞因子水平。此外,我们还测量了TBL个体的基线(BL)和治疗后(PT)全身水平。我们证明,与LTBI和HC个体相比,TBL个体的特征是促炎(IL-12、IL-23、IFNα、IFNβ)细胞因子增加。我们还表明,在完成抗结核治疗(ATT)后,TBL个体的全身促炎细胞因子水平得到了显著调节。受试者工作特征(ROC)分析显示,IL-23、IFNα和IFNβ能显著区分TBL疾病与LTBI和/或HC个体。因此,我们的研究表明促炎细胞因子的全身水平发生了改变,且在ATT后得到逆转,这表明它们是TBL疾病发病机制/严重程度以及免疫调节改变的标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85dd/10053505/31f54dc25872/tropicalmed-08-00150-g001.jpg

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