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耐多药结核病患者细胞因子飙升,表明存在过度炎症和疾病严重程度。

Cytokine upsurge among drug-resistant tuberculosis endorse the signatures of hyper inflammation and disease severity.

机构信息

Department of Immunology, ICMR-National Institute for Research in Tuberculosis (ICMR-NIRT), No.1. Mayor Sathyamoorthy Road, Chetpet, Chennai, 600 031, India.

ICMR-NIRT-NIH-International Center for Excellence in Research, Chennai, India.

出版信息

Sci Rep. 2023 Jan 16;13(1):785. doi: 10.1038/s41598-023-27895-8.

Abstract

Tuberculosis (TB) elimination is possible with the discovery of accurate biomarkers that define the stages of infection. Drug-resistant TB impair the current treatment strategies and worsen the unfavourable outcomes. The knowledge on host immune responses between drug-sensitive and drug-resistant infection is inadequate to understand the pathophysiological differences and disease severity. The secreted proteins, cytokines display versatile behaviour upon infection with Mycobacterium tuberculosis (MTB) and their imbalances often tend to assist disease pathology than protection. Therefore, studying these soluble proteins across TB infection spectrum (drug-resistant TB, drug-sensitive TB, and latent TB) may unveil the disease mediated responses and unique stage specific cytokine signatures. Thus, we sought to determine the plasma cytokine levels from healthy, latently infected, drug-sensitive, and drug-resistant TB individuals. Our study revealed top 8 cytokines (IL-17, IL-1α, IL-2, IL-10, IL-5, IFN-γ, TNF-α and IL-6) and their biomarker abilities to discriminate different stages of infection.

摘要

结核病(TB)的消除是有可能的,只要发现能够定义感染阶段的准确生物标志物。耐药性结核病会损害当前的治疗策略,并导致不良后果恶化。对于宿主对敏感和耐药感染的免疫反应的了解还不足以理解病理生理学差异和疾病严重程度。分泌蛋白、细胞因子在感染结核分枝杆菌(MTB)时表现出多种行为,它们的失衡往往倾向于协助疾病病理学,而不是保护。因此,研究这些可溶性蛋白在结核病感染谱(耐药结核病、敏感结核病和潜伏性结核病)中的变化情况,可能揭示疾病介导的反应和独特的阶段特异性细胞因子特征。因此,我们试图确定来自健康人、潜伏感染者、敏感结核病患者和耐药结核病患者的血浆细胞因子水平。我们的研究揭示了前 8 种细胞因子(IL-17、IL-1α、IL-2、IL-10、IL-5、IFN-γ、TNF-α 和 IL-6)及其作为生物标志物的能力,可以区分感染的不同阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ee/9842614/6a5c18e504f7/41598_2023_27895_Fig1_HTML.jpg

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