期刊
CYTOKINE
卷 157, 期 -, 页码 -出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2022.155960
关键词
Tuberculosis; Caspase-3; Cytokine; Oxidative stress; Antioxidant; XIAP
资金
- Sanjay Gandhi Postgraduate Institute of Medical Sciences [A-04-PGI/IMP/76/2018]
This study indicates that there is an up-regulation of death signals and suppression of survival signals in patients with tuberculous meningitis.
Background: The balancing factor of apoptosis, survival, inflammatory and oxidative stress biomarkers may determine the clinico-radiological severity and death in the patients with tuberculous meningitis (TBM). Aim: We report the relationship of death [caspase-3, malondialdehyde (MDA), tumor necrosis factor-alpha (TNF alpha), interleukin 6 (IL6)] and survival biomarkers [X-linked inhibitory apoptotic protein (XIAP), IL10, glutathione (GSH) and catalase] in TBM, and its role in determining disease severity and death. Methods: The diagnosis of TBM was based on clinical, MRI and cerebrospinal fluid (CSF) findings. Their clinical and MRI findings were noted. The severity of TBM was categorized as stages I to III. Serum and CSF caspase-3 and XIAP were measured by ELISA, and TNF alpha, IL6 and IL10 gene expression in peripheral blood mononuclear cells using RT-PCR (reverse-transcriptase polymerase chain reaction). Plasma MDA, GSH and catalase were measured by spectrophotometer. Results: There were 40 patients with TBM whose mean age was 31.6 years and 50% were females. TBM patients had higher expression of death (caspase-3, TNF alpha, IL6, and MDA) and suppression of survival biomarkers (XIAP, catalase and GSH) compared to the healthy controls. Caspase-3 positively correlated with TNF alpha, IL6 and MDA, and negatively with XIAP, GSH and catalase. Patients with longer duration of illness and definite TBM had higher expression of caspase-3. Patients who died has higher expression of caspase-3 and suppression of XIAP compared to those who survived. Conclusion: It can be concluded from this study that there is up-regulation of death signals and suppression of survival signals in TBM.
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