Potential mechanism of CARD16 protein action and susceptibility to sepsis in the elderly infected population: Through transcriptome analysis of blood

转录组 机制(生物学) 败血症 作用机理 人口 动作(物理) 生物 计算生物学 遗传学 医学 免疫学 基因 基因表达 环境卫生 哲学 物理 认识论 量子力学 体外
作者
Yuhan Sun,Jiahuan Lu,Jing Wu,Xiao Qi,Yanfang Huang,Ke Lin,Jing Wang,Jiajia Wang,Jinwei Li,Shuyu Fang,Ali Yang,Shuqing Chen,Wenhong Zhang,Jialin Jin,Zhongqing Xu,Sen Wang
出处
期刊:International Journal of Biological Macromolecules [Elsevier]
卷期号:: 136578-136578
标识
DOI:10.1016/j.ijbiomac.2024.136578
摘要

As global aging accelerates, the super-elderly population is at higher risk of infectious diseases, especially sepsis, a condition that may be associated with declining immune system function and abnormal inflammatory responses. The aim of this study was to investigate the role of CARD16 protein in sepsis susceptibility in the elderly population and its potential mechanism, and to reveal the expression characteristics of CARD16-related genes through blood transcriptomic analysis. Transcriptome sequencing was conducted on peripheral blood samples obtained from patients suffering from senile sepsis, along with samples from a healthy elderly control group. To examine the differences in gene expression, bioinformatics techniques were employed to compare the expression levels of CARD16-related genes between the two groups. Additionally, a comprehensive analysis was performed on the downstream inflammatory pathways and cytokines that are regulated by CARD16.The findings from the transcriptome analysis indicated that the expression of CARD16 was markedly upregulated in the cohort of patients experiencing hypersenile sepsis. This upregulation was associated with an increase in a variety of pro-inflammatory factors. Further network analysis suggested that CARD16 may potentiate the inflammatory response by modulating the NF-κB signaling pathway, which could consequently heighten the patients' vulnerability to sepsis.In comparison to the healthy elderly control group, the levels of anti-inflammatory genes in the super-elderly cohort were found to be significantly diminished. This observation points to a notable imbalance in immune regulation, further emphasizing the altered immune response in individuals with senile sepsis.
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