Bioinformatics analyses of immune-related genes and immune infiltration associated with lung ischemia-reperfusion injury.

BACKGROUND: Ischemia-reperfusion injury (IRI) is a significant complication that can occur following lung transplantation and is known to contribute to poor prognosis. Our research aimed to investigate the potential molecular targets and mechanisms involved in lung IRI (LIRI), in order to improve our understanding of this condition. METHOD: We downloaded gene expression datasets (GSE127003 and GSE18995) linked to LIRI from the GEO database. Using WGCNA, we identified LIRI-related modules. Functional enrichment analyses were performed on the modules showing significant correlation with LIRI. Core immune-related genes (IRGs) were identified and validated using the GSE18995 dataset. A rat LIRI model was established to validate the expression changes of core IRGs. The LIRI groups were subjected to 60 min of warm ischemia followed by 120 min of reperfusion. Additionally, the xCell algorithm was used to characterize the immune landscape and analyze the relationships between hub IRGs and infiltrating immune cells. RESULTS: A total of 483 genes from the turquoise module were identified through WGCNA, with a predominant enrichment in immune- and inflammation-related pathways. Three IRGs (PTGS2, CCL2, and RELB) were found to be up-regulated after reperfusion in both GSE127003 and GSE18995 datasets, and this was further confirmed using the rat LIRI model. The xCell analysis revealed that immune score, CD8+ naive T cells, eosinophils, neutrophils, NK cells, and Tregs were upregulated after reperfusion. PTGS2, CCL2, and RELB showed positive correlations with CD8+ naive T cells, monocytes, neutrophils, and Tregs. CONCLUSION: PTGS2, CCL2, and RELB were found to be potential biomarkers for LIRI. Immune and microenvironment scores were higher after reperfusion compared to before reperfusion. PTGS2, CCL2, and RELB appear to play a crucial role in the development of LIRI and may contribute to it by increasing the number of immune cells. Our findings offer new perspectives on potential treatment targets and the pathogenesis of LIRI.

[Research progress on the mechanism of two-component systems in regulating carbapenem resistance of Klebsiella pneumoniae].

Carbapenem-resistant Klebsiella pneumoniae (CRKP) leads to high mortality of infected patients. How to deal with CRKP is an urgent problem in clinical practice, and it is imperative to carry out researchon carbapenem resistance mechanism of CRKP. The two-component systems (TCSs) areassociated with the development of drug resistance in a variety of bacteria, and TCSs were expected to be important therapeutic targets for CRKP. Therefore, this article reviewed the mechanisms of TCSs in the regulation of CRKP from the following several aspects: common mechanisms of carbapenem resistance of CRKP, research progress in drug resistance of TCSs, relationships between Klebsiella pneumoniae and TCSs, and so on. It may provide some research ideas for future research and the references for clinical diagnosis and treatment.