Transcriptome landscape reveals the chronic inflammatory response in kidneys affected by the combinatory effect of leptospirosis and nephrotoxic injury

Leptospirosis can cause chronic kidney damage, putting patients at risk of additional kidney injury due to other factors that can lead to renal failure. To understand the combined effect, the transcriptome profiles of kidneys of mice with adenine-induced and chronically Leptospira-infected kidneys were analysed. Chronic inflammation and T-helper 17 immune responses were activated and a high-level expression of Indoleamine 2,3-dioxygenase 1 protein was found. The results indicate that the combination may predispose patients to chronic inflammation, kidney function disruption, and symptoms seen in progressive chronic kidney disease (CKD). Furthermore, immunometabolic regulation may contribute to renal injury caused by chronic leptospirosis with secondary nephrotoxic injury. This study identified several significantly disrupted genes that could serve as potential targets for the diagnosis or treatment of CKD. Our work provides insight into the combined effect of leptospirosis and secondary kidney damage and the molecular basis for rapid progression of CKD.

Automated summary

This study analyzed the transcriptome profiles of mice kidneys with adenine-induced and chronically Leptospira-infected kidneys to understand the combined effect. The findings showed that chronic inflammation and T-helper 17 immune responses were activated, and there was high expression of Indoleamine 2,3-dioxygenase 1 protein. These results suggest that the combination may lead to chronic inflammation, kidney function disruption, and symptoms of chronic kidney disease. Additionally, immunometabolic regulation may contribute to renal injury caused by chronic leptospirosis with secondary nephrotoxic injury. The study identified disrupted genes that could be potential targets for CKD diagnosis or treatment, providing insight into the molecular basis for rapid progression of CKD.