Protective effects of interleukin-22 on oxalate-induced crystalline renal injury via alleviating mitochondrial damage and inflammatory response

• Published in: Applied microbiology and biotechnology Vol. 106; no. 7; pp. 2637 - 2649
• Main Authors: Gu, Yuting, Shen, Yilan, Chen, Wei, He, Haidong, Ma, Yulei, Mei, Xiaobin, Ju, Dianwen, Liu, Hongrui
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.04.2022; Springer; Springer Nature B.V
• Subjects: Analysis; Animal models; Animals; Applied Microbial and Cell Physiology; Biocompatibility; Biomedical and Life Sciences; Biotechnology; Calcium oxalate; Calcium Oxalate - metabolism; Calcium Oxalate - pharmacology; Calcium Oxalate - therapeutic use; Care and treatment; Cell culture; Crystal structure; Crystallinity; Crystals; Cytokines; Cytotoxicity; Damage accumulation; Humans; Identification and classification; IL-1β; Inflammasomes; Inflammation; Inflammation - drug therapy; Inflammatory response; Injury prevention; Interleukin 18; Interleukin 22; Interleukins; Kidney; Kidney diseases; Kidney stones; Kidneys; Life Sciences; Membrane potential; Microbial Genetics and Genomics; Microbiology; Mitochondria; Mitochondrial membranes; Nephropathy; Oxalates; Oxalic acid; Oxidative Stress; Properties; Reactive Oxygen Species - metabolism; Sodium; Sodium oxalate; Toxicity; Tumor necrosis factor-α; China; Crystalline renal injury; Inflammation; Interleukin-22; Oxalate; Mitochondrial damage
• ISSN: 0175-7598; 1432-0614
• DOI: 10.1007/s00253-022-11876-4

Oxalate-induced crystalline kidney injury is one of the most common types of crystalline nephropathy. Unfortunately, there is no effective treatment to reduce the deposition of calcium oxalate crystals and alleviate kidney damage. Thus, proactive therapeutic is urgently needed to alleviate the suffering it causes to patient. Here, we investigated whether IL-22 exerted nephroprotective effects to sodium oxalate-mediated kidney damage and its potential mechanism. Crystalline kidney injury models were developed in vitro and in vivo that was often observed in clinic. We provided evidence that IL-22 could effectively decrease the accumulation of ROS and mitochondrial damage in cell and animal models and reduce the death of TECs. Moreover, IL-22 decreased the expression of the NLRP3 inflammasome and mature IL-1β in renal tissue induced by sodium oxalate. Further studies confirmed that IL-22 could play an anti-inflammatory role by reducing the levels of cytokines such as IL-1β, IL-18, and TNF-α in serum. In conclusion, our study confirmed that IL-22 has protective effects on sodium oxalate-induced crystalline kidney injury by reducing the production of ROS, protecting mitochondrial membrane potential, and inhibiting the inflammatory response. Therefore, IL-22 may play a potential preventive role in sodium oxalate-induced acute renal injury. Key points • IL-22 could reduce sodium oxalate-mediated cytotoxicity and ameliorate renal injury. • IL-22 could alleviate oxidative stress and mitochondrial dysfunction induced by sodium oxalate. • IL-22 could inhibit inflammatory response of renal injury caused by sodium oxalate.