Feng Gao1, Yuan-Zheng Yang2, Xuan-Yun Feng3, Ting-Ting Fan4, Long Jiang5, Rui Guo6, Qiong Liu7. 1. Department of Anesthesia, Stomatology Hospital of Chongqing Medical University, No. 426 Songshibei Road, Yubei District, Chongqing 401146, China. Electronic address: gaofeng61647093@126.com. 2. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China; Department of Critical Care Medicine, The Affiliated Hospital of Hainan Medical College, No. 31 Hualong Road, Xinhua District, Hainan 571101, China. Electronic address: 362383118@qq.com. 3. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China. Electronic address: 625764852@qq.com. 4. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China. Electronic address: 358097112@qq.com. 5. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China. Electronic address: 276173466@qq.com. 6. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China. Electronic address: guo-rui5@163.com. 7. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing 400016, China. Electronic address: liuqiong0219@163.com.
Abstract
INTRODUCTION: Interleukin (IL)-27 is an important cytokine involved in many human inflammatory diseases. In this study, we investigated its role in the pathogenesis of sepsis-induced myocardial dysfunction (SIMD). METHODS: Twenty patients with SIMD and 24healthy donors were prospectively enrolled. Expression of IL-27 was detected in serum from SIMD patients by ELISA. Cardiac dysfunction was induced by administration of Escherichia coli lipopolysaccharide (LPS) to C57BL/6 (wild type) or IL-27R-/- mice. IL-27 mRNA in the myocardium was measured by RT-PCR. Cytokine levels in serum were determined by ELISA. RESULTS: Expression of IL-27 in the serum was markedly increased in patients with SIMD compared with that in controls. Serum IL-27 levels and cardiac IL-27 mRNA expression were significantly increased after LPS injection compared with control specimens. Compared with wild-type mice, IL-27R-/- mice had higher expression of brain natriuretic peptide, cardiac troponin I, IL-6, IL-12, tumor necrosis factor-α and transforming growth factor-β. CONCLUSIONS: IL-27 is an important protective mediator of SIMD.
INTRODUCTION:Interleukin (IL)-27 is an important cytokine involved in many human inflammatory diseases. In this study, we investigated its role in the pathogenesis of sepsis-induced myocardial dysfunction (SIMD). METHODS: Twenty patients with SIMD and 24healthy donors were prospectively enrolled. Expression of IL-27 was detected in serum from SIMD patients by ELISA. Cardiac dysfunction was induced by administration of Escherichia colilipopolysaccharide (LPS) to C57BL/6 (wild type) or IL-27R-/- mice. IL-27 mRNA in the myocardium was measured by RT-PCR. Cytokine levels in serum were determined by ELISA. RESULTS: Expression of IL-27 in the serum was markedly increased in patients with SIMD compared with that in controls. Serum IL-27 levels and cardiac IL-27 mRNA expression were significantly increased after LPS injection compared with control specimens. Compared with wild-type mice, IL-27R-/- mice had higher expression of brain natriuretic peptide, cardiac troponin I, IL-6, IL-12, tumor necrosis factor-α and transforming growth factor-β. CONCLUSIONS:IL-27 is an important protective mediator of SIMD.
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