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Interleukin‐5 deletion promotes sepsis‐induced M1 macrophage differentiation, deteriorates cardiac dysfunction, and exacerbates cardiac injury via the NF‐κB p65 pathway in mice

Inflammation plays a crucial role in sepsis‐induced cardiac injury. The purpose of this study was to determine whether interleukin‐5 (IL‐5) affected lipopolysaccharide (LPS)‐induced cardiac injury by regulating the inflammatory response. First, the expression level and source of cardiac IL‐5 were examined, and the results showed that LPS treatment and cecal ligation decreased cardiac IL‐5 expression in macrophages. In addition, LPS was used to establish a mouse sepsis model, and the effects of IL‐5 deletion on cardiac injury, M1 macrophage differentiation and myocardial cell apoptosis were analyzed. The results showed that IL‐5 deficiency significantly increased cardiac injury marker expression, worsened cardiac dysfunction, promoted M1 macrophage differentiation and exacerbated myocardial cell apoptosis in LPS‐induced septic mice. The nuclear factor‐kappa B (NF‐κB) p65 pathway was inhibited by JSH‐23, and the results showed that treatment with JSH‐23 inhibited M1 macrophage differentiation and alleviated cardiac injury in LPS‐treated IL‐5‐knockout mice. Furthermore, the effects of IL‐5 deficiency on M1 macrophage differentiation and myocardial cell apoptosis were measured in vitro. The IL‐5‐mediated promotion of M1 macrophage differentiation was also reversed by S31‐201, and the pro‐apoptotic effect of IL‐5 knockout on macrophage‐mediated myocardial cell apoptosis was also reversed by JSH‐23. In conclusion, we found that IL‐5 knockout may exacerbate sepsis‐induced cardiac injury by promoting M1 macrophage differentiation in mice. IL‐5 may be a potential target for the clinical prevention of sepsis‐related cardiac injury.