KMID : 0545120140240081133
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Journal of Microbiology and Biotechnology 2014 Volume.24 No. 8 p.1133 ~ p.1142
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Interleukin-32¥ã Transgenic Mice Resist LPS-Mediated Septic Shock
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Kim Sun-Jong
Lee Si-Young Kwak A-Reum Kim Eun-Som Jo Seung-Hyun Bae Su-Young Lee Young-Min Ryoo So-Yoon Choi Ji-Da Kim Soo-Hyun
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Abstract
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Interleukin-32 (IL-32) is a cytokine and inducer of various proinflammatory cytokines such as TNF¥á, IL-1¥â, and IL-6 as well as chemokines. There are five splicing variants (¥á, ¥â, ¥ã, ¥ä, and ¥å) and IL-32¥ã is the most active isoform. We generated human IL-32¥ã transgenic (IL-32¥ã TG) mice to express high level of IL-32¥ã in various tissues, including immune cells. The pathology of sepsis is based on the systemic inflammatory response that is characterized by upregulating inflammatory cytokines in whole body, particularly in response to gram-negative bacteria. We investigated the role of IL-32¥ã in a mouse model of experimental sepsis by using lipopolysaccharides (LPS). We found that IL-32¥ãTG mice resisted LPS-induced lethal endotoxemia. IL-32¥ã reduced systemic cytokines release after LPS administration but not the local immune response. IL-32¥ãTG increased neutrophil influx into the initial foci of the primary injected site, and prolonged local cytokines and chemokines production. These results suggest that neutrophil recruitment in IL-32¥ãTG occurred as a result of the local induction of chemokines but not the systemic inflammatory cytokine circulation. Together, our results suggest that IL-32¥ã enhances an innate immune response against local infection but inhibits the spread of immune responses, leading to systemic immune disorder.
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KEYWORD
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Interleukin-32, Inflammatory cytokine, IL-32¥ã transgenic mice, Lipopolysaccharides, Mouse model of sepsis
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