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An immunosuppressive peptide from the horsefly inhibits inflammation by repressing macrophage maturation and phagocytosis
Author(s) -
Chen Ran,
Yuan Long,
Cao Nengqi,
Li Pengpeng,
Chen Huilin,
Zhou Jiaxin,
Hao Xue,
Liu Tong,
Yang WenHao,
Cui Shuzhong,
Yan Xiuwen
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28687
Subject(s) - phagocytosis , macrophage , inflammation , proinflammatory cytokine , immune system , lipopolysaccharide , microbiology and biotechnology , secretion , biology , immunopotentiator , immunology , stimulation , extracellular , chemistry , biochemistry , endocrinology , in vitro
Ectoparasites repress host immune responses while they obtain nutrition from their hosts. Understanding the immunosuppressive mechanisms between ectoparasites and their hosts will provide new strategies to develop potential immunosuppressive drugs against immune disorder diseases. Previously, we have discovered that a small peptide, immunoregulin HA, from the horsefly ( Hybomitra atriperoides ) may play an immunosuppressive role in rat splenocytes. However, the targeting cells and detailed mechanisms of immunoregulin HA in immunosuppressive reactions are not well defined. Here, we show that immunoregulin HA reduces the secretion of proinflammatory cytokines upon lipopolysaccharide (LPS) stimulation. Interestingly, we discover that the major cytokines repressed by immunoregulin HA are secreted by macrophages, rather than by T cells. Furthermore, immunoregulin HA inhibits macrophage maturation and phagocytosis. Mechanically, the activations of c‐JUN N‐terminal kinase and extracellular signal‐regulated kinase upon LPS stimulation are decreased by immunoregulin HA. Consistently, immunoregulin HA treatment exhibits an anti‐inflammatory activity in a mouse model of adjuvant‐induced paw inflammation. Taken together, our data reveal that immunoregulin HA conducts the anti‐inflammatory activity by blocking macrophage functions.