Regulation of neutrophil-mediated killing of Staphylococcus aureus and chemotaxis by c-jun NH2 terminal kinase

Journal of Leukocyte Biology

Violet Mukaro²  Antonio Ferrante¹  Mei-Chun Yeh²  Charles S. Hii² 

[1] Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Sansom Institute, University of South Australia, Adelaide, South Australia, Australia Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Sansom Institute, University of South Australia, Adelaide, South Australia, Australia Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Sansom Institute, University of South Australia, Adelaide, South Australia, Australia Sansom Institute, University of South Australia, Adelaide, South Australia, Australia Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Sansom Institute, University of South Australia, Adelaide, South Australia, Australia;Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and Department of Immunopathology, Children, Youth and Women’s Health Service, North Adelaide, South Australia, Australia; Discipline of Paediatrics, Faculty of Health Sciences, University of Adelaide, South Australia; and

关键词: JNK;    TAT-JIP peptide;    superoxide production;    phagocytosis;    adherence;    mechanism of bactericidal activity;   

DOI  :  10.1189/jlb.0609399

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

The role of JNK in neutrophil chemotaxis and killing of microbial pathogens remains unclear. Using a recently described cell-permeable peptide inhibitor of the JNK pathway, based on the JBD of JIP-1, coupled to the protein transduction domain of HIV-TAT (TAT-JIP), in association with control peptides, we demonstrate that the JNK pathway plays a major role in regulating human neutrophil chemotaxis and killing of microbial pathogens. Serum-opsonized Staphylococcus aureus elicited JNK activation and c-jun phosphorylation. The activation of the JNK pathway and bactericidal activity were inhibited by the TAT-JIP peptide. The stimulation of oxygen radical generation by S. aureus was dependent on the JNK signaling pathway, as was the phagocytosis of serum-opsonized bacteria. Chemotaxis to activated serum complement but not random migration was inhibited by the TAT-JIP peptide. The findings demonstrate a major role for the JNK signaling pathway in neutrophil-mediated defense against microbial pathogens.

【 授权许可】

Unknown