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Paper| Volume 29, ISSUE 1, P35-40, January 1998

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Intact autocrine activation and cytokine production by PMNs from injured adults with elevated Candida antigen titres

  • John F. Sweeney
    Correspondence
    Requests for reprints should be addressed to: J. F. Sweeney, md, Chief, General Surgery Service, 112G, Ann Arbor VA Medical Center, Ann Arbor, MI 48105, USA.
    Affiliations
    Department of Surgery and Medical Microbiology and Immunology, University of South Florida College of Medicine, Florida, USA

    Immunology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA
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  • Alexander S. Rosemurgy
    Affiliations
    Department of Surgery and Medical Microbiology and Immunology, University of South Florida College of Medicine, Florida, USA

    Immunology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA
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  • Sheng Wei
    Affiliations
    Department of Surgery and Medical Microbiology and Immunology, University of South Florida College of Medicine, Florida, USA

    Immunology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA
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  • Julie Y. Djeu
    Affiliations
    Department of Surgery and Medical Microbiology and Immunology, University of South Florida College of Medicine, Florida, USA

    Immunology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA
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      Abstract

      Injured patients with Candida antigen titres have increased mortality due to sepsis. Polymorphonuclear leucocytes (PMNs) from injured patients with elevated Candida antigen titres demonstrate impaired function against Candida albicans growth when compared with PMNs from injury matched controls. To determine if PMN dysfunction is global, PMNs from patients with positive Candida antigen titres were evaluated for their ability to activate the anticandidal function of normal PMNs (autocrine activation) and to produce tumour necrosis factor (TNF) and interleukin 8 (IL8), known activators of PMN anticandidal function, this study demonstrates that the PMN dysfunction is not global, as PMN cytokine production and autocrine activation remain intact.
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