NDLI: Loss of the oxygen sensor PHD3 enhances the innate immune response to abdominal sepsis.

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Loss of the oxygen sensor PHD3 enhances the innate immune response to abdominal sepsis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Weitz, Jürgen Kirchberg, Johanna Walmsley, Sarah R. Whyte, Moira K. B. Niemietz, Thomas Kiss, Judit Schneider, Martin Mollenhauer, Martin Mazzone, Massimiliano Steinert, Gunnar Carmeliet, Peter Radhakrishnan, Praveen Dudda, Johanna
Description	Author Affiliation: Kiss J ( Department of General and Transplantation Surgery, University of Heidelberg, Heidelberg, D-69120 Germany.)
Abstract	Hypoxia and HIFs (HIF-1 and HIF-2 ) modulate innate immune responses in the setting of systemic inflammatory responses and sepsis. The HIF prolyl hydroxylase enzymes PHD1, PHD2 and PHD3 regulate the mammalian adaptive response to hypoxia; however, their significance in the innate immune response has not been elucidated. We demonstrate in this study that deficiency of PHD3 (PHD3(-/-)) specifically shortens the survival of mice subjected to various models of abdominal sepsis because of an overwhelming innate immune response, leading to premature organ dysfunction. By contrast, this phenotype was absent in mice deficient for PHD1 (PHD1(-/-)) or PHD2 (PHD2(+/-)). In vivo, plasma levels of proinflammatory cytokines were enhanced, and recruitment of macrophages to internal organs was increased in septic PHD3-deficient mice. Reciprocal bone marrow transplantation in sublethally irradiated mice revealed that enhanced susceptibility of PHD3-deficient mice to sepsis-related lethality was specifically caused by loss of PHD3 in myeloid cells. Several in vitro assays revealed enhanced cytokine production, migration, phagocytic capacity, and proinflammatory activation of PHD3-deficient macrophages. Increased proinflammatory activity of PHD3-deficient macrophages occurred concomitantly with enhanced HIF-1 protein stabilization and increased NF-κB activity, and interference with the expression of HIF-1 or the canonical NF-κB pathway blunted their proinflammatory phenotype. It is concluded that impairment of PHD3 enzyme function aggravates the clinical course of abdominal sepsis via HIF-1 - and NF-κB-mediated enhancement of the innate immune response.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	4
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Immunity, Innate Immunology Macrophages Procollagen-proline Dioxygenase Sepsis Signal Transduction Animals Blotting, Western Chemotaxis, Leukocyte Cytokines Biosynthesis Hypoxia-inducible Factor 1, Alpha Subunit Metabolism Immunohistochemistry Mice Mice, Knockout Nf-kappa B Real-time Polymerase Chain Reaction Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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