title: Impact of short-term systemic hypoxia on phagocytosis, cytokine production, and transcription factor activation in peripheral blood cells.
abstract: Hypoxia frequently associated with certain physiologic and pathologic conditions influences numerous cellular functions. Because the effects of short-term hypoxia are incompletely understood, we examined phagocytosis and cytokine production as well as the activation of the transcription factors HIF-1 and NFκB in peripheral blood cells of healthy volunteers exposed to an oxygen concentration equivalent to that found at a height of 5500 m. Furthermore, we analysed plasma HIF-1 and serum concentrations of various HIF-1-dependent genes. Results showed that short-term hypoxia increased phagocytosis in neutrophils without affecting monocyte phagocytosis. Hypoxia decreased basal TNFα concentration in monocytes and basal interferon γ concentration in CD4(+) T lymphocytes. In contrast, plasma HIF and serum VEGF concentrations were not affected by hypoxia, although serum EPO concentration was raised. In PBMC, hypoxia increased cytosolic HIF-1 concentration without affecting nuclear HIF-1 concentration and led to a rise in the nuclear NFκB in PBMC. Our results show that short-term hypoxia affects immune functions in healthy individuals. Furthermore, we speculate that the effects of hypoxia are not due to HIF-1, but are caused by the activation of NFκB .
authors.affiliation: Department of Internal Medicine I, Division of Cardiology, Friedrich-Schiller-University, Erlanger Allee 101, 07740 Jena, Germany. michael.fritzenwanger@med.uni-jena.de
authors.forename: Michael
authors.initials: M
authors.lastname: Fritzenwanger
authors.forename: Christian
authors.initials: C
authors.lastname: Jung
authors.forename: Bjoern
authors.initials: B
authors.lastname: Goebel
authors.forename: Alexander
authors.initials: A
authors.lastname: Lauten
authors.forename: Hans R
authors.initials: HR
authors.lastname: Figulla
mesh_terms: D000328:Adult; D001274:Atmospheric Pressure; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D004921:Erythropoietin / Q000097:blood; D005260:Female; D016650:Fluorescein-5-isothiocyanate; D005456:Fluorescent Dyes; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000276:immunology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000097:blood / Q000235:genetics / Q000276:immunology*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009000:Monocytes / Q000502:physiology; D052002:NF-kappa B p50 Subunit / Q000235:genetics / Q000276:immunology*; D009504:Neutrophils / Q000502:physiology; D010587:Phagocytosis / Q000235:genetics / Q000276:immunology*; D051996:Transcription Factor RelA / Q000235:genetics / Q000276:immunology*; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D055815:Young Adult; D015054:Zymosan / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D005456:Fluorescent Dyes; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D052002:NF-kappa B p50 Subunit; D051996:Transcription Factor RelA; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D004921:Erythropoietin; D019344:Lactic Acid; D015054:Zymosan; D016650:Fluorescein-5-isothiocyanate