title: Inflammatory response to acute hypoxia in humans.
abstract: BACKGROUND
  In animal studies hypoxia is known to cause an inflammatory response, inducing multiple transcription factors and activating molecular processes at the cellular level. However, it is not known whether acute hypoxia causes similar inflammatory effects in humans, although such an assumption is commonly made.
  
  
  METHODS
  The effects of acute hypoxic exposure were studied in 12 healthy adults: Each subject was studied on 2 different days. Group 1 (mean age 33 ± 5.5 years; 2 females, 4 males) was exposed either to a hypoxic gas mixture or room air for 30 min and Group 2 (mean age 26.5 ± 7.5 years; 3 females, 3 males) for 60 min. Measurements of circulating adhesion molecules (AMs), Clara cell secretory protein (CC16), hypoxia inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and C reactive protein (hsCRP) were made at baseline and at intervals following exposure for 240 min.
  
  
  RESULTS
  No significant changes were seen in circulating AMs, CC16, TNF-α, IL-6 or hsCRP, although both HIF-1α and VEGF levels increased significantly (p < 0.05) after hypoxic exposure.
  
  
  CONCLUSIONS
  Acute hypoxic exposure in normal man does not induce a measurable change in inflammatory or epithelial biomarkers, in contrast to studies at the cellular level in animals. However, acute hypoxic exposure does induce the expression of HIF-1α and VEGF. These results indicate that in humans acute hypoxic exposure for up to 60 min does not induce a generalized inflammatory response, indicating that the human response to hypoxia is more complex than inferred from animal/cellular studies.
authors.affiliation: Division of Pulmonary & Critical Care Medicine, University of Connecticut Health Center, Farmington, CT 06030-1321, USA. Electronic address: nburki@uchc.edu.
authors.forename: Nausherwan K
authors.initials: NK
authors.lastname: Burki
authors.affiliation: Division of Pulmonary & Critical Care Medicine, University of Connecticut Health Center, Farmington, CT 06030-1321, USA. Electronic address: Sodienye.Tetenta@crmcwy.org.
authors.forename: Sodienye U
authors.initials: SU
authors.lastname: Tetenta
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000150:complications*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism*; D007249:Inflammation / Q000209:etiology / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D018836:Inflammation Mediators; D042461:Vascular Endothelial Growth Factor A
keywords: Acute hypoxia; Adhesion molecules; Clara cell protein; HIF-1α; Inflammation