title: Impact of Systemic Normobaric Short-Term Hypoxia on Pro-Inflammatory and Anti-Inflammatory Cytokines in Healthy Volunteers.
abstract: BACKGROUND
  Hypoxia has been shown to induce a microvascular inflammation, affect the cell count of different types of immune cells, and influence cytokine production in blood. In the present study, serum levels of different cytokines were investigated to achieve insights into the effect of hypoxia on the balance of inflammation and anti-inflammation.
  
  
  METHODS
  Pro- (IL-8) and anti-inflammatory (IL-10) cytokines were measured in an experiment exposing 12 healthy subjects (35 ± 9 yr, 176 ± 7 cm, 73 ± 16 kg, BMI 23 ± 4 kg/m2) to systemic, normobaric hypoxia in a hypoxic chamber. In this chamber oxygen was replaced by nitrogen to reach an oxygen content of 9.9% that is equivalent to an altitude of 5500 m during 7 hours. Serum cytokine concentrations were analyzed using ELISA.
  
  
  RESULTS
  As expected, a significant decrease in peripheral oxygen saturation accompanied by a significant increase in breathing frequency and heart rate were observed in the subjects during hypoxia compared to baseline (BL). Blood leukocytes increased slightly, but significantly in the course of hypoxia. A statistically significant increase was measured for IL-8 serum level during hypoxia compared to the baseline measurements (BL 12.0 ± 1.1 pg/mL, hypoxia 16.2 ± 1.6 pg/mL, p = 0.006). For IL-10 a statistically significant decrease was measured upon hypoxia compared to baseline (BL 11.6 [6.2 - 43.31 pg/mL, hypoxia 8.3 [4.4 - 26.6] pg/mL, p = 0.016). Additionally, a significant inverse correlation was found comparing the anti-inflammatory cytokine IL-10 with the pro-inflammatory cytokine IL-8 (r = -0.69, p < 0.001).
  
  
  CONCLUSIONS
  The results of this study demonstrate a hypoxia-induced increase in pro- and decrease in anti-inflammatory cytokines reflecting an increased pro-inflammatory status during hypoxia.
authors.forename: Ilonka
authors.initials: I
authors.lastname: Rohm
authors.forename: Josephine
authors.initials: J
authors.lastname: Ratka
authors.forename: Rudin
authors.initials: R
authors.lastname: Pistulli
authors.forename: Bjoern
authors.initials: B
authors.lastname: Goebel
authors.forename: Thomas
authors.initials: T
authors.lastname: Gecks
authors.forename: Hans Reiner
authors.initials: HR
authors.lastname: Figulla
authors.forename: Atilla
authors.initials: A
authors.lastname: Yilmaz
authors.forename: Christian
authors.initials: C
authors.lastname: Jung
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D064368:Healthy Volunteers; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000150:complications* / Q000276:immunology; D007249:Inflammation / Q000097:blood / Q000209:etiology* / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D016209:Interleukin-8 / Q000097:blood*; D008297:Male; D013997:Time Factors
chemical_list: D015415:Biomarkers; C508606:CXCL8 protein, human; C508609:IL10 protein, human; D018836:Inflammation Mediators; D016209:Interleukin-8; D016753:Interleukin-10