title: Diabetes increases inflammation and lung injury associated with protective ventilation strategy in mice.
abstract: BACKGROUND
  Mechanical ventilation may paradoxically cause lung injury. Protective mechanical ventilation strategy utilizing low tidal volume and high frequency has been shown to attenuate inflammation and reduce mortality in non-diabetic patients. The purpose of this present study was to observe the effects of diabetes on inflammation and lung injury in mice with protective ventilation strategy.
  
  
  METHODS
  Forty mice were included in our study. The mice in Group Dia-MV and Con-MV were subjected to 4 hour-ventilation. And the mice in Group Dia-SB and Con-SB were exposed to room air breathing spontaneously for 4h. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), superoxide dismutase (SOD) and malondialdehyde (MDA) levels in serum were detected and the expression of inflammatory cytokine mRNA was also determined in lung tissue. Lung damage was assessed using a modified lung injury score.
  
  
  RESULTS
  The serum levels of TNF-α, IL-6, and IL-10 in Group Dia-MV were significantly higher than those in Group Dia-SB or Group Con-MV or Group Con-SB (P<0.05). Quantitative RT-PCR analysis of pro-inflammatory cytokines in lung homogenates presented similar results. The mice in Group Dia-MV suffered obvious lung histological changes, whose lung injury scores were significantly higher in Group Dia-SB as compared to Group Con-SB , Group Con-MV or Group Dia-SB (P<0.05).
  
  
  CONCLUSIONS
  Diabetes increased the inflammation reaction and associated lung injury in mice in spite of the protective mechanical ventilation strategy based on low tidal volumes and high frequency.
authors.affiliation: Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, Zhejiang, China.
authors.forename: Xiang-qing
authors.initials: XQ
authors.lastname: Xiong
authors.forename: Wan-tie
authors.initials: WT
authors.lastname: Wang
authors.forename: Liang-rong
authors.initials: LR
authors.lastname: Wang
authors.forename: Li-da
authors.initials: LD
authors.lastname: Jin
authors.forename: Li-na
authors.initials: LN
authors.lastname: Lin
mesh_terms: D000818:Animals; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000276:immunology* / Q000503:physiopathology*; D007249:Inflammation / Q000209:etiology* / Q000276:immunology; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000276:immunology; D055370:Lung Injury / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012121:Respiration, Artificial / Q000009:adverse effects* / Q000379:methods; D013990:Tidal Volume; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; C556062:IL10 protein, mouse; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10