Diabetes increases inflammation and lung injury associated with protective ventilation strategy in mice

Int Immunopharmacol. 2012 Jul;13(3):280-3. doi: 10.1016/j.intimp.2012.04.020. Epub 2012 May 9.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / biosynthesis
  • Cytokines / blood
  • Cytokines / genetics
  • Diabetes Mellitus, Experimental / complications
  • Diabetes Mellitus, Experimental / immunology*
  • Diabetes Mellitus, Experimental / physiopathology*
  • Inflammation / etiology*
  • Inflammation / immunology
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Lung / immunology
  • Lung Injury / etiology*
  • Lung Injury / pathology
  • Lung Injury / physiopathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Respiration, Artificial / adverse effects*
  • Respiration, Artificial / methods
  • Tidal Volume
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • IL10 protein, mouse
  • Interleukin-6
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interleukin-10