Effect of stress on eotaxin and expression of adhesion molecules in a murine model of allergic airway inflammation

J Neuroimmunol. 2007 Jan;182(1-2):55-62. doi: 10.1016/j.jneuroim.2006.09.010. Epub 2006 Nov 7.

Abstract

Recently we have shown that sound stress enhances allergic airway inflammation in a combined murine model. In the current study we investigated mediating factors and early kinetics of stress exacerbated allergic airway inflammation. Stress significantly increased allergen induced airway inflammation as identified by leukocyte numbers in BAL fluids. Eotaxin levels from stressed mice were significantly higher 24 h after stress. No differences were found for vascular or cellular adhesion molecule expression or cytokine levels. Our data indicate that the effect of stress on allergic airway inflammation might be mediated by the chemoattractant eotaxin, while Th2 cytokines and expression of adhesion molecules seem not to be differently regulated in stressed and non-stressed mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / immunology*
  • Animals
  • Blood Cells / pathology
  • Bronchitis / complications
  • Bronchitis / immunology*
  • Bronchitis / metabolism*
  • Bronchitis / pathology
  • Bronchoalveolar Lavage Fluid / chemistry
  • Cell Adhesion Molecules / analysis
  • Cell Adhesion Molecules / metabolism*
  • Cell Count
  • Chemokine CCL11
  • Chemokines, CC / metabolism*
  • Corticosterone / blood
  • Eosinophils / metabolism
  • Eosinophils / pathology
  • Interleukin-4 / analysis
  • Interleukin-5 / analysis
  • Lung / pathology
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / immunology
  • Stress, Physiological / complications
  • Stress, Physiological / metabolism*

Substances

  • Allergens
  • Ccl11 protein, mouse
  • Cell Adhesion Molecules
  • Chemokine CCL11
  • Chemokines, CC
  • Interleukin-5
  • Interleukin-4
  • Ovalbumin
  • Corticosterone