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Rat tracheal epithelial responses to water avoidance stress
Hiroshi Akiyama1, Hiroo Amano, John Bienenstock
1Division of Foods, National Institute of Health Sciences, Tokyo, Japan. akiyama@nihs.go.jp
The Journal of Allergy and Clinical Immunology
|August 9, 2005
Summary
Acute stress activates tracheal mast cells and sensitizes the airway epithelium to substance P, partly via corticotropin-releasing factor (CRF). This suggests stress may contribute to lung inflammation, like asthma.
Area of Science:
- Pulmonary Medicine
- Neuroimmunology
- Cellular Biology
Background:
- Psychological stress impacts multiple organ systems, including the gut via the hypothalamic-pituitary-adrenal axis, mast cells, and nerves.
- Limited research exists on the effects of stress on the lung.
Purpose of the Study:
- To examine Wistar rat tracheal epithelial responses to acute water avoidance stress.
- To elucidate the role of corticotropin-releasing factor (CRF) and mast cells in stress-induced airway changes.
Main Methods:
- Tracheal tissue was analyzed using Ussing chambers.
- Electron microscopy was employed to assess mast cell activation.
- Responses to substance P were measured following stress and CRF administration.
Main Results:
- Acute stress increased short-circuit current in tracheal epithelium, indicating altered ion transport.
- Stress led to mast cell activation and degranulation in the trachea.
- Both stress and CRF enhanced substance P responses, but CRF receptor antagonism did not fully block these effects.
Conclusions:
- Acute stress affects tracheal epithelium, partly through CRF and mast cell activation.
- Stress sensitizes the airway epithelium to substance P, potentially exacerbating inflammatory responses.
- These findings suggest a potential role for stress in lung inflammatory diseases such as asthma.