This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mitchell, G. B.
Right arrow Articles by Caswell, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mitchell, G. B.
Right arrow Articles by Caswell, J. L.

 Previous Article  |  Next Article 

Infection and Immunity, March 2007, p. 1325-1334, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.00686-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Effect of Corticosteroids and Neuropeptides on the Expression of Defensins in Bovine Tracheal Epithelial Cells{triangledown}

Gordon B. Mitchell,* Muthafar H. Al-Haddawi, Mary Ellen Clark, Jennifer D. Beveridge, and Jeff L. Caswell

Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada

Received 28 April 2006/ Returned for modification 4 June 2006/ Accepted 1 December 2006

Susceptibility to bacterial pneumonia in cattle is enhanced by stressors such as transportation, weaning, and commingling, which trigger a physiologic stress response resulting in elevated levels of endogenous corticosteroids and catecholamines. To determine the effect of neuroendocrine mediators on the expression of innate defense peptides in the lung, bovine tracheal epithelial cells were exposed to dexamethasone, catecholamines, acetylcholine, or substance P, and then ß-defensin expression was quantified using real-time reverse transcription-PCR. Basal expression of tracheal antimicrobial peptide (TAP) mRNA was not affected by any of the mediators tested. However, induction of TAP expression by lipopolysaccharide was significantly inhibited by pretreatment with dexamethasone. Bronchial biopsy specimens from dexamethasone-treated calves had significantly lower expression of TAP and lingual antimicrobial peptide (LAP) mRNA than saline-treated controls following 48 h of treatment. Lipopolysaccharide-elicited neutrophil recruitment was enhanced in the lungs of dexamethasone-treated calves compared to saline-treated controls. These findings indicate that modulation of epithelial antimicrobial peptide expression is one mechanism through which corticosteroids and stress may impair innate pulmonary defenses.

* Corresponding author. Mailing address: Department of Pathobiology, University of Guelph, Guelph, ON N1G 2W1, Canada. Phone: (519) 824-4120. Fax: (519) 824-5930. E-mail: gmitchel{at}uoguelph.ca.

{triangledown} Published ahead of print on 11 December 2006.

Editor: J. L. Flynn

Infection and Immunity, March 2007, p. 1325-1334, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.00686-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»