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Comparative and Functional Genomics - Volume 6 2005, Issue 4, Pages 244-250

Conference paper

Genome Prairie, Suite 115, 3553-31 St., NW, Calgary, AB T2L 2K7, Canada

Vaccine and Infectious Disease Organization, 120 Veterinary Road, University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada

Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada

Central Institute for Research on Buffalo, Sirsa Road, Hisar, Haryana 125001, India

Received 17 February 2005; Accepted 14 March 2005

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The severity of bovine respiratory infections has been linked to a variety offactors, including environmental and nutritional changes, transportation, and socialreorganization of weaned calves. Fatal respiratory infections, however, usually occurwhen a primary viral infection compromises host defences and enhances the severityof a secondary bacterial infection. This viral–bacterial synergy can occur by a numberof different mechanisms and disease challenge models have been developed to analysehost responses during these respiratory infections. A primary bovine herpesvirus-1BHV-1 respiratory infection followed by a secondary challenge with Mannheimia haemolyticaresults in fatal bovine respiratory disease BRD and host responses to these two pathogens have been studied extensively. We used this disease model todemonstrate that stress significantly altered the viral–bacterial synergy resulting infatal BRD. Functional genomic analysis revealed that BHV-1 infection enhanced toll-likereceptors TLR expression and increased pro-inflammatory responses whichcontribute to the severity of a Mannheimia haemolytica infection. TLRs play a criticalrole in detecting bacterial infections and inducing pro-inflammatory responses. It isdifficult to understand, however, how stress-induced corticosteroids could enhancethis form of viral–bacterial synergy. Nuclear translocation of the glucocorticoidreceptor activates cell signalling pathways which inhibit both TLR signallingand pro-inflammatory responses. The apparent conundrum between stress-inducedcorticosteroids and enhanced BRD susceptibility is discussed in terms of present dataand previous investigations of stress and respiratory disease.

Autor: P. D. Hodgson, P. Aich, A. Manuja, K. Hokamp, F. M. Roche, F. S. L. Brinkman, A. Potter, L. A. Babiuk, and P. J. Griebel

Fuente: https://www.hindawi.com/


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