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Infection and Immunity, October 1999, p. 5041-5047, Vol. 67, No. 10
Department of Pathobiology, University of
Guelph, Guelph, Ontario N1G 2W1, Canada
Received 21 April 1999/Returned for modification 25 May
1999/Accepted 15 July 1999
The ability of Rhodococcus equi to induce pneumonia in
foals depends on the presence of an 85- to 90-kb plasmid. In this
study, we evaluated whether plasmid-encoded products mediate virulence by modulating the cytokine response of foals. Foals infected
intrabronchially with a virulence plasmid-containing strain of R. equi had similar gamma interferon (IFN-
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Modulation of Cytokine Response of Pneumonic Foals
by Virulent Rhodococcus equi

) and interleukin-12
(IL-12) p35 but significantly higher IL-1
, IL-10, IL-12 p40, and
tumor necrosis factor alpha (TNF-
) mRNA expression in lung tissue
compared to foals infected with the plasmid-cured derivative. IFN-
mRNA expression levels in CD4+ T lymphocytes isolated from
bronchial lymph nodes (BLN) were similar for the two groups of R. equi-infected foals on day 3 postinfection. However, on day 14, in association with pneumonia and marked multiplication of virulent
R. equi but with complete clearance of the plasmid-cured
derivative, IFN-
mRNA expression in BLN CD4+ T
lymphocytes was significantly (P < 0.001) higher in
foals infected with the plasmid-cured derivative. These results
suggests an immunomodulating role for R. equi virulence
plasmid-encoded products in downregulating IFN-
mRNA expression by
CD4+ T lymphocytes.
*
Corresponding author. Mailing address: Department of
Pathobiology, University of Guelph, Guelph, Ontario N1G 2W1, Canada. Phone: (519) 824-4120, ext. 4717. Fax: (519) 767-0809. E-mail: jprescott{at}ovcnet.uoguelph.ca.
Present address: Department of Large Animal Clinical Sciences,
College of Veterinary Medicine, University of Florida, Gainesville, FL
32610-0136.
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