| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
R Gene-Deleted Mice1
* Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;
Western College of Veterinary Medicine, Saskatoon, Saskatchewan, Canada;
State University of New York, Upstate Medical University, Syracuse, NY 13210; and
Department of Biological Sciences, University of Warwick, Coventry, United Kingdom
Pneumonia virus of mice (PVM; family Paramyxoviridae) is a natural pathogen of rodents that reproduces important clinical features of severe respiratory syncytial virus infection in humans. As anticipated, PVM infection induces transcription of IFN antiviral response genes preferentially in wild-type over IFN-
R gene-deleted (IFN-R–/–) mice. However, we demonstrate that PVM infection results in enhanced expression of eotaxin-2 (CCL24), thymus and activation-regulated chemokine (CCL17), and the proinflammatory RNase mouse eosinophil-associated RNase (mEar) 11, and decreased expression of monocyte chemotactic protein-5, IFN-
-inducible protein-10, and TLR-3 in lung tissue of IFN-R–/– mice when compared with wild type. No differential expression of chemokines MIP-1 or MIP-2 or Th2 cytokines IL-4 or IL-5 was observed. Differential expression of proinflammatory mediators was associated with distinct patterns of lung pathology. The widespread granulocytic infiltration and intra-alveolar edema observed in PVM-infected, wild-type mice are replaced with patchy, dense inflammatory foci localized to the periphery of the larger blood vessels. Bronchoalveolar lavage fluid from IFN-R–/– mice yielded 7- to 8-fold fewer leukocytes overall, with increased percentages of eosinophils, monocytes, and CD4+ T cells, and decreased percentage of CD8+ T cells. Differential pathology is associated with prolonged survival of the IFN-R–/– mice (50% survival at 10.8 ± 0.6 days vs the wild type at 9.0 ± 0.3 days; p < 0.02) despite increased virus titers. Overall, our findings serve to identify novel transcripts that are differentially expressed in the presence or absence of IFN-R-mediated signaling, further elucidating interactions between the IFN and antiviral inflammatory responses in vivo.
This article has been cited by other articles:
|
|
 |
|
  H. Qiu, Y. Fan, A. G. Joyee, S. Wang, X. Han, H. Bai, L. Jiao, N. Van Rooijen, and X. Yang Type I IFNs Enhance Susceptibility to Chlamydia muridarum Lung Infection by Enhancing Apoptosis of Local Macrophages J. Immunol., August 1, 2008; 181(3): 2092 - 2102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. F. Rosenberg RNase A ribonucleases and host defense: an evolving story J. Leukoc. Biol., May 1, 2008; 83(5): 1079 - 1087. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Xu, M. Johansson, and A. Karlsson Human UMP-CMP Kinase 2, a Novel Nucleoside Monophosphate Kinase Localized in Mitochondria J. Biol. Chem., January 18, 2008; 283(3): 1563 - 1571. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Austin, W. P. Halford, B. R. G. Williams, and D. J. J. Carr Oligoadenylate Synthetase/Protein Kinase R Pathways and {alpha}beta TCR+ T Cells Are Required for Adenovirus Vector: IFN-{gamma} Inhibition of Herpes Simplex Virus-1 in Cornea J. Immunol., April 15, 2007; 178(8): 5166 - 5172. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
