AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 289: L111-L124, 2005. First published March 25, 2005; doi:10.1152/ajplung.00318.2004
1040-0605/05 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
289/1/L111    most recent
00318.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Teske, S.
Right arrow Articles by Lawrence, B. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Teske, S.
Right arrow Articles by Lawrence, B. P.

Activation of the aryl hydrocarbon receptor increases pulmonary neutrophilia and diminishes host resistance to influenza A virus

Sabine Teske,1 Andrea A. Bohn,2 Jean F. Regal,3 Joshua J. Neumiller,1 and B. Paige Lawrence1,2

1Department of Pharmaceutical Sciences, Pharmacology/Toxicology Graduate Program, College of Pharmacy, and 2Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington; and 3Department of Biochemistry and Molecular Biology, University of Minnesota, Duluth, Minnesota

Submitted 25 August 2004 ; accepted in final form 18 March 2005

Unlike their role in bacterial infection, less is known about the role of neutrophils during pulmonary viral infection. Exposure to pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) results in excess neutrophils in the lungs of mice infected with influenza A virus. TCDD is the most potent agonist for the aryl hydrocarbon receptor (AhR), and exposure to AhR ligands has been correlated with exacerbated inflammatory lung diseases. However, knowledge of the effects of AhR agonists on neutrophils is limited. Likewise, the factors regulating neutrophil responses during respiratory viral infections are not well characterized. To address these knowledge gaps, we determined the in vivo levels of KC, MIP-1{alpha}, MIP-2, LIX, IL-6, and C5a in infected mouse lungs. Our data show that these neutrophil chemoattractants are generally produced transiently in the lung within 12–24 h of infection. We also report that expression of CD11a, CD11b, CD49d, CD31, and CD38 is increased on pulmonary neutrophils in response to influenza virus. Using AhR-deficient mice, we demonstrate that excess neutrophilia in the lung is mediated by activation of the AhR and that this enhanced neutrophilia correlates directly with decreased survival in TCDD-exposed mice. Although AhR activation results in more neutrophils in the lungs, we show that this is not mediated by deregulation in levels of common neutrophil chemoattractants, expression of adhesion molecules on pulmonary neutrophils, or delayed death of neutrophils. Likewise, exposure to TCDD did not enhance pulmonary neutrophil function. This study provides an important first step in elucidating the mechanisms by which AhR agonists exacerbate pulmonary inflammatory responses.

pulmonary inflammation; chemokines; adhesion molecules; aryl hydrocarbon receptor-knockout mice; dioxin


Address for reprint requests and other correspondence: B. P. Lawrence, Dept. of Pharmaceutical Sciences, Wegner Hall, Washington State Univ., Pullman, WA 99164-6534 (E-mail bpl{at}mail.wsu.edu)




This article has been cited by other articles:


Home page
 BloodHome page
B. P. Lawrence, M. S. Denison, H. Novak, B. A. Vorderstrasse, N. Harrer, W. Neruda, C. Reichel, and M. Woisetschlager
Activation of the aryl hydrocarbon receptor is essential for mediating the anti-inflammatory effects of a novel low-molecular-weight compound
Blood, August 15, 2008; 112(4): 1158 - 1165.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
M. A. O'Reilly, S. H. Marr, M. Yee, S. A. McGrath-Morrow, and B. P. Lawrence
Neonatal Hyperoxia Enhances the Inflammatory Response in Adult Mice Infected with Influenza A Virus
Am. J. Respir. Crit. Care Med., May 15, 2008; 177(10): 1103 - 1110.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
S. Teske, A. A. Bohn, J. P. Hogaboam, and B. P. Lawrence
Aryl Hydrocarbon Receptor Targets Pathways Extrinsic to Bone Marrow Cells to Enhance Neutrophil Recruitment during Influenza Virus Infection
Toxicol. Sci., March 1, 2008; 102(1): 89 - 99.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
B. A. Vorderstrasse and B. P. Lawrence
Protection against Lethal Challenge with Streptococcus pneumoniae Is Conferred by Aryl Hydrocarbon Receptor Activation but Is Not Associated with an Enhanced Inflammatory Response.
Infect. Immun., October 1, 2006; 74(10): 5679 - 5686.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.