Allergic airway inflammation is exacerbated during acute influenza infection and correlates with increased allergen presentation and recruitment of allergen-specific T-helper type 2 cells

B. J. Marsland, C. B. Scanga, M. Kopf, G. Le Gros

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Background: Respiratory viral infections are a leading cause of the hospitalization of asthmatics, however, the cellular immunological interactions which underlie these two diseases remain elusive. Objective: We sought to characterize the effect influenza viral infection has on allergic airway inflammation and to identify the cellular pathways involved. Methods: We have used an ovalbumin (OVA) model of allergic airway inflammation, which involves sensitization of animals with OVA adsorbed in alum adjuvant followed by an intranasal challenge with OVA in phosphate-buffered saline. To study T cell recruitment into the lung, we adoptively transferred in vitro activated T cell receptor-transgenic T cells, which were subsequently identified by fluorescence-activated cell sorting (FACS) analysis. In addition, to study in vivo dendritic cell (DC) migration, we administered fluorescently labelled dextran and identified DCs that had phagocytosed it by FACS analysis. Results: We found that different stages of influenza infection had contrasting effects upon the outcome of OVA-induced allergic airway inflammation. The allergic response against OVA was exacerbated during the acute stage of influenza infection; however, mice were protected against the development of airway eosinophilia at late time-points following infection. We investigated the mechanisms responsible for the virus-induced exacerbation and found that the response was partially independent of IL-4 and that there was increased delivery of inhaled allergens to the draining lymph node during the acute stage of the infection. In addition, virus-induced inflammation in the lung and draining lymph node resulted in the non-specific recruitment of circulating allergen-specific effector/ memory cells. Conclusion: In addition to virus-mediated damage to the lung and airways, influenza viral infection can also enhance unrelated local allergic responses.

Original languageEnglish
Pages (from-to)1299-1306
Number of pages8
JournalClinical and Experimental Allergy
Volume34
Issue number8
DOIs
Publication statusPublished - 1 Aug 2004
Externally publishedYes

Keywords

  • Asthma
  • Exacerbation
  • Influenza
  • T cell
  • Virus

Cite this

@article{89bc8065db9f4080ad1ea63ea8451c99,
title = "Allergic airway inflammation is exacerbated during acute influenza infection and correlates with increased allergen presentation and recruitment of allergen-specific T-helper type 2 cells",
abstract = "Background: Respiratory viral infections are a leading cause of the hospitalization of asthmatics, however, the cellular immunological interactions which underlie these two diseases remain elusive. Objective: We sought to characterize the effect influenza viral infection has on allergic airway inflammation and to identify the cellular pathways involved. Methods: We have used an ovalbumin (OVA) model of allergic airway inflammation, which involves sensitization of animals with OVA adsorbed in alum adjuvant followed by an intranasal challenge with OVA in phosphate-buffered saline. To study T cell recruitment into the lung, we adoptively transferred in vitro activated T cell receptor-transgenic T cells, which were subsequently identified by fluorescence-activated cell sorting (FACS) analysis. In addition, to study in vivo dendritic cell (DC) migration, we administered fluorescently labelled dextran and identified DCs that had phagocytosed it by FACS analysis. Results: We found that different stages of influenza infection had contrasting effects upon the outcome of OVA-induced allergic airway inflammation. The allergic response against OVA was exacerbated during the acute stage of influenza infection; however, mice were protected against the development of airway eosinophilia at late time-points following infection. We investigated the mechanisms responsible for the virus-induced exacerbation and found that the response was partially independent of IL-4 and that there was increased delivery of inhaled allergens to the draining lymph node during the acute stage of the infection. In addition, virus-induced inflammation in the lung and draining lymph node resulted in the non-specific recruitment of circulating allergen-specific effector/ memory cells. Conclusion: In addition to virus-mediated damage to the lung and airways, influenza viral infection can also enhance unrelated local allergic responses.",
keywords = "Asthma, Exacerbation, Influenza, T cell, Virus",
author = "Marsland, {B. J.} and Scanga, {C. B.} and M. Kopf and {Le Gros}, G.",
year = "2004",
month = "8",
day = "1",
doi = "10.1111/j.1365-2222.2004.02021.x",
language = "English",
volume = "34",
pages = "1299--1306",
journal = "Clinical and Experimental Allergy",
issn = "0954-7894",
publisher = "Wiley-Blackwell",
number = "8",

}

Allergic airway inflammation is exacerbated during acute influenza infection and correlates with increased allergen presentation and recruitment of allergen-specific T-helper type 2 cells. / Marsland, B. J.; Scanga, C. B.; Kopf, M.; Le Gros, G.

In: Clinical and Experimental Allergy, Vol. 34, No. 8, 01.08.2004, p. 1299-1306.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Allergic airway inflammation is exacerbated during acute influenza infection and correlates with increased allergen presentation and recruitment of allergen-specific T-helper type 2 cells

AU - Marsland, B. J.

AU - Scanga, C. B.

AU - Kopf, M.

AU - Le Gros, G.

PY - 2004/8/1

Y1 - 2004/8/1

N2 - Background: Respiratory viral infections are a leading cause of the hospitalization of asthmatics, however, the cellular immunological interactions which underlie these two diseases remain elusive. Objective: We sought to characterize the effect influenza viral infection has on allergic airway inflammation and to identify the cellular pathways involved. Methods: We have used an ovalbumin (OVA) model of allergic airway inflammation, which involves sensitization of animals with OVA adsorbed in alum adjuvant followed by an intranasal challenge with OVA in phosphate-buffered saline. To study T cell recruitment into the lung, we adoptively transferred in vitro activated T cell receptor-transgenic T cells, which were subsequently identified by fluorescence-activated cell sorting (FACS) analysis. In addition, to study in vivo dendritic cell (DC) migration, we administered fluorescently labelled dextran and identified DCs that had phagocytosed it by FACS analysis. Results: We found that different stages of influenza infection had contrasting effects upon the outcome of OVA-induced allergic airway inflammation. The allergic response against OVA was exacerbated during the acute stage of influenza infection; however, mice were protected against the development of airway eosinophilia at late time-points following infection. We investigated the mechanisms responsible for the virus-induced exacerbation and found that the response was partially independent of IL-4 and that there was increased delivery of inhaled allergens to the draining lymph node during the acute stage of the infection. In addition, virus-induced inflammation in the lung and draining lymph node resulted in the non-specific recruitment of circulating allergen-specific effector/ memory cells. Conclusion: In addition to virus-mediated damage to the lung and airways, influenza viral infection can also enhance unrelated local allergic responses.

AB - Background: Respiratory viral infections are a leading cause of the hospitalization of asthmatics, however, the cellular immunological interactions which underlie these two diseases remain elusive. Objective: We sought to characterize the effect influenza viral infection has on allergic airway inflammation and to identify the cellular pathways involved. Methods: We have used an ovalbumin (OVA) model of allergic airway inflammation, which involves sensitization of animals with OVA adsorbed in alum adjuvant followed by an intranasal challenge with OVA in phosphate-buffered saline. To study T cell recruitment into the lung, we adoptively transferred in vitro activated T cell receptor-transgenic T cells, which were subsequently identified by fluorescence-activated cell sorting (FACS) analysis. In addition, to study in vivo dendritic cell (DC) migration, we administered fluorescently labelled dextran and identified DCs that had phagocytosed it by FACS analysis. Results: We found that different stages of influenza infection had contrasting effects upon the outcome of OVA-induced allergic airway inflammation. The allergic response against OVA was exacerbated during the acute stage of influenza infection; however, mice were protected against the development of airway eosinophilia at late time-points following infection. We investigated the mechanisms responsible for the virus-induced exacerbation and found that the response was partially independent of IL-4 and that there was increased delivery of inhaled allergens to the draining lymph node during the acute stage of the infection. In addition, virus-induced inflammation in the lung and draining lymph node resulted in the non-specific recruitment of circulating allergen-specific effector/ memory cells. Conclusion: In addition to virus-mediated damage to the lung and airways, influenza viral infection can also enhance unrelated local allergic responses.

KW - Asthma

KW - Exacerbation

KW - Influenza

KW - T cell

KW - Virus

UR - http://www.scopus.com/inward/record.url?scp=4143070170&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2222.2004.02021.x

DO - 10.1111/j.1365-2222.2004.02021.x

M3 - Article

VL - 34

SP - 1299

EP - 1306

JO - Clinical and Experimental Allergy

JF - Clinical and Experimental Allergy

SN - 0954-7894

IS - 8

ER -