A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse

Hua Hao H. Shen, Sergei I. Ochkur, Michael P. McGarry, Jeffrey R. Crosby, Edie M. Hines, Michael T. Borchers, Huiying Wang, Travis L. Biechelle, Katie R. O'Neill, Tracy L. Ansay, Dana C. Colbert, Stephania Cormier, J. Paul Justice, Nancy A. Lee, James J. Lee

Research output: Contribution to journalArticle

130 Citations (Scopus)

Abstract

Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5 -/- mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5 -/- mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5 -/- mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5 -/- mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4 + T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.

Original languageEnglish (US)
Pages (from-to)3296-3305
Number of pages10
JournalJournal of Immunology
Volume170
Issue number6
DOIs
StatePublished - Mar 15 2003

Fingerprint

Eosinophils
Pathology
Lung
Interleukin-5
Pulmonary Eosinophilia
Adoptive Transfer
Mucus
T-Lymphocytes
Wild Animals
Bronchoalveolar Lavage
Allergens
Asthma
Cytokines
Inflammation

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Shen, H. H. H., Ochkur, S. I., McGarry, M. P., Crosby, J. R., Hines, E. M., Borchers, M. T., ... Lee, J. J. (2003). A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse. Journal of Immunology, 170(6), 3296-3305. https://doi.org/10.4049/jimmunol.170.6.3296

A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse. / Shen, Hua Hao H.; Ochkur, Sergei I.; McGarry, Michael P.; Crosby, Jeffrey R.; Hines, Edie M.; Borchers, Michael T.; Wang, Huiying; Biechelle, Travis L.; O'Neill, Katie R.; Ansay, Tracy L.; Colbert, Dana C.; Cormier, Stephania; Justice, J. Paul; Lee, Nancy A.; Lee, James J.

In: Journal of Immunology, Vol. 170, No. 6, 15.03.2003, p. 3296-3305.

Research output: Contribution to journalArticle

Shen, HHH, Ochkur, SI, McGarry, MP, Crosby, JR, Hines, EM, Borchers, MT, Wang, H, Biechelle, TL, O'Neill, KR, Ansay, TL, Colbert, DC, Cormier, S, Justice, JP, Lee, NA & Lee, JJ 2003, 'A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse', Journal of Immunology, vol. 170, no. 6, pp. 3296-3305. https://doi.org/10.4049/jimmunol.170.6.3296
Shen, Hua Hao H. ; Ochkur, Sergei I. ; McGarry, Michael P. ; Crosby, Jeffrey R. ; Hines, Edie M. ; Borchers, Michael T. ; Wang, Huiying ; Biechelle, Travis L. ; O'Neill, Katie R. ; Ansay, Tracy L. ; Colbert, Dana C. ; Cormier, Stephania ; Justice, J. Paul ; Lee, Nancy A. ; Lee, James J. / A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse. In: Journal of Immunology. 2003 ; Vol. 170, No. 6. pp. 3296-3305.
@article{537c39e51738494e9be7339f2083750d,
title = "A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse",
abstract = "Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5 -/- mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5 -/- mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5 -/- mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5 -/- mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4 + T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.",
author = "Shen, {Hua Hao H.} and Ochkur, {Sergei I.} and McGarry, {Michael P.} and Crosby, {Jeffrey R.} and Hines, {Edie M.} and Borchers, {Michael T.} and Huiying Wang and Biechelle, {Travis L.} and O'Neill, {Katie R.} and Ansay, {Tracy L.} and Colbert, {Dana C.} and Stephania Cormier and Justice, {J. Paul} and Lee, {Nancy A.} and Lee, {James J.}",
year = "2003",
month = "3",
day = "15",
doi = "10.4049/jimmunol.170.6.3296",
language = "English (US)",
volume = "170",
pages = "3296--3305",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "6",

}

TY - JOUR

T1 - A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse

AU - Shen, Hua Hao H.

AU - Ochkur, Sergei I.

AU - McGarry, Michael P.

AU - Crosby, Jeffrey R.

AU - Hines, Edie M.

AU - Borchers, Michael T.

AU - Wang, Huiying

AU - Biechelle, Travis L.

AU - O'Neill, Katie R.

AU - Ansay, Tracy L.

AU - Colbert, Dana C.

AU - Cormier, Stephania

AU - Justice, J. Paul

AU - Lee, Nancy A.

AU - Lee, James J.

PY - 2003/3/15

Y1 - 2003/3/15

N2 - Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5 -/- mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5 -/- mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5 -/- mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5 -/- mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4 + T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.

AB - Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5 -/- mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5 -/- mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5 -/- mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5 -/- mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4 + T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.

UR - http://www.scopus.com/inward/record.url?scp=0037443649&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037443649&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.170.6.3296

DO - 10.4049/jimmunol.170.6.3296

M3 - Article

VL - 170

SP - 3296

EP - 3305

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 6

ER -