Neutrophils Regulate Airway Responses in a Model of Fungal Allergic Airways Disease

Park, Stacy J; Wiekowski, Maria T; Lira, Sergio A; Mehrad, Borna

doi:10.4049/jimmunol.176.4.2538

Cited by 51Asthma and respiratory diseasesAllergic Rhinitis and SensitizationIL-33, ST2, and ILC Pathways

Neutrophils Regulate Airway Responses in a Model of Fungal Allergic Airways Disease

Park, Stacy J, Wiekowski, Maria T, Lira, Sergio A, Mehrad, Borna·2006·The Journal of Immunology

DOI 10.4049/jimmunol.176.4.2538

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Abstract

Neutrophils infiltrate airway walls in patients with allergic airway diseases and in animal models of these illnesses, but their contribution to the pathogenesis of airway allergy is not established. We hypothesized that, in a mouse model of airway allergy to the ubiquitous environmental mold, Aspergillus fumigatus, airway neutrophils contribute to disease severity. Ab-mediated neutrophil depletion resulted in reduced airway hyperresponsiveness and remodeling, whereas conditional transgenic overexpression of the neutrophil chemotactic molecule, CXCL1, in airway walls resulted in worsened allergic responses. This worsened phenotype was associated with a marked increase in the number of airway neutrophils but not other lung leukocytes, including eosinophils and lymphocyte subsets, and depletion of neutrophils in sensitized mice with transgenic overexpression of CXCL1 resulted in attenuated airway responses. The number of lung neutrophils correlated with lung matrix metalloproteinase 9 (MMP-9) activity both in the context of neutrophil depletion and with augmented neutrophil recruitment to the airways. Although wild-type and MMP-9-deficient neutrophils homed to the inflamed airways to a similar extent, transfer of wild-type, but not MMP-9-deficient, neutrophils to MMP-9-deficient animals resulted in augmented allergic airway responses. Taken together, these data implicate neutrophils in the pathogenesis of fungal allergic airway disease.

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CXCR2-deficient mice that are defective in neutrophil chemotaxis are highly susceptible to development of invasive aspergillosis.
“Accordingly, CXCR2-deficient mice that are defective in neutrophil chemotaxis are highly susceptible to development of invasive aspergillosis (242, 276).”
From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [276]

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Authors: Park, S. J., Wiekowski, M. T., Lira, S. A., & Mehrad, B.
Affiliations: The University of Texas Southwestern Medical Center (US)
Department of Immunology, Schering-Plough Research Institute , Kenilworth, NJ 07033
Immunobiology Center, Mount Sinai School of Medicine , New York, NY 10029
Corresponding author: Mehrad, Borna
ORCID: Wiekowski, Maria T
Mehrad, Borna
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2006-02
Volume: 176
Issue: 4
Pages: 2538-2545
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.176.4.2538
OpenAlex: W1911091032
Cited by: 51
References: 74
Citations by year: 2025: 1 · 2020: 4 · 2019: 3 · 2017: 2 · 2016: 3 · 2015: 5 · 2014: 2 · 2013: 7 · 2012: 3
FWCI: 2.66
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (HL04220, HL-73848, R01HL073848)
Topics: Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords: neutrophils, allergic airway disease, Aspergillus fumigatus, fungal allergy, airway hyperresponsiveness, airway remodeling, CXCL1, neutrophil chemotaxis, MMP-9, neutrophil depletion, neutrophil recruitment, eosinophils, mouse model
MeSH terms: Animals, Aspergillosis, Aspergillus fumigatus, Disease Models, Animal, T-Lymphocytes, Helper-Inducer, Hypersensitivity, Immunoglobulin E, Lung Diseases, Neutrophils, Cytokines, Transgenes, Matrix Metalloproteinase 9, Mice

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Neutrophils Regulate Airway Responses in a Model of Fungal Allergic Airways Disease

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