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Anti-inflammatory role of CD11b + Ly6G + neutrophilic cells in allergic airway inflammation in mice.
- Source :
-
Immunology letters [Immunol Lett] 2018 Dec; Vol. 204, pp. 67-74. Date of Electronic Publication: 2018 Oct 28. - Publication Year :
- 2018
-
Abstract
- Asthma is a chronic inflammatory disease driven by overactivation of T helper cell type 2 (Th2) responses. In the present study, we investigated the functional relevance of CD11b <superscript>+</superscript> Ly6G <superscript>+</superscript> neutrophilic cells in allergic airway inflammation in vivo. Allergic airway inflammation in mice was induced by house dust mite (HDM) or ovalbumin (OVA) sensitization and challenge. CD11b <superscript>+</superscript> Ly6G <superscript>+</superscript> neutrophilic cells and T cell phenotypes were quantified by flow cytometry. To assess the functional in vivo relevance, CD11b <superscript>+</superscript> Ly6G <superscript>+</superscript> neutrophilic cells were adoptively transferred intravenously or intratracheally and consequences on airway inflammation were studied. Adoptively transferred CD11b <superscript>+</superscript> Ly6G <superscript>+</superscript> neutrophilic cells attenuated Th2 and Th17 responses and airway inflammation in vivo. Collectively, our results demonstrate that CD11b <superscript>+</superscript> Ly6G <superscript>+</superscript> neutrophilic cells suppress airway inflammation in allergic mice in vivo. Adoptive cellular transfer of suppressive neutrophilic cells may represent an attractive therapeutic strategy for allergic airway inflammation.<br /> (Copyright © 2018 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.)
- Subjects :
- Adoptive Transfer
Animals
Biomarkers
Cytokines metabolism
Female
Immunophenotyping
Inflammation Mediators metabolism
Mice
Antigens, Ly metabolism
CD11b Antigen metabolism
Neutrophils immunology
Neutrophils metabolism
Respiratory Hypersensitivity immunology
Respiratory Hypersensitivity metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1879-0542
- Volume :
- 204
- Database :
- MEDLINE
- Journal :
- Immunology letters
- Publication Type :
- Academic Journal
- Accession number :
- 30392943
- Full Text :
- https://doi.org/10.1016/j.imlet.2018.10.007