| Resistin-Like Molecule Alpha Regulates IL-13-Induced Chemokine Production but not Allergen-Induced Airway Responses. | |
| | |
MedLine Citation:
|
PMID: 22246861 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
|
Resistin-like molecule alpha (Relm-α) is one of the most up-regulated gene products in allergen and parasite-associated Th2 responses. Localized to alternatively activated macrophages, Relm-α has been shown to have an anti-inflammatory effect in parasite-induced Th2 responses, but its role in experimental asthma remains unexplored. Herein, we analyzed the cellular source, IL-4 receptors required to stimulate Relm-α production, and the role of Relm-α following experimental asthma induction by IL-4, IL-13 or multiple experimental regimes, including OVA and Aspergillus fumigatus immunization. We demonstrate that Relm-α was secreted into the airway lumen, dependent upon both IL-13Rα1 and likely the type I IL-4 receptor, and differentially localized to epithelial cells and myeloid cells, depending upon the specific cytokine and/or aeroallergen trigger. Studies performed with Retnla gene-targeted mice demonstrated that Relm-α was largely redundant in terms of inducing Th2 cytokines, mucus and inflammatory cell infiltration into the lung. These results mirror the dispensable role that other alternatively-activated macrophage products (such as arginase 1) have in allergen induced experimental asthma and contrast with their role in the setting of parasitic infections. Taken together, our findings demonstrate distinct utilization of IL-4/IL-13 receptors for Relm-α induction in the lungs. Differential regulation of Relm-α expression is likely determined by the relative expression levels of IL-4, IL-13 and their corresponding receptors which are differentially expressed by divergent cells (i.e. epithelial cells and macrophages.) Finally, we identify a largely redundant functional role for Relm-α in acute experimental models of allergen-associated Th2-immune responses. |
| | |
Authors:
|
Ariel Munitz; Eric T Cole; Danielle Atar-Karo; Fred D Finkelman; Marc E Rothenberg |
Publication Detail:
|
Type: JOURNAL ARTICLE Date: 2012-1-12 |
Journal Detail:
|
Title: American journal of respiratory cell and molecular biology Volume: - ISSN: 1535-4989 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
|
Created Date: 2012-1-16 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: - |
Other Details:
|
Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
|
Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Hypercapnia - a Non-permissive Environment for the Lung.
Next Document: Prenatal Nicotine Exposure Alters Lung Function and Airway Geometry Through ?7 Nicotinic Receptors.