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Allergic airway disease is unaffected by the absence of IL-4R -dependent alternatively activated macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nieuwenhuizen, Natalie E. Kirstein, Frank Jayakumar, Jaisubash Emedi, Babele Hurdayal, Ramona Horsnell, William G. C. Lopata, Andreas L. Brombacher, Frank
Description	Country affiliation: South Africa Author Affiliation: Nieuwenhuizen NE ( International Center for Genetic Engineering and Biotechnology, Cape Town, South Africa.)
Abstract	BACKGROUND: Markers of alternatively activated macrophages (AAMs) are upregulated in the lungs of asthmatic patients and in mice with allergic airway disease. AAMs are thought to contribute to the pathogenesis of allergic airway disease by virtue of their decreased NO production and increased production of proline and polyamines, which are important in the synthesis of connective tissues such as collagen. OBJECTIVE: We aimed to define the role of AAMs in the pathogenesis of allergic airway disease. METHODS: The IL-4 receptor alpha (IL-4R ) gene is genetically abrogated in macrophages in LysM(cre)IL-4R (-/lox) mice, which therefore have impaired IL-4/IL-13 activation of AAMs through IL-4R types 1 and 2. Responses of LysM(cre)IL-4R (-/lox) mice and IL-4R (-/lox) littermate controls were examined in ovalbumin- and house dust mite-induced allergic airway disease. RESULTS: IL-4R expression was shown to be efficiently depleted from alveolar macrophages, interstitial macrophages, and CD11b(+)MHCII(+) inflammatory macrophages. Although the expression of markers of AAMs such as Ym-1, arginase and found in inflammatory zone 1 was decreased in macrophages of LysM(cre)IL-4R (-/lox) mice in chronic ovalbumin-induced allergic airway disease, airway hyperreactivity, T(H)2 responses, mucus hypersecretion, eosinophil infiltration, and collagen deposition were not significantly reduced. LysM(cre)IL-4R (-/lox) mice and littermate controls also developed similar responses in acute ovalbumin- and house dust mite-induced allergic airway disease. CONCLUSION: Our results suggest that the presence of AAMs in allergic airway disease may be only an association, as a result of the increased T(H)2 responses present during disease, and that IL-4R -dependent AAMs do not play an important role in the pathology of disease.
File Format	HTM / HTML
ISSN	00916749
e-ISSN	10976825
Journal	Journal of Allergy and Clinical Immunology
Issue Number	3
Volume Number	130
Language	English
Publisher	Elsevier
Publisher Date	2012-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Immunology Asthma Immunology Macrophages Physiology Receptors, Cell Surface Airway Resistance Animals Etiology Collagen Metabolism Cytokines Macrophage Activation Mice Mice, Inbred Balb C Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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