Impact of endobronchial allergen provocation on macrophage phenotype in asthmatics

BMC Immunology

Jens M Hohlfeld²  Frank Schaumann¹  Olaf Holz²  Meike Müller¹  Conny Faulenbach¹  Natali Moraw¹  Lena Witte¹  Carla Winkler¹ 

[1] Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany;Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research, Hannover, Germany

关键词: Segmental allergen challenge;    Endobronchial allergen provocation;    M2 macrophages;    Asthma;   

Others  :  1077721
DOI  :  10.1186/1471-2172-15-12

 received in 2013-08-14, accepted in 2014-02-21,  发布年份 2014

【 摘 要 】

Background

The role of M2 polarized macrophages (MΦ) during the allergic airway inflammation has been discussed in various animal models. However, their presence and relevance during the chronic and acute phase of allergic airway inflammation in humans has not been fully elucidated so far. In the present study we phenotypically characterized macrophages with regard to M2 polarization in mice, a human in vitro and a human ex vivo model with primary lung cells after endobronchial provocation.

Results

Macrophages remained polarized beyond clearance of the acute allergic airway inflammation in mice. Alveolar macrophages of asthmatics revealed increased mRNA expression of CCL13, CCL17 and CLEC10A in response to allergen challenge as well as increased surface expression of CD86. Further, mRNA expression of CCL13, CCL17, and CLEC10A was increased in asthmatics at baseline compared to healthy subjects. The mRNA expression of CCL17 and CLEC10A correlated significantly with the degree of eosinophilia (each P < .01). Furthermore, macrophages from asthmatics released significant amounts of CCL17 protein in vitro which was also found increased in BAL fluid after allergen provocation.

Conclusions

This study supports previous findings of M2 macrophage polarization in asthmatic subjects during the acute course of the allergic inflammation and provides evidence for their contribution to the Th2 inflammation.

【 授权许可】

   
2014 Winkler et al.; licensee BioMed Central Ltd.

【 图 表 】

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