Alveolar macrophages modulate allergic inflammation in a murine model of asthma.
10.3858/emm.2011.43.5.028
- Author:
Bo Ram BANG
1
;
Eunyoung CHUN
;
Eun Jin SHIM
;
Hyun Seung LEE
;
Soo Yeon LEE
;
Sang Heon CHO
;
Kyung Up MIN
;
You Young KIM
;
Heung Woo PARK
Author Information
1. Department of Internal Medicine, College of Medicine, Seoul National University, Seoul 110-744, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
adoptive transfer;
airway inflammation;
alveolar macrophage;
asthma;
GM-CSF
- MeSH:
Animals;
Asthma/*immunology;
Bronchoalveolar Lavage Fluid/chemistry/cytology/immunology;
Cytokines/biosynthesis/immunology;
Disease Models, Animal;
Female;
Immunization;
Immunomodulation/*immunology;
Inflammation/*immunology;
Leukocytes/immunology;
Macrophages, Alveolar/*immunology;
Mice;
Mice, Inbred C57BL;
Ovalbumin/immunology
- From:Experimental & Molecular Medicine
2011;43(5):275-280
- CountryRepublic of Korea
- Language:English
-
Abstract:
The role of alveolar macrophages (AMs) in the pathogenesis of asthma is still unknown. The aim of the present study was to investigate the effects of AM in the murine model of asthma. AMs were selectively depleted by liposomes containing clodronate just before allergen challenges, and changes in inflammatory cells and cytokine concentrations in bronchoalveolar lavage (BAL) fluid were measured. AMs were then adoptively transferred to AM-depleted sensitized mice and changes were measured. Phenotypic changes in AMs were evaluated after in vitro allergen stimulation. AM-depletion after sensitization significantly increased the number of eosinophils and lymphocytes and the concentrations of IL-4, IL-5 and GM-CSF in BAL fluid. These changes were significantly ameliorated only by adoptive transfer of unsensitized AMs, not by sensitized AMs. In addition, in vitro allergen stimulation of AMs resulted in their gaining the ability to produce inflammatory cytokines, such as IL-1beta, IL-6 and TNF-alpha, and losing the ability to suppress GM-CSF concentrations in BAL fluid. These findings suggested that AMs worked probably through GM-CSF-dependent mechanisms, although further confirmatory experiments are needed. Our results indicate that the role of AMs in the context of airway inflammation should be re-examined.
