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. 2011 May 31;43(5):275-80.
doi: 10.3858/emm.2011.43.5.028.

Alveolar macrophages modulate allergic inflammation in a murine model of asthma

Affiliations

Alveolar macrophages modulate allergic inflammation in a murine model of asthma

Bo Ram Bang et al. Exp Mol Med. .

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-1β, IL-6 and TNF-α, 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.

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Figures

Figure 1
Figure 1
Changes in inflammatory cells in BAL fluid after alveolar macrophage depletion and after adoptive transfer of sensitized or unsensitized alveolar macrophage to alveolar macrophage depleted mice (A) total cell, (B) macrophages, (C) eosinophils, (D) neutrophils, (E) lymphocytes, LPS, lipopolysaccharide; sAM, sensitized alveolar macrophages; uAM, unsensitized alveolar macrophages; OVA, ovalbumin, *, P < 0.05)
Figure 2
Figure 2
Changes in inflammatory cytokine levels in BAL fluid after alveolar macrophage depletion and after adoptive transfer of sensitized or unsensitized alveolar macrophage to alveolar macrophage depleted mice (A, IL-4; B, IL-5; C, IFN-γ; D, GM-CSF; LPS, lipopolysaccharide; sAM, sensitized alveolar macrophages; uAM, unsensitized alveolar macrophages; OVA, ovalbumin; *, P < 0.05)
Figure 3
Figure 3
Pro-inflammatory cytokine production from alveolar macrophages after in vitro ovalbumin stimulation (*, P < 0.05).

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References

    1. Busse WW, Lemanske RF., Jr Asthma. N Engl J Med. 2001;344:350–362. - PubMed
    1. Careau E, Proulx LI, Pouliot P, Spahr A, Turmel V, Bissonnette EY. Antigen sensitization modulates alveolar macrophage functions in an asthma model. Am J Physiol Lung Cell Mol Physiol. 2006;290:L871–L879. - PubMed
    1. Careau E, Turmel V, Lauzon-Joset JF, Bissonnette EY. Alveolar macrophages reduce airway hyperresponsiveness and modulate cytokine levels. Exp Lung Res. 2010;36:255–261. - PubMed
    1. Elder AC, Gelein R, Oberdorster G, Finkelstein J, Notter R, Wang Z. Efficient depletion of alveolar macrophages using intratracheally inhaled aerosols of liposome-encapsulated clodronate. Exp Lung Res. 2004;30:105–120. - PubMed
    1. Gosset P, Tsicopoulos A, Wallaert B, Vannimenus C, Joseph M, Tonnel AB, Capron A. Increased secretion of tumor necrosis factor alpha and interleukin-6 by alveolar macrophages consecutive to the development of the late asthmatic reaction. J Allergy Clin Immunol. 1991;88:561–571. - PubMed

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