The role of alveolar macrophages and dendritic cells in allergic airway sensitization

Jansen, Henk M.

doi:10.1111/j.1398-9995.1996.tb04611.x

Cited by 18 publications

(17 citation statements)

References 119 publications

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“…The role played by alveolar macrophages in allergic lung inflammation pertains to their ability to serve as an antigen-presenting cell. More important, however, is their ability to produce pro-and antiinflammatory cytokines, lipid mediators, radical oxygen species, and chemokines (Lukacs et al 1995;Jansen 1996;Gosset et al 1999). Chemokine receptors expressed on monocytes/macrophages not only play a crucial role in the selective recruitment of these cells to sites of inflammation (Kurihara et al 1997), but are also important in the regulation of adhesion molecule expression and the release of inflammatory mediators by monocytes/macrophages (Jiang et al 1992;Mackay 2001).…”

Section: Discussionmentioning

confidence: 99%

Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation

Oostendorp

Hylkema

Luinge

et al. 2004

J Histochem Cytochem.

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Section: Discussionmentioning

confidence: 99%

Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation

Oostendorp

Hylkema

Luinge

et al. 2004

J Histochem Cytochem.

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“…On the one hand, it could be argued that genetics can predispose individuals to allergic disease; on the other, epidemiological studies suggest that environmental influences should not be dismissed. Moreover, it has been well established that mucosal surfaces, such as the lung, have immunosuppressive capacity (1,(8)(9)(10)12). Indeed, in experimental models it has been shown that exposure to aerosolized OVA does not lead to the development of airway histopathology (11), but may in fact elicit the phenomenon known as inhalation tolerance (12).…”

Section: /Cd8mentioning

confidence: 99%

“…The airways, like all mucosal surfaces, represent a site of initial exposure to environmental agents (1). It is at the mucosal surface that antigens are captured by antigen-presenting cells (APCs).…”

Section: Introductionmentioning

confidence: 99%

“…It is at the mucosal surface that antigens are captured by antigen-presenting cells (APCs). 1 They are subsequently processed and presented to lymphocytes in the lymphoid tissue, where they ultimately initiate a specific immunological response (1,2). The airways, in particular, are in continuous contact with a large number of airborne particles, both pathogenic and innocuous.…”

Section: Introductionmentioning

confidence: 99%

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GM-CSF transgene expression in the airway allows aerosolized ovalbumin to induce allergic sensitization in mice.

Stämpfli¹,

Wiley²,

Neigh³

et al. 1998

J. Clin. Invest.

238

175

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The purpose of this study was to explore whether repeated exposure to aerosolized ovalbumin (OVA) in the context of local expression of GM-CSF can initiate a Th2-driven, eosinophilic inflammation in the airways. On day Ϫ 1, Balb/c mice were infected intranasally with an adenovirus construct expressing GM-CSF (Ad/GM-CSF). From day 0 to day 9 mice were exposed daily to an OVA aerosol. Mice exposed to OVA alone did not show any evidence of airway inflammation. Mice receiving both Ad/GM-CSF and aerosolized OVA exhibited marked airway inflammation characterized by eosinophilia and goblet cell hyperplasia. Migration of eosinophils into the airway was preceded by a rise in IL-5 and IL-4. Both IL-5 and class II MHC were critically required to generate airway eosinophilia. After resolution, airway eosinophilia was reconstituted after a single OVA exposure. Flow cytometric analysis of dispersed lung cells revealed an increase in macrophages and dendritic cells expressing B7.1 and B7.2, and expansion of activated (CD69-expressing) CD4 and CD8 T cells in mice exposed to OVA and Ad/GM-CSF. Our data indicate that expression of GM-CSF in the airway compartment increases local antigen presentation capacity, and concomitantly facilitates the development of an antigen-specific, eosinophilic inflammatory response to an otherwise innocuous antigen. ( J. Clin. Invest.

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“…Although the pathogenesis of bronchial asthma is not fully understood, studies have shown that innate immunity is involved in the activation and recruitment of cells that are important for the development of allergic sensitization and inflammation (3)(4)(5)(6).…”

mentioning

confidence: 99%

Activation of Mast Cells Is Essential for Development of House Dust Mite Dermatophagoides farinae-Induced Allergic Airway Inflammation in Mice

Chen

2003

The Journal of Immunology

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In this study, we demonstrate that Dermatophagoides farinae (Der f), a major source of airborne allergens, but not OVA, could rapidly activate mast cells in mice. This was indicated by an elevation of serum mouse mast cell protease 1, a mast cell-specific proteinase, as early as 30 min after intratracheal challenge. Administration of sodium cromoglycate (40 mg/kg, i.p., 1 h before Der f instillation), a mast cell stabilizer, not only suppressed acute mouse mast cell protease 1 production but also attenuated the allergic airway inflammation provoked by repetitive Der f challenge in mice (five times at 1-wk interval). Der f induced the expression of mRNA for TNF-α, IL-1β, IL-4, IL-6, IL-9, and IL-13 in mastocytoma P815 cells and stimulated both P815 cells and bone marrow-derived mast cells to produce IL-4, IL-6, and TNF-α in a dose- and time-dependent manner. Cycloheximide as well as sodium cromoglycate blocked the Der f-induced IL-4 production, indicating a de novo protein synthesis process. Supernatants of Der f-stimulated mast cells chemoattracted monocytes and T lymphocytes; they up-regulated the expression of costimulatory B7 molecules, eotaxin, RANTES, monocyte chemoattractant protein 1, and IFN-inducible protein 10 mRNA of alveolar macrophages; they supported PHA-induced T cell proliferation; and they promoted Th2 cell development. Our data indicate that mast cells may be an important cell type during the initiation of Der f sensitization in the airway by modulating the function of alveolar macrophages and T cells.

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The role of alveolar macrophages and dendritic cells in allergic airway sensitization

Cited by 18 publications

References 119 publications

Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation

Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation

GM-CSF transgene expression in the airway allows aerosolized ovalbumin to induce allergic sensitization in mice.

Activation of Mast Cells Is Essential for Development of House Dust Mite Dermatophagoides farinae-Induced Allergic Airway Inflammation in Mice

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