ArticleProceedings of the National Academy of Sciences of the United States of America1998
Autologously up-regulated Fc receptor expression and action in airway smooth muscle mediates its altered responsiveness in the atopic asthmatic sensitized state.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 60 citations in OpenAlex.
- Impaired anti-inflammatory action of glucocorticoid in neutrophil from patients with steroid-resistant asthma.Respiratory research · 2016Article
- G Protein βγ-subunit signaling mediates airway hyperresponsiveness and inflammation in allergic asthma.PloS one · 2012Article
- CC-chemokine CCL15 expression and possible implications for the pathogenesis of IgE-related severe asthma.Mediators of inflammation · 2012Review
- Pentraxin 3 (PTX3) expression in allergic asthmatic airways: role in airway smooth muscle migration and chemokine production.PloS one · 2012Article
- Functional expression of IgG-Fc receptors in human airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2011Article
- Is there a regulatory role of immunoglobulins on tissue forming cells relevant in chronic inflammatory lung diseases?Journal of allergy · 2011Article
- Article
- Research upregulation of CD23 (FcepsilonRII) expression in human airway smooth muscle cells (huASMC) in response to IL-4, GM-CSF, and IL-4/GM-CSF.Clinical and molecular allergy : CMA · 2005Article
- Endothelin-1 increases cholinergic nerve-mediated contraction of human bronchi via tachykinin synthesis induction.British journal of pharmacology · 2001Article
- Autocrine interaction between IL-5 and IL-1beta mediates altered responsiveness of atopic asthmatic sensitized airway smooth muscle.The Journal of clinical investigation · 1999Article
- Regulation of TH1- and TH2-type cytokine expression and action in atopic asthmatic sensitized airway smooth muscle.The Journal of clinical investigation · 1999Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
To elucidate the role of IgE-dependent mechanisms in inducing altered airway responsiveness in the atopic asthmatic state, the expression and actions of Fc receptor activation were examined in isolated rabbit tracheal smooth muscle (TSM) tissue and cultured cells passively sensitized with sera from atopic asthmatic patients or nonatopic/nonasthmatic (control) subjects. Relative to control tissues, the atopic asthmatic-sensitized TSM exhibited significantly increased maximal isometric contractility to acetylcholine (P < 0. 01) and attenuated maximal relaxation responses and sensitivity (i.e.,-log ED50) to isoproterenol (P < 0.005). These changes in agonist responsiveness in atopic sensitized TSM were ablated by pretreating the tissues with a blocking mAb to the low affinity receptor for IgE, FcepsilonRII (i.e., CD23) or by depleting the sensitizing serum of its immune complexes. Moreover, in complimentary experiments, exogenous administration of IgE immune complexes to naive TSM produced changes in agonist responsiveness that were qualitatively similar to those obtained in the atopic asthmatic-sensitized state. Extended studies further demonstrated that, in contrast to their respective controls, atopic asthmatic serum-sensitized human and rabbit TSM tissue and cultured cells exhibited markedly induced mRNA and cell surface expression of FcepsilonRII, whereas constitutive expression of the IgG receptor subtype, FcgammaRIII, was unaltered. Finally, the up-regulated mRNA expression of FcepsilonRII observed following exposure of TSM to atopic asthmatic serum or to exogenously administered IgE immune complexes was significantly inhibited by pretreating the tissues or cells with anti-CD23 mAb. Collectively, these observations provide evidence demonstrating that the altered agonist responsiveness in atopic asthmatic sensitized airway smooth muscle is largely attributed to IgE-mediated induction of the autologous expression and activation of FcepsilonRII receptors in the airway smooth muscle itself.
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