ArticlePloS one2009
Proinflammatory and Th2 cytokines regulate the high affinity IgE receptor (FcepsilonRI) and IgE-dependant activation of human airway smooth muscle cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Basophil FCER1A and PTAFR Gene Expression Profiles Correlate With Disease Severity in Chronic Spontaneous Urticaria.Clinical and translational allergy · 2026Article
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Article
- An Update on Anti-IgE Therapy in Pediatric Respiratory Diseases.Current respiratory medicine reviews · 2017Review
- Inhibition of spleen tyrosine kinase attenuates IgE-mediated airway contraction and mediator release in human precision cut lung slices.British journal of pharmacology · 2016Article
- The impact of vitamin D on asthmatic human airway smooth muscle.Expert review of respiratory medicine · 2016Article
- Effects of phthalate exposure on asthma may be mediated through alterations in DNA methylation.Clinical epigenetics · 2015Article
- Article
- IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2013Article
- Pentraxin 3 (PTX3) expression in allergic asthmatic airways: role in airway smooth muscle migration and chemokine production.PloS one · 2012Article
- Targeting airway smooth muscle in airways diseases: an old concept with new twists.Expert review of respiratory medicine · 2011Review
- Functional expression of IgG-Fc receptors in human airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2011Article
- Does airway smooth muscle express an inflammatory phenotype in asthma?British journal of pharmacology · 2011Review
- Direct evidence for functional smooth muscle myosin II in the 10S self-inhibited monomeric conformation in airway smooth muscle cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Is there a regulatory role of immunoglobulins on tissue forming cells relevant in chronic inflammatory lung diseases?Journal of allergy · 2011Article
- Th2 but not Th1 immune bias results in altered lung functions in a murine model of pulmonary Cryptococcus neoformans infection.Infection and immunity · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundThe high affinity IgE receptor (FcepsilonRI) is a crucial structure for IgE-mediated allergic reactions. We have previously demonstrated that human airway smooth muscle (ASM) cells express the tetrameric (alphabetagamma2) FcepsilonRI, and its activation leads to marked transient increases in intracellular Ca(2+) concentration, release of Th-2 cytokines and eotaxin-1/CCL11. Therefore, it was of utmost importance to delineate the factors regulating the expression of FcepsilonRI in human (ASM) cells. METHODOLOGY/PRINCIPAL
findingsIncubation of human bronchial and tracheal smooth muscle (B/TSM) cells with TNF-alpha, IL-1beta or IL-4 resulted in a significant increase in FcepsilonRI-alpha chain mRNA expression (p<0.05); and TNF-alpha, IL-4 enhanced the FcepsilonRI-alpha protein expression compared to the unstimulated control at 24, 72 hrs after stimulation. Interestingly, among all other cytokines, only TNF-alpha upregulated the FcepsilonRI-gamma mRNA expression. FcepsilonRI-gamma protein expression remained unchanged despite the nature of stimulation. Of note, as a functional consequence of FcepsilonRI upregulation, TNF-alpha pre-sensitization of B/TSM potentially augmented the CC (eotaxin-1/CCL11 and RANTES/CCL5, but not TARC/CCL17) and CXC (IL-8/CXCL8, IP-10/CXCL10) chemokines release following IgE stimulation (p<0.05, n = 3). Furthermore, IgE sensitization of B/TSM cells significantly enhanced the transcription of selective CC and CXC chemokines at promoter level compared to control, which was abolished by Lentivirus-mediated silencing of Syk expression. CONCLUSIONS/SIGNIFICANCE: Our data depict a critical role of B/TSM in allergic airway inflammation via potentially novel mechanisms involving proinflammatory, Th2 cytokines and IgE/FcepsilonRI complex.
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