Transient Receptor Potential Ankyrin 1 Channel Localized to Non-Neuronal Airway Cells Promotes Non-Neurogenic Inflammation
| Autor: | Camilla Fusi, Pierangelo Geppetti, Susan Stokesberry, Anna Rita Pisano, Nadia Moretto, Chiara Carnini, Naila Svitacheva, Fabrizio Facchinetti, Riccardo Patacchini, Arturo R. Viscomi, Pamela Pedretti, Lorcan McGarvey, Charlott Brunmark, Romina Nassini, Anders B. Damholt, Serena Materazzi |
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| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Transient receptor potential ankyrin 1 channel
non-neuronal airway cells non-neurogenic inflammation Pathology Anatomy and Physiology Pulmonology Chronic Obstructive Pulmonary Diseases Respiratory System lcsh:Medicine Substance P Biochemistry Ion Channels Transient receptor potential channel chemistry.chemical_compound Mice Transient Receptor Potential Channels lcsh:Science TRPA1 Cation Channel Neurogenic inflammation Multidisciplinary Smoking food and beverages respiratory system Immunohistochemistry medicine.anatomical_structure Medicine medicine.symptom Bronchoalveolar Lavage Fluid psychological phenomena and processes Sensory nerve Research Article medicine.medical_specialty Immunology TRPV1 TRPV Cation Channels Inflammation Mice Transgenic Nerve Tissue Proteins Biology Environmental and Occupational Lung Diseases medicine Animals Humans Interleukin 8 lcsh:R Interleukin-8 Immunity Proteins Smoking Related Disorders Epithelial Cells Muscle Smooth Fibroblasts Asthma respiratory tract diseases chemistry Gene Expression Regulation Capsaicin Cellular Neuroscience lcsh:Q Calcium Channels Neuroscience |
| Zdroj: | PLoS ONE PLoS ONE, Vol 7, Iss 8, p e42454 (2012) Nassini, R, Pedretti, P, Moretto, N, Fusi, C, Carnini, C, Facchinetti, F, Viscomi, A R, Pisano, A R, Stokesberry, S, Brunmark, C, Svitacheva, N, McGarvey, L, Patacchini, R, Damholt, A B, Geppetti, P & Materazzi, S 2012, ' Transient receptor potential ankyrin 1 channel localized to non-neuronal airway cells promotes non-neurogenic inflammation ', PLOS ONE, vol. 7, no. 8, e42454 . https://doi.org/10.1371/journal.pone.0042454 |
| ISSN: | 1932-6203 |
| Popis: | Background: The transient receptor potential ankyrin 1 (TRPA1) channel, localized to airway sensory nerves, has been proposed to mediate airway inflammation evoked by allergen and cigarette smoke (CS) in rodents, via a neurogenic mechanism. However the limited clinical evidence for the role of neurogenic inflammation in asthma or chronic obstructive pulmonary disease raises an alternative possibility that airway inflammation is promoted by non-neuronal TRPA1. Methodology/Principal Findings: By using Real-Time PCR and calcium imaging, we found that cultured human airway cells, including fibroblasts, epithelial and smooth muscle cells express functional TRPA1 channels. By using immunohistochemistry, TRPA1 staining was observed in airway epithelial and smooth muscle cells in sections taken from human airways and lung, and from airways and lung of wild-type, but not TRPA1-deficient mice. In cultured human airway epithelial and smooth muscle cells and fibroblasts, acrolein and CS extract evoked IL-8 release, a response selectively reduced by TRPA1 antagonists. Capsaicin, agonist of the transient receptor potential vanilloid 1 (TRPV1), a channel co-expressed with TRPA1 by airway sensory nerves, and acrolein or CS (TRPA1 agonists), or the neuropeptide substance P (SP), which is released from sensory nerve terminals by capsaicin, acrolein or CS), produced neurogenic inflammation in mouse airways. However, only acrolein and CS, but not capsaicin or SP, released the keratinocyte chemoattractant (CXCL-1/KC, IL-8 analogue) in bronchoalveolar lavage (BAL) fluid of wild-type mice. This effect of TRPA1 agonists was attenuated by TRPA1 antagonism or in TRPA1-deficient mice, but not by pharmacological ablation of sensory nerves. Conclusions: Our results demonstrate that, although either TRPV1 or TRPA1 activation causes airway neurogenic inflammation, solely TRPA1 activation orchestrates an additional inflammatory response which is not neurogenic. This finding suggests that non-neuronal TRPA1 in the airways is functional and potentially capable of contributing to inflammatory airway diseases. (Less) |
| Databáze: | OpenAIRE |
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