Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium |
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| Affiliation: | 1. Department of Oral Biology, Yonsei University College of Dentistry, Seoul, Republic of Korea;2. BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Republic of Korea;3. Department of Advanced General Dentistry, Yonsei University College of Dentistry, Seoul, Republic of Korea;4. Department of Pediatric Dentistry, Yonsei University College of Dentistry, Seoul, Republic of Korea;1. Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Belmeloro, 8, 40126 Bologna, Italy;2. Medical Genetics Laboratory, Alzahra University Hospital, Isfahan University of Medical Sciences, 81745-319 Isfahan, Iran;3. Plastic Surgery Unit, Sant’Orsola Malpighi University Hospital, Via Massarenti, 9, 40138 Bologna, Italy;4. Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Via Luigi Borsari, 46, 44121 Ferrara, Italy;5. Department of Genetics and Molecular Biology, Medical School, Isfahan University of Medical Sciences, 81745-319 Isfahan, Iran;1. Faculty of Sciences and Technology, State University of São Paulo, Unesp, Presidente Prudente, SP, Brazil;2. São Carlos Institute of Physics, University of São Paulo, São Carlos, SP, Brazil;1. Research Programme on Biomedical Informatics (GRIB), Hospital Del Mar Medical Research Institute (IMIM)—Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), 08003 Barcelona, Spain;2. InterAx Biotech AG, PARK InnovAARE, 5234 Villigen, Switzerland;3. Faculty of Chemistry, Biological and Chemical Research Centre, University of Warsaw, 02-093 Warsaw, Poland;4. Department of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark;1. Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases, Bethesda, Md;2. Rho Federal Systems Division, Chapel Hill, MC;3. Division of Allergy and Immunology, Johns Hopkins University School of Medicine, Baltimore, Md;4. Department of Pediatrics, Boston University School of Medicine, Boston, Mass;5. Division of Allergy and Immunology, Ann and Robert H. Lurie Children''s Hospital of Chicago, Chicago, Ill;6. Division of Asthma Research and Division of Pulmonary Medicine, Cincinnati Children''s Hospital, Cincinnati, Ohio;7. University of Texas Southwestern Medical Center, Dallas, Tex;8. Division of Allergy and Immunology, National Jewish Health, Denver, and the Department of Allergy and Immunology, Children''s Hospital Colorado and University of Colorado School of Medicine, Aurora, Colo;9. Division of Allergy and Immunology, Henry Ford Health System, Detroit, Mich;10. Department of Pediatrics, College of Physicians and Surgeons, New York, NY;11. Division of Allergy, Immunology, and Pulmonary Medicine, St Louis Children''s Hospital, St Louis, Mo;12. Department of Pulmonary Medicine, Children''s National Health System, Washington, DC;13. Division of Allergy and Immunology, University of Wisconsin School of Medicine and Public Health, Madison, Wis;1. Department of Urology, The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Second Chinese Medicine Hospital, Nanjing, China;2. Department of Urology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China |
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| Abstract: | ObjectiveIn reaching the airways inhaled allergens pass through and contact with the oral mucosa. Although they are often responsible for initiating asthmatic attacks, it is unknown whether airborne allergens can also trigger chronic inflammation of gingival epithelial cells leading to chronic periodontitis. In this study, we investigated the inflammatory responses of human gingival epithelial cells (HGECs) to airborne allergens, particularly German cockroach extract (GCE) with a focus on calcium signaling.DesignHGECs isolated from healthy donors were stimulated with GCE. Intracellular Ca2+ concentration ([Ca2+]i) was measured with Fura-2-acetoxymethyl ester (Fura-2/AM) staining. Expression of inflammatory cytokines interleukin (IL)-8, IL-1β, IL-6, and NOD-like receptor family, pyridine domain-containing (NLRP) 3 was analyzed using reverse transcription-polymerase chain reaction (RT-PCR).ResultsGCE promoted increase in the [Ca2+]i in a dose-dependent manner. Depletion of endoplasmic reticulum (ER) Ca2+ by the ER Ca2+ ATPase inhibitor thapsigargin (Tg) but not the depletion of extracellular Ca2+ abolished the GCE-induced increase in [Ca2+]i. Treatment of phospholipase C (PLC) inhibitor (U73122) or 1,4,5-trisinositolphosphate (IP3) receptor inhibitor (2-APB) also prevented GCE-induced increase in [Ca2+]i. Protease activated receptor (PAR)-2 activation mainly mediated the GCE-induced increase in [Ca2+]i and enhanced the expression of IL-8, NLRP3, IL-1β, and IL-6 in HGECs.ConclusionsGCE activates PAR-2, which can induce PLC/IP3-dependent Ca2+ signaling pathway, ultimately triggering inflammation via the production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-8, and NLRP 3 in HGECs. |
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| Keywords: | Calcium Allergens Gingival epithelial cells Inflammation PAR-2 |
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