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Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium

 Ga-Yeon Sona  ;  Aran Son  ;  Yu-Mi Yang  ;  Wonse Park  ;  Inik Chang  ;  Jae-Ho Lee  ;  Dong Min Shin 
 Archives of Oral Biology, Vol.61(1) : 138-143, 2016 
Journal Title
 Archives of Oral Biology 
Issue Date
Adolescent ; Adult ; Allergens/immunology* ; Animals ; Boron Compounds/pharmacology ; Calcium/metabolism ; Cockroaches/immunology* ; Cytokines/metabolism* ; Epithelial Cells/immunology* ; Estrenes/pharmacology ; Female ; Fura-2 ; Gingiva/cytology ; Gingiva/immunology* ; Humans ; Inhalation Exposure ; Male ; Pyrrolidinones/pharmacology ; Receptor, PAR-2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Thapsigargin/pharmacology
Allergens ; Calcium ; Gingival epithelial cells ; Inflammation ; PAR-2
OBJECTIVE: In 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. DESIGN: HGECs isolated from healthy donors were stimulated with GCE. Intracellular Ca(2+) concentration ([Ca(2+)]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). RESULTS: GCE promoted increase in the [Ca(2+)]i in a dose-dependent manner. Depletion of endoplasmic reticulum (ER) Ca(2+) by the ER Ca(2+) ATPase inhibitor thapsigargin (Tg) but not the depletion of extracellular Ca(2+) abolished the GCE-induced increase in [Ca(2+)]i. Treatment of phospholipase C (PLC) inhibitor (U73122) or 1,4,5-trisinositolphosphate (IP3) receptor inhibitor (2-APB) also prevented GCE-induced increase in [Ca(2+)]i. Protease activated receptor (PAR)-2 activation mainly mediated the GCE-induced increase in [Ca(2+)]i and enhanced the expression of IL-8, NLRP3, IL-1β, and IL-6 in HGECs. CONCLUSIONS: GCE activates PAR-2, which can induce PLC/IP3-dependent Ca(2+) 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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2. College of Dentistry (치과대학) > Dept. of Advanced General Dentistry (통합치의학과) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Pediatric Dentistry (소아치과학교실) > 1. Journal Papers
Yonsei Authors
박원서(Park, Wonse) ORCID logo https://orcid.org/0000-0002-2081-1156
신동민(Shin, Dong Min) ORCID logo https://orcid.org/0000-0001-6042-0435
이제호(Lee, Jae Ho) ORCID logo https://orcid.org/0000-0002-1556-3485
장인익(Chang, In Ik)
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