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 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). Results GCE 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. Conclusions GCE 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.
All Science Journal Classification (ASJC) codes
- Cell Biology