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

Ga Yeon Son, Aran Son, Yu Mi Yang, Wonse Park, Inik Chang, Jae Ho Lee, DongMin Shin

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

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 (IP 3 ) 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/IP 3 -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.

Original languageEnglish
Pages (from-to)138-143
Number of pages6
JournalArchives of Oral Biology
Volume61
DOIs
Publication statusPublished - 2016 Jan 1

Fingerprint

Blattellidae
PAR-2 Receptor
Allergens
Epithelium
Cytokines
Epithelial Cells
Interleukin-8
Interleukin-1
Interleukin-6
Type C Phospholipases
Endoplasmic Reticulum
Inflammation
Chronic Periodontitis
Thapsigargin
Calcium Signaling
Fura-2
Mouth Mucosa
Reverse Transcription
Adenosine Triphosphatases
Esters

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology
  • Dentistry(all)
  • Cell Biology

Cite this

Son, Ga Yeon ; Son, Aran ; Yang, Yu Mi ; Park, Wonse ; Chang, Inik ; Lee, Jae Ho ; Shin, DongMin. / Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium. In: Archives of Oral Biology. 2016 ; Vol. 61. pp. 138-143.
@article{b80e63b25c364749863269580a59b7e5,
title = "Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium",
abstract = "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 (IP 3 ) 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/IP 3 -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.",
author = "Son, {Ga Yeon} and Aran Son and Yang, {Yu Mi} and Wonse Park and Inik Chang and Lee, {Jae Ho} and DongMin Shin",
year = "2016",
month = "1",
day = "1",
doi = "10.1016/j.archoralbio.2015.10.015",
language = "English",
volume = "61",
pages = "138--143",
journal = "Archives of Oral Biology",
issn = "0003-9969",
publisher = "Elsevier Limited",

}

Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium. / Son, Ga Yeon; Son, Aran; Yang, Yu Mi; Park, Wonse; Chang, Inik; Lee, Jae Ho; Shin, DongMin.

In: Archives of Oral Biology, Vol. 61, 01.01.2016, p. 138-143.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium

AU - Son, Ga Yeon

AU - Son, Aran

AU - Yang, Yu Mi

AU - Park, Wonse

AU - Chang, Inik

AU - Lee, Jae Ho

AU - Shin, DongMin

PY - 2016/1/1

Y1 - 2016/1/1

N2 - 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 (IP 3 ) 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/IP 3 -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.

AB - 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 (IP 3 ) 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/IP 3 -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.

UR - http://www.scopus.com/inward/record.url?scp=84946600423&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84946600423&partnerID=8YFLogxK

U2 - 10.1016/j.archoralbio.2015.10.015

DO - 10.1016/j.archoralbio.2015.10.015

M3 - Article

VL - 61

SP - 138

EP - 143

JO - Archives of Oral Biology

JF - Archives of Oral Biology

SN - 0003-9969

ER -