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Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammato...

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Autores principales: Son, Aran, Shin, Dong Min, Hong, Jeong Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Physiological Society and The Korean Society of Pharmacology 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297762/
https://www.ncbi.nlm.nih.gov/pubmed/25605997
http://dx.doi.org/10.4196/kjpp.2015.19.1.51
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author Son, Aran
Shin, Dong Min
Hong, Jeong Hee
author_facet Son, Aran
Shin, Dong Min
Hong, Jeong Hee
author_sort Son, Aran
collection PubMed
description The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of gram-positive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.
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spelling pubmed-42977622015-01-20 Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium Son, Aran Shin, Dong Min Hong, Jeong Hee Korean J Physiol Pharmacol Original Article The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of gram-positive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells. The Korean Physiological Society and The Korean Society of Pharmacology 2015-01 2014-12-31 /pmc/articles/PMC4297762/ /pubmed/25605997 http://dx.doi.org/10.4196/kjpp.2015.19.1.51 Text en Copyright © 2015 The Korean Physiological Society and The Korean Society of Pharmacology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Son, Aran
Shin, Dong Min
Hong, Jeong Hee
Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title_full Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title_fullStr Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title_full_unstemmed Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title_short Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
title_sort peptidoglycan induces the production of interleukin-8 via calcium signaling in human gingival epithelium
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297762/
https://www.ncbi.nlm.nih.gov/pubmed/25605997
http://dx.doi.org/10.4196/kjpp.2015.19.1.51
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