Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.

<h4>Purpose</h4>To characterize the effects of benzalkonium chloride (BAK) in THP-1 differentiated cells in vitro.<h4>Methods</h4>Macrophages were obtained after differentiation of THP-1 cells, a human monocytic leukemia cell line. Macrophages were exposed for 24 h to 33 nM (...

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Autores principales:	Sylvain Michée, Françoise Brignole-Baudouin, Luisa Riancho, William Rostene, Christophe Baudouin, Antoine Labbé
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3a806f464216409980ba32b60a573f3e
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spelling	oai:doaj.org-article:3a806f464216409980ba32b60a573f3e2021-11-18T08:58:52ZEffects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.1932-620310.1371/journal.pone.0072459https://doaj.org/article/3a806f464216409980ba32b60a573f3e2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23991114/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Purpose</h4>To characterize the effects of benzalkonium chloride (BAK) in THP-1 differentiated cells in vitro.<h4>Methods</h4>Macrophages were obtained after differentiation of THP-1 cells, a human monocytic leukemia cell line. Macrophages were exposed for 24 h to 33 nM (10(-5)%) benzalkonium chloride (BAK), 10 nM dinitrochlorobenzene (DNCB), 100 ng/mL lipopolysaccharide (LPS), 5 ng/mL tumor necrosis factor alpha (TNF-α) or phosphate buffered saline (PBS) as controls. The expression of CD11b, CD11c, CD33 and CD54 was evaluated using immunohistochemistry and flow cytometry (FCM). Phagocytosis function was analyzed using carboxylate-modified fluorescent microspheres and quantified by FCM. Migration was evaluated in cocultures with conjunctival epithelial cells. Cytokine production was detected and quantified in culture supernatants using a human cytokine array.<h4>Results</h4>Stimulation of THP-1-derived macrophages with a low concentration of BAK increased CD11b and CD11c expression and decreased CD33. Macrophages exposed to BAK, LPS and TNF-α had increased phagocytosis. In contrast to LPS, BAK and TNF-α increased macrophage migration. Cytokines in supernatants of macrophages exposed to BAK revealed an increased release of CCL1, CCL4/MIP-1β, TNF-α, soluble CD54/ICAM-1 and IL-1β.<h4>Conclusion</h4>In vitro, BAK has a direct stimulating effect on macrophages, increasing phagocytosis, cytokine release, migration and expression of CD11b and CD11c. Long-term exposure to low concentrations of BAK should be considered as a stimulating factor responsible for inflammation through macrophage activation.Sylvain MichéeFrançoise Brignole-BaudouinLuisa RianchoWilliam RosteneChristophe BaudouinAntoine LabbéPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e72459 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sylvain Michée Françoise Brignole-Baudouin Luisa Riancho William Rostene Christophe Baudouin Antoine Labbé Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
description	<h4>Purpose</h4>To characterize the effects of benzalkonium chloride (BAK) in THP-1 differentiated cells in vitro.<h4>Methods</h4>Macrophages were obtained after differentiation of THP-1 cells, a human monocytic leukemia cell line. Macrophages were exposed for 24 h to 33 nM (10(-5)%) benzalkonium chloride (BAK), 10 nM dinitrochlorobenzene (DNCB), 100 ng/mL lipopolysaccharide (LPS), 5 ng/mL tumor necrosis factor alpha (TNF-α) or phosphate buffered saline (PBS) as controls. The expression of CD11b, CD11c, CD33 and CD54 was evaluated using immunohistochemistry and flow cytometry (FCM). Phagocytosis function was analyzed using carboxylate-modified fluorescent microspheres and quantified by FCM. Migration was evaluated in cocultures with conjunctival epithelial cells. Cytokine production was detected and quantified in culture supernatants using a human cytokine array.<h4>Results</h4>Stimulation of THP-1-derived macrophages with a low concentration of BAK increased CD11b and CD11c expression and decreased CD33. Macrophages exposed to BAK, LPS and TNF-α had increased phagocytosis. In contrast to LPS, BAK and TNF-α increased macrophage migration. Cytokines in supernatants of macrophages exposed to BAK revealed an increased release of CCL1, CCL4/MIP-1β, TNF-α, soluble CD54/ICAM-1 and IL-1β.<h4>Conclusion</h4>In vitro, BAK has a direct stimulating effect on macrophages, increasing phagocytosis, cytokine release, migration and expression of CD11b and CD11c. Long-term exposure to low concentrations of BAK should be considered as a stimulating factor responsible for inflammation through macrophage activation.
format	article
author	Sylvain Michée Françoise Brignole-Baudouin Luisa Riancho William Rostene Christophe Baudouin Antoine Labbé
author_facet	Sylvain Michée Françoise Brignole-Baudouin Luisa Riancho William Rostene Christophe Baudouin Antoine Labbé
author_sort	Sylvain Michée
title	Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
title_short	Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
title_full	Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
title_fullStr	Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
title_full_unstemmed	Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.
title_sort	effects of benzalkonium chloride on thp-1 differentiated macrophages in vitro.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/3a806f464216409980ba32b60a573f3e
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_version_	1718421074966740992

Effects of benzalkonium chloride on THP-1 differentiated macrophages in vitro.

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