TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.

Members of the mammalian nucleotide binding domain, leucine-rich repeat (LRR)-containing receptor family of proteins are key modulators of innate immunity regulating inflammation. To date, microbial pathogen-associated molecules and toxins have been identified as key triggers of activation of inflam...

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Autores principales:	Susana Álvarez, Ma Ángeles Muñoz-Fernández
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b7d4965c5a0f413a9ac01cbfd823be8c
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spelling	oai:doaj.org-article:b7d4965c5a0f413a9ac01cbfd823be8c2021-11-18T09:00:53ZTNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.1932-620310.1371/journal.pone.0071477https://doaj.org/article/b7d4965c5a0f413a9ac01cbfd823be8c2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23940760/?tool=EBIhttps://doaj.org/toc/1932-6203Members of the mammalian nucleotide binding domain, leucine-rich repeat (LRR)-containing receptor family of proteins are key modulators of innate immunity regulating inflammation. To date, microbial pathogen-associated molecules and toxins have been identified as key triggers of activation of inflammasomes. However, recently, environmental, and neurodegenerative stimuli have been identified that lead to IL-1β release by means of inflammasomes. IL-1β plays a crucial role during brain inflammation, and caspase-1 appears to be a key modulator of IL-1β bioactivity and the consequent transcriptional regulation of gene expression within the brain during inflammation. We show here that exposure of a human neuroblastoma cell line (SK-N-MC cells) to TNF-α promotes ROS-mediated caspase-1 activation and IL-1β secretion. The involvement of NF-κB in the regulation of IL-1β synthesis is investigated through specific inhibition of this transcription factor. The effect of TNF-α was abolished in the presence of ROS inhibitors as NAC, or DPI. Remarkably, SK-N-MC cells do not respond to ATP stimulation in spite of P2X7R expression. These results provide a mechanism by which danger signals and particulate matter mediate inflammation via the inflammasome in the absence of microbial infection.Susana ÁlvarezMa Ángeles Muñoz-FernándezPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e71477 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Susana Álvarez Ma Ángeles Muñoz-Fernández TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
description	Members of the mammalian nucleotide binding domain, leucine-rich repeat (LRR)-containing receptor family of proteins are key modulators of innate immunity regulating inflammation. To date, microbial pathogen-associated molecules and toxins have been identified as key triggers of activation of inflammasomes. However, recently, environmental, and neurodegenerative stimuli have been identified that lead to IL-1β release by means of inflammasomes. IL-1β plays a crucial role during brain inflammation, and caspase-1 appears to be a key modulator of IL-1β bioactivity and the consequent transcriptional regulation of gene expression within the brain during inflammation. We show here that exposure of a human neuroblastoma cell line (SK-N-MC cells) to TNF-α promotes ROS-mediated caspase-1 activation and IL-1β secretion. The involvement of NF-κB in the regulation of IL-1β synthesis is investigated through specific inhibition of this transcription factor. The effect of TNF-α was abolished in the presence of ROS inhibitors as NAC, or DPI. Remarkably, SK-N-MC cells do not respond to ATP stimulation in spite of P2X7R expression. These results provide a mechanism by which danger signals and particulate matter mediate inflammation via the inflammasome in the absence of microbial infection.
format	article
author	Susana Álvarez Ma Ángeles Muñoz-Fernández
author_facet	Susana Álvarez Ma Ángeles Muñoz-Fernández
author_sort	Susana Álvarez
title	TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
title_short	TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
title_full	TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
title_fullStr	TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
title_full_unstemmed	TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
title_sort	tnf-α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/b7d4965c5a0f413a9ac01cbfd823be8c
work_keys_str_mv	AT susanaalvarez tnfamaymediateinflammasomeactivationintheabsenceofbacterialinfectioninmorethanoneway AT maangelesmunozfernandez tnfamaymediateinflammasomeactivationintheabsenceofbacterialinfectioninmorethanoneway
_version_	1718421045176696832

TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.

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