The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.

Humans inhale hundreds of Aspergillus conidia without adverse consequences. Powerful protective mechanisms may ensure prompt control of the pathogen and inflammation. Here we reveal a previously unknown mechanism by which the danger molecule S100B integrates pathogen- and danger-sensing pathways to...

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Autores principales:	Guglielmo Sorci, Gloria Giovannini, Francesca Riuzzi, Pierluigi Bonifazi, Teresa Zelante, Silvia Zagarella, Francesco Bistoni, Rosario Donato, Luigina Romani
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/17d27567bec24af39fe09f81ab17676f
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spelling	oai:doaj.org-article:17d27567bec24af39fe09f81ab17676f2021-11-18T06:03:32ZThe danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.1553-73661553-737410.1371/journal.ppat.1001315https://doaj.org/article/17d27567bec24af39fe09f81ab17676f2011-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21423669/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Humans inhale hundreds of Aspergillus conidia without adverse consequences. Powerful protective mechanisms may ensure prompt control of the pathogen and inflammation. Here we reveal a previously unknown mechanism by which the danger molecule S100B integrates pathogen- and danger-sensing pathways to restrain inflammation. Upon forming complexes with TLR2 ligands, S100B inhibited TLR2 via RAGE, through a paracrine epithelial cells/neutrophil circuit that restrained pathogen-induced inflammation. However, upon binding to nucleic acids, S100B activated intracellular TLRs eventually resolve danger-induced inflammation via transcriptional inhibition of S100B. Thus, the spatiotemporal regulation of TLRs and RAGE by S100B provides evidence for an evolving braking circuit in infection whereby an endogenous danger protects against pathogen-induced inflammation and a pathogen-sensing mechanism resolves danger-induced inflammation.Guglielmo SorciGloria GiovanniniFrancesca RiuzziPierluigi BonifaziTeresa ZelanteSilvia ZagarellaFrancesco BistoniRosario DonatoLuigina RomaniPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 3, p e1001315 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Guglielmo Sorci Gloria Giovannini Francesca Riuzzi Pierluigi Bonifazi Teresa Zelante Silvia Zagarella Francesco Bistoni Rosario Donato Luigina Romani The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
description	Humans inhale hundreds of Aspergillus conidia without adverse consequences. Powerful protective mechanisms may ensure prompt control of the pathogen and inflammation. Here we reveal a previously unknown mechanism by which the danger molecule S100B integrates pathogen- and danger-sensing pathways to restrain inflammation. Upon forming complexes with TLR2 ligands, S100B inhibited TLR2 via RAGE, through a paracrine epithelial cells/neutrophil circuit that restrained pathogen-induced inflammation. However, upon binding to nucleic acids, S100B activated intracellular TLRs eventually resolve danger-induced inflammation via transcriptional inhibition of S100B. Thus, the spatiotemporal regulation of TLRs and RAGE by S100B provides evidence for an evolving braking circuit in infection whereby an endogenous danger protects against pathogen-induced inflammation and a pathogen-sensing mechanism resolves danger-induced inflammation.
format	article
author	Guglielmo Sorci Gloria Giovannini Francesca Riuzzi Pierluigi Bonifazi Teresa Zelante Silvia Zagarella Francesco Bistoni Rosario Donato Luigina Romani
author_facet	Guglielmo Sorci Gloria Giovannini Francesca Riuzzi Pierluigi Bonifazi Teresa Zelante Silvia Zagarella Francesco Bistoni Rosario Donato Luigina Romani
author_sort	Guglielmo Sorci
title	The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
title_short	The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
title_full	The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
title_fullStr	The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
title_full_unstemmed	The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.
title_sort	danger signal s100b integrates pathogen- and danger-sensing pathways to restrain inflammation.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/17d27567bec24af39fe09f81ab17676f
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The danger signal S100B integrates pathogen- and danger-sensing pathways to restrain inflammation.

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