IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.

Salmonella enterica subspecies 1 serovar Typhimurium (S. Typhimurium) causes diarrhea and acute inflammation of the intestinal mucosa. The pro-inflammatory cytokines IL-17A and IL-17F are strongly induced in the infected mucosa but their contribution in driving the tissue inflammation is not underst...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Pascal Songhet, Manja Barthel, Till A Röhn, Laurye Van Maele, Delphine Cayet, Jean-Claude Sirard, Martin Bachmann, Manfred Kopf, Wolf-Dietrich Hardt
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/40b58373429a4828a167a5798ac77528
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:40b58373429a4828a167a5798ac77528
record_format	dspace
spelling	oai:doaj.org-article:40b58373429a4828a167a5798ac775282021-11-18T07:36:35ZIL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.1932-620310.1371/journal.pone.0013804https://doaj.org/article/40b58373429a4828a167a5798ac775282010-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21124903/?tool=EBIhttps://doaj.org/toc/1932-6203Salmonella enterica subspecies 1 serovar Typhimurium (S. Typhimurium) causes diarrhea and acute inflammation of the intestinal mucosa. The pro-inflammatory cytokines IL-17A and IL-17F are strongly induced in the infected mucosa but their contribution in driving the tissue inflammation is not understood. We have used the streptomycin mouse model to analyze the role of IL-17A and IL-17F and their cognate receptor IL-17RA in S. Typhimurium enterocolitis. Neutralization of IL-17A and IL-17F did not affect mucosal inflammation triggered by infection or spread of S. Typhimurium to systemic sites by 48 h p.i. Similarly, Il17ra(-/-) mice did not display any reduction in infection or inflammation by 12 h p.i. The same results were obtained using S. Typhimurium variants infecting via the TTSS1 type III secretion system, the TTSS1 effector SipA or the TTSS1 effector SopE. Moreover, the expression pattern of 45 genes encoding chemokines/cytokines (including CXCL1, CXCL2, IL-17A, IL-17F, IL-1α, IL-1β, IFNγ, CXCL-10, CXCL-9, IL-6, CCL3, CCL4) and antibacterial molecules was not affected by Il17ra deficiency by 12 h p.i. Thus, in spite of the strong increase in Il17a/Il17f mRNA in the infected mucosa, IL-17RA signaling seems to be dispensable for eliciting the acute disease. Future work will have to address whether this is attributable to redundancy in the cytokine signaling network.Pascal SonghetManja BarthelTill A RöhnLaurye Van MaeleDelphine CayetJean-Claude SirardMartin BachmannManfred KopfWolf-Dietrich HardtPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 11, p e13804 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pascal Songhet Manja Barthel Till A Röhn Laurye Van Maele Delphine Cayet Jean-Claude Sirard Martin Bachmann Manfred Kopf Wolf-Dietrich Hardt IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
description	Salmonella enterica subspecies 1 serovar Typhimurium (S. Typhimurium) causes diarrhea and acute inflammation of the intestinal mucosa. The pro-inflammatory cytokines IL-17A and IL-17F are strongly induced in the infected mucosa but their contribution in driving the tissue inflammation is not understood. We have used the streptomycin mouse model to analyze the role of IL-17A and IL-17F and their cognate receptor IL-17RA in S. Typhimurium enterocolitis. Neutralization of IL-17A and IL-17F did not affect mucosal inflammation triggered by infection or spread of S. Typhimurium to systemic sites by 48 h p.i. Similarly, Il17ra(-/-) mice did not display any reduction in infection or inflammation by 12 h p.i. The same results were obtained using S. Typhimurium variants infecting via the TTSS1 type III secretion system, the TTSS1 effector SipA or the TTSS1 effector SopE. Moreover, the expression pattern of 45 genes encoding chemokines/cytokines (including CXCL1, CXCL2, IL-17A, IL-17F, IL-1α, IL-1β, IFNγ, CXCL-10, CXCL-9, IL-6, CCL3, CCL4) and antibacterial molecules was not affected by Il17ra deficiency by 12 h p.i. Thus, in spite of the strong increase in Il17a/Il17f mRNA in the infected mucosa, IL-17RA signaling seems to be dispensable for eliciting the acute disease. Future work will have to address whether this is attributable to redundancy in the cytokine signaling network.
format	article
author	Pascal Songhet Manja Barthel Till A Röhn Laurye Van Maele Delphine Cayet Jean-Claude Sirard Martin Bachmann Manfred Kopf Wolf-Dietrich Hardt
author_facet	Pascal Songhet Manja Barthel Till A Röhn Laurye Van Maele Delphine Cayet Jean-Claude Sirard Martin Bachmann Manfred Kopf Wolf-Dietrich Hardt
author_sort	Pascal Songhet
title	IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
title_short	IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
title_full	IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
title_fullStr	IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
title_full_unstemmed	IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.
title_sort	il-17a/f-signaling does not contribute to the initial phase of mucosal inflammation triggered by s. typhimurium.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/40b58373429a4828a167a5798ac77528
work_keys_str_mv	AT pascalsonghet il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT manjabarthel il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT tillarohn il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT lauryevanmaele il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT delphinecayet il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT jeanclaudesirard il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT martinbachmann il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT manfredkopf il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium AT wolfdietrichhardt il17afsignalingdoesnotcontributetotheinitialphaseofmucosalinflammationtriggeredbystyphimurium
_version_	1718423218017009664

IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium.

Ejemplares similares