Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection

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dc.contributor.authorSegueni, Noriaen_ZA
dc.contributor.authorVigne, Solenneen_ZA
dc.contributor.authorPalmer, Gabyen_ZA
dc.contributor.authorBourigault, Marie-Laureen_ZA
dc.contributor.authorOlleros, Maria L.en_ZA
dc.contributor.authorVesin, Dominiqueen_ZA
dc.contributor.authorGarcia, Ireneen_ZA
dc.contributor.authorRyffel, Bernharden_ZA
dc.contributor.authorQuesniaux, Valérie F. J.en_ZA
dc.contributor.authorGabay, Cemen_ZA
dc.date.accessioned2015-11-09T13:21:31Z
dc.date.available2015-11-09T13:21:31Z
dc.date.issued2015en_ZA
dc.description.abstractIL-36 cytokines are members of the IL-1 family of cytokines that stimulate dendritic cells and T cells leading to enhanced T helper 1 responses in vitro and in vivo ; however, their role in host defense has not been fully addressed thus far. The objective of this study was to examine the role of IL-36R signaling in the control of mycobacterial infection, using models of systemic attenuated M . bovis BCG infection and virulent aerogenic M . tuberculosis infection. IL-36γ expression was increased in the lung of M . bovis BCG infected mice. However, IL-36R deficient mice infected with M . bovis BCG showed similar survival and control of the infection as compared to wild-type mice, although their lung pathology and CXCL1 response were transiently different. While highly susceptible TNF-α deficient mice succumbed with overwhelming M . tuberculosis infection, and IL-1RI deficient mice showed intermediate susceptibility, IL-36R-deficient mice controlled the infection, with bacterial burden, lung inflammation and pathology, similar to wild-type controls. Therefore, IL-36R signaling has only limited influence in the control of mycobacterial infection.en_ZA
dc.identifier.apacitationSegueni, N., Vigne, S., Palmer, G., Bourigault, M., Olleros, Maria L., Vesin, D., ... Gabay, C. (2015). Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. <i>PLoS One</i>, http://hdl.handle.net/11427/14788en_ZA
dc.identifier.chicagocitationSegueni, Noria, Solenne Vigne, Gaby Palmer, Marie-Laure Bourigault, Maria L. Olleros, Dominique Vesin, Irene Garcia, Bernhard Ryffel, Valérie F. J. Quesniaux, and Cem Gabay "Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection." <i>PLoS One</i> (2015) http://hdl.handle.net/11427/14788en_ZA
dc.identifier.citationSegueni, N., Vigne, S., Palmer, G., Bourigault, M. L., Olleros, M. L., Vesin, D., ... & Gabay, C. (2015). Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. PloS one, 10(5). doi:10.1371/journal.pone.0126058en_ZA
dc.identifier.ris TY - Journal Article AU - Segueni, Noria AU - Vigne, Solenne AU - Palmer, Gaby AU - Bourigault, Marie-Laure AU - Olleros, Maria L. AU - Vesin, Dominique AU - Garcia, Irene AU - Ryffel, Bernhard AU - Quesniaux, Valérie F. J. AU - Gabay, Cem AB - IL-36 cytokines are members of the IL-1 family of cytokines that stimulate dendritic cells and T cells leading to enhanced T helper 1 responses in vitro and in vivo ; however, their role in host defense has not been fully addressed thus far. The objective of this study was to examine the role of IL-36R signaling in the control of mycobacterial infection, using models of systemic attenuated M . bovis BCG infection and virulent aerogenic M . tuberculosis infection. IL-36γ expression was increased in the lung of M . bovis BCG infected mice. However, IL-36R deficient mice infected with M . bovis BCG showed similar survival and control of the infection as compared to wild-type mice, although their lung pathology and CXCL1 response were transiently different. While highly susceptible TNF-α deficient mice succumbed with overwhelming M . tuberculosis infection, and IL-1RI deficient mice showed intermediate susceptibility, IL-36R-deficient mice controlled the infection, with bacterial burden, lung inflammation and pathology, similar to wild-type controls. Therefore, IL-36R signaling has only limited influence in the control of mycobacterial infection. DA - 2015 DB - OpenUCT DO - 10.1371/journal.pone.0126058 DP - University of Cape Town J1 - PLoS One LK - https://open.uct.ac.za PB - University of Cape Town PY - 2015 T1 - Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection TI - Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection UR - http://hdl.handle.net/11427/14788 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/14788
dc.identifier.urihttp://dx.doi.org/10.1371/journal.pone.0126058
dc.identifier.vancouvercitationSegueni N, Vigne S, Palmer G, Bourigault M, Olleros Maria L, Vesin D, et al. Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. PLoS One. 2015; http://hdl.handle.net/11427/14788.en_ZA
dc.language.isoengen_ZA
dc.publisherPublic Library of Scienceen_ZA
dc.publisher.departmentDivision of Immunologyen_ZA
dc.publisher.facultyFaculty of Health Sciencesen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_ZA
dc.rights.holder© 2015 Segueni et alen_ZA
dc.rights.urihttp://creativecommons.org/licenses/by/4.0en_ZA
dc.sourcePLoS Oneen_ZA
dc.source.urihttp://journals.plos.org/plosoneen_ZA
dc.subject.otherMycobacterium tuberculosisen_ZA
dc.subject.otherMycobacterium bovisen_ZA
dc.subject.otherInflammationen_ZA
dc.subject.otherCytokinesen_ZA
dc.subject.otherT cellsen_ZA
dc.subject.otherMiceen_ZA
dc.subject.otherInfectious disease controlen_ZA
dc.subject.otherPsoriasisen_ZA
dc.titleLimited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infectionen_ZA
dc.typeJournal Articleen_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceArticleen_ZA
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