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

 

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dc.contributor.author Segueni, Noria en_ZA
dc.contributor.author Vigne, Solenne en_ZA
dc.contributor.author Palmer, Gaby en_ZA
dc.contributor.author Bourigault, Marie-Laure en_ZA
dc.contributor.author Olleros, Maria L. en_ZA
dc.contributor.author Vesin, Dominique en_ZA
dc.contributor.author Garcia, Irene en_ZA
dc.contributor.author Ryffel, Bernhard en_ZA
dc.contributor.author Quesniaux, Valérie F. J. en_ZA
dc.contributor.author Gabay, Cem en_ZA
dc.date.accessioned 2015-11-09T13:21:31Z
dc.date.available 2015-11-09T13:21:31Z
dc.date.issued 2015 en_ZA
dc.identifier.citation Segueni, 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.0126058 en_ZA
dc.identifier.uri http://hdl.handle.net/11427/14788
dc.identifier.uri http://dx.doi.org/10.1371/journal.pone.0126058
dc.description.abstract 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. en_ZA
dc.language.iso eng en_ZA
dc.publisher Public Library of Science en_ZA
dc.rights This 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.uri http://creativecommons.org/licenses/by/4.0 en_ZA
dc.source PLoS One en_ZA
dc.source.uri http://journals.plos.org/plosone en_ZA
dc.subject.other Mycobacterium tuberculosis en_ZA
dc.subject.other Mycobacterium bovis en_ZA
dc.subject.other Inflammation en_ZA
dc.subject.other Cytokines en_ZA
dc.subject.other T cells en_ZA
dc.subject.other Mice en_ZA
dc.subject.other Infectious disease control en_ZA
dc.subject.other Psoriasis en_ZA
dc.title Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection en_ZA
dc.type Journal Article en_ZA
dc.rights.holder © 2015 Segueni et al en_ZA
uct.type.publication Research en_ZA
uct.type.resource Article en_ZA
dc.publisher.institution University of Cape Town
dc.publisher.faculty Faculty of Health Sciences en_ZA
dc.publisher.department Division of Immunology en_ZA
uct.type.filetype Text
uct.type.filetype Image
dc.identifier.apacitation Segueni, 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/11427/14788 en_ZA
dc.identifier.chicagocitation Segueni, 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/11427/14788 en_ZA
dc.identifier.vancouvercitation Segueni 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.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


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This 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. Except where otherwise noted, this item's license is described as This 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.