Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection.
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-3...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2015-01-01
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| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0126058 |
| _version_ | 1818725242350075904 |
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| author | Noria Segueni Solenne Vigne Gaby Palmer Marie-Laure Bourigault Maria L Olleros Dominique Vesin Irene Garcia Bernhard Ryffel Valérie F J Quesniaux Cem Gabay |
| author_facet | Noria Segueni Solenne Vigne Gaby Palmer Marie-Laure Bourigault Maria L Olleros Dominique Vesin Irene Garcia Bernhard Ryffel Valérie F J Quesniaux Cem Gabay |
| author_sort | Noria Segueni |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-17T21:39:12Z |
| format | Article |
| id | doaj.art-e359e0440cd5423284a6e29002d4342f |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-17T21:39:12Z |
| publishDate | 2015-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-e359e0440cd5423284a6e29002d4342f2022-12-21T21:31:40ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01105e012605810.1371/journal.pone.0126058Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection.Noria SegueniSolenne VigneGaby PalmerMarie-Laure BourigaultMaria L OllerosDominique VesinIrene GarciaBernhard RyffelValérie F J QuesniauxCem GabayIL-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.https://doi.org/10.1371/journal.pone.0126058 |
| spellingShingle | Noria Segueni Solenne Vigne Gaby Palmer Marie-Laure Bourigault Maria L Olleros Dominique Vesin Irene Garcia Bernhard Ryffel Valérie F J Quesniaux Cem Gabay Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. PLoS ONE |
| title | Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. |
| title_full | Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. |
| title_fullStr | Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. |
| title_full_unstemmed | Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. |
| title_short | Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. |
| title_sort | limited contribution of il 36 versus il 1 and tnf pathways in host response to mycobacterial infection |
| url | https://doi.org/10.1371/journal.pone.0126058 |
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