Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection
| Autor: | Bernhard Ryffel, Gaby Palmer, Dominique Vesin, Marie-Laure Bourigault, Irene Garcia, Solenne Vigne, Cem Gabay, Valérie F. J. Quesniaux, Noria Segueni, Maria L. Olleros |
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| Přispěvatelé: | Division of Immunology, Faculty of Health Sciences |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Tuberculosis
Science T cells Inflammation ddc:616.07 Biology Mycobacterium tuberculosis Mice In vivo Infectious disease control medicine Animals Psoriasis ddc:616 Tumor Necrosis Factor-alpha/metabolism Mice Knockout Mycobacterium bovis Mycobacterium Infections Multidisciplinary Tumor Necrosis Factor-alpha Interleukin biology.organism_classification medicine.disease 3. Good health CXCL1 Mice Inbred C57BL Immunology Host-Pathogen Interactions Cytokines Medicine Tumor necrosis factor alpha Mycobacterium Infections/metabolism Interleukin-1/metabolism medicine.symptom Interleukin-1 Research Article |
| Zdroj: | PLoS ONE, Vol 10, Iss 5, p e0126058 (2015) PLoS One PLoS ONE PLosone PloS one PLOS ONE, Vol. 10, No 5 (2015) P. e0126058 |
| ISSN: | 1932-6203 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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