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...

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Published in:PloS one 2015-05, Vol.10 (5), p.e0126058-e0126058
Main Authors: Segueni, Noria, Vigne, Solenne, Palmer, Gaby, Bourigault, Marie-Laure, Olleros, Maria L, Vesin, Dominique, Garcia, Irene, Ryffel, Bernhard, Quesniaux, Valérie F J, Gabay, Cem
Format: Article
Language:English
Subjects:
Animal models
Animals
Bacillus Calmette-Guerin vaccine
Bacteria
BCG
Cytokines
Dendritic cells
Disease
Gene expression
Hospitals
Host-Pathogen Interactions
Immune response
Immune system
Immunology
Infections
Interleukin 1
Interleukin 1 receptors
Interleukin-1 - metabolism
Interleukins
Internal medicine
Lungs
Lymphocytes
Lymphocytes T
Medical schools
Medicine
Mice
Mice, Inbred C57BL
Mice, Knockout
Mycobacterium bovis
Mycobacterium infections
Mycobacterium Infections - metabolism
Mycobacterium tuberculosis
Pathology
Physiological aspects
Psoriasis
Rheumatology
Rodents
Signaling
Tuberculosis
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factor-TNF
Tumor necrosis factor-α
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cited_by cdi_FETCH-LOGICAL-c692t-84ebb38cdfb02e21379bbad4de057fa6b81c8705f0aed254a9702fff955d3a623
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container_end_page e0126058
container_issue 5
container_start_page e0126058
container_title PloS one
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creator Segueni, Noria
Vigne, Solenne
Palmer, Gaby
Bourigault, Marie-Laure
Olleros, Maria L
Vesin, Dominique
Garcia, Irene
Ryffel, Bernhard
Quesniaux, Valérie F J
Gabay, Cem
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.
doi_str_mv 10.1371/journal.pone.0126058
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1932-6203
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source Publicly Available Content Database; PubMed Central
subjects Animal models
Animals
Bacillus Calmette-Guerin vaccine
Bacteria
BCG
Cytokines
Dendritic cells
Disease
Gene expression
Hospitals
Host-Pathogen Interactions
Immune response
Immune system
Immunology
Infections
Interleukin 1
Interleukin 1 receptors
Interleukin-1 - metabolism
Interleukins
Internal medicine
Lungs
Lymphocytes
Lymphocytes T
Medical schools
Medicine
Mice
Mice, Inbred C57BL
Mice, Knockout
Mycobacterium bovis
Mycobacterium infections
Mycobacterium Infections - metabolism
Mycobacterium tuberculosis
Pathology
Physiological aspects
Psoriasis
Rheumatology
Rodents
Signaling
Tuberculosis
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factor-TNF
Tumor necrosis factor-α
title Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection
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