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

Segueni, Noria
Bourigault, Marie-Laure
Olleros, Maria L
Vesin, Dominique
Ryffel, Bernhard
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Published in PLOS ONE. 2015, vol. 10, no. 5, p. e0126058
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.
Keywords AnimalsHost-Pathogen InteractionsInterleukin-1/metabolismMiceMice, Inbred C57BLMice, KnockoutMycobacterium Infections/metabolismTumor Necrosis Factor-alpha/metabolism
PMID: 25950182
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Article (Published version) (24.3 MB) - public document Free access
Research group Mécanisme de l'inflammation articulaire (44)
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SEGUENI, Noria et al. Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection. In: PLOS ONE, 2015, vol. 10, n° 5, p. e0126058. https://archive-ouverte.unige.ch/unige:87957

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Deposited on : 2016-10-04

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