Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection
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2015
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PLoS One
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Public Library of Science
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University of Cape Town
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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.
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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