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Scientific article
Open access
English

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

Published inPloS one, vol. 10, no. 5, e0126058
Publication date2015
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
  • Animals
  • Host-Pathogen Interactions
  • Interleukin-1/metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mycobacterium Infections/metabolism
  • Tumor Necrosis Factor-alpha/metabolism
Citation (ISO format)
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. doi: 10.1371/journal.pone.0126058
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Article (Published version)
Identifiers
ISSN of the journal1932-6203
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