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The AIM2 inflammasome is critical for innate immunity to Francisella tularensis.

  • Author(s): Fernandes-Alnemri, Teresa
  • Yu, Je-Wook
  • Juliana, Christine
  • Solorzano, Leobaldo
  • Kang, Seokwon
  • Wu, Jianghong
  • Datta, Pinaki
  • McCormick, Margaret
  • Huang, Lan
  • McDermott, Erin
  • Eisenlohr, Laurence
  • Landel, Carlisle P
  • Alnemri, Emad S
  • et al.

Published Web Location

https://doi.org/10.1038/ni.1859
Abstract

Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F. tularensis and elicit this proinflammatory response. Using mice deficient in the DNA-sensing inflammasome component AIM2, we demonstrate here that AIM2 is required for sensing F. tularensis. AIM2-deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bacterial burden than that of wild-type mice. Caspase-1 activation, IL-1beta secretion and cell death were absent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic DNA. Our study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of its critical role in host innate immunity to intracellular pathogens.

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