title: the AIM2 inflammasome is involved in macrophage activation during infection with virulent Mycobacterium bovis strain.
abstract: BACKGROUND
  Mycobacterium bovis, the causative agent of bovine tuberculosis, infects host macrophages and triggers production of the proinflammatory cytokine interleukin 1β (IL-1β). The mechanism by which macrophages become activated and secrete IL-1β in tuberculosis has not yet been elucidated.
  
  
  METHODS
  In this study, we investigated the role of the absence in melanoma 2 (AIM2) inflammasome in IL-1β release from macrophages infected with pathogenic M. bovis strain.
  
  
  RESULTS
  We found that the AIM2 inflammasome activation is involved in the production of IL-1β in primary and immortalized mouse macrophage upon M. bovis infection; that the activation process requires cytoplasmic potassium efflux, mycobacterial internalization, but not reactive oxygen species (ROS) or IFN-β release; that the AIM2 inflammasome contributes to the synthesis of proinflammatory and chemotatic factors in M. bovis-infected macrophages; and that the activation of the AIM2 inflammasome is due, at least in part, to mycobacterial translocation into the cytosol.
  
  
  CONCLUSIONS
  We conclude that the AIM2 inflammasome is involved in macrophage activation during infection with virulent M. bovis strain. To our knowledge, this is the first evidences for the involvement of the AIM2 inflammasome in M. bovis infection.
authors.affiliation: State Key Laboratories for Agrobiotechnology, Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.forename: Xiangmei
authors.initials: X
authors.lastname: Zhou
authors.forename: Mohammed
authors.initials: M
authors.lastname: Kouadir
authors.forename: Fushan
authors.initials: F
authors.lastname: Shi
authors.forename: Tianjian
authors.initials: T
authors.lastname: Ding
authors.forename: Chunfa
authors.initials: C
authors.lastname: Liu
authors.forename: Jin
authors.initials: J
authors.lastname: Liu
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: Lifeng
authors.initials: L
authors.lastname: Yang
authors.forename: Xiaomin
authors.initials: X
authors.lastname: Yin
authors.forename: Deming
authors.initials: D
authors.lastname: Zhao
mesh_terms: D000818:Animals; D020170:Caspase 1 / Q000235:genetics / Q000378:metabolism; D002417:Cattle; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D003600:Cytosol / Q000382:microbiology; D004268:DNA-Binding Proteins; D058847:Inflammasomes / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology / Q000382:microbiology; D051379:Mice; D009163:Mycobacterium bovis / Q000276:immunology* / Q000472:pathogenicity; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D010588:Phagosomes / Q000382:microbiology; D011188:Potassium / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D014380:Tuberculosis, Bovine / Q000276:immunology* / Q000382:microbiology; D015854:Up-Regulation; D014774:Virulence
chemical_list: C540422:Aim2 protein, mouse; D016207:Cytokines; D004268:DNA-Binding Proteins; D058847:Inflammasomes; D053583:Interleukin-1beta; D009687:Nuclear Proteins; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D020170:Caspase 1; D011188:Potassium
keywords: AIM2; IL-1β; M. bovis; inflammasome; macrophage