title: [TLR-4 involvement in pyroptosis of mice with pulmonary inflammation infected by Actinobacillus pleuropneumoniae].
abstract: OBJECTIVE
  Pyroptosis is a caspase-1 dependent programmed cell death and involves pathogenesis of infectious diseases by releasing many pro-inflammatory cytokines to induced inflammation. TLR-4 plays an important role in mediating pathogenesis of some infectious diseases. In this study, we detected the expression of TLR-4 and some molecules (e. g caspase-1, TNF-α, IL-1β, IL-6, IL-18 ) related with pyroptosis to determine its involvement and mechanisms of pulmonary inflammation in mice infected by A. pleuropneumoniae.
  
  
  METHODS
  Mice were intranasally infected by A. pleuropneumoniae and killed 48 hours post infection. Pulmonary gross lesion and histological pathology by H-E were observed. Expression levels of caspase-1 , caspase-3, TNF-α, IL-1β, IL-6, IL-18, and TLR-4 in lung of mice were detected by RT-PCR and qPCR.
  
  
  RESULTS
  Serious pulmonary hemorrhage and inflammation in infected mice were observed. Expression levels of caspase-1, caspase-3, TNF-α, IL-1β, IL-6, IL-18 and TLR-4 increased, and expression levels of caspase-3 were not changed in lung of infected mice.
  
  
  CONCLUSIONS
  TLR-4 might be involved in pulmonary inflammation of mice infected by A. pleuropneumoniae. After induced by activated TLR-4 some cells in this lesion expressed pro-inflammatory cytokines. These cytokines would induce pulmonary inflammation. This lesion might involve pyroptosis with caspase-1 expression.
authors.forename: Peipei
authors.initials: P
authors.lastname: Hu
authors.forename: Fushen
authors.initials: F
authors.lastname: Huang
authors.forename: Junchao
authors.initials: J
authors.lastname: Niu
authors.forename: Zhaoshan
authors.initials: Z
authors.lastname: Tang
mesh_terms: D000189:Actinobacillus Infections / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D016977:Actinobacillus pleuropneumoniae / Q000235:genetics / Q000502:physiology*; D000818:Animals; D017209:Apoptosis; D005260:Female; D006801:Humans; D020382:Interleukin-18 / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D008168:Lung / Q000166:cytology / Q000276:immunology / Q000382:microbiology; D008297:Male; D051379:Mice; D011014:Pneumonia / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D020382:Interleukin-18; D015850:Interleukin-6; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha