title: AIM2 inflammasome is dispensable for the host defense against Pseudomonas aeruginosa infection.
abstract: Respiratory tract infection with Pseudomonas aeruginosa is a major cause of hospital&mdash;acquired pneumonia in immune&mdash;compromised individuals. Lung infection with P. aeruginosa is often associated with production of various inflammatory cytokines including IL&mdash;1&#946;. Production of IL&mdash;1&#946; requires proteolytic cleavage by a multiprotein complex termed inflammasome. AIM2 inflammasome recognizes foreign cytosolic double stranded DNA. A role of AIM2 in P. aeruginosa infection has not been reported previously. In this study, we found that P. aeruginosa infection induced degradation of AIM2 protein in macrophages and induction of AIM2 mRNA expression in macrophages and in the lung of mice. Interestingly, P. aeruginosa infection induced a similar level of IL&mdash;1&#946;, IL&mdash;6 and TNF production in wild&mdash;type and AIM2&mdash;deficient mice. Similarly, no significant differences in bacterial clearance, neutrophil infiltration and NF&mdash;&#954;B activation were observed between wild&mdash;type and AIM2&mdash;deficient mice following P. aeruginosa lung infection. Our data suggest that AIM2 inflammasome is dispensable for the host defense against P. aeruginosa infection.
authors.affiliation: Saint Mary&apos;s University Biology Department Halifax Canada.
authors.forename: Z
authors.initials: Z
authors.lastname: Pang
authors.affiliation: Saint Mary&apos;s University Biology Department Halifax Canada genlou.sun&commat;smu.ca.
authors.forename: G
authors.initials: G
authors.lastname: Sun
authors.affiliation: Dalhousie University Department of Microbiology and Immunology Halifax Canada.
authors.forename: R D
authors.initials: RD
authors.lastname: Junkins
authors.affiliation: Dalhousie University Department of Microbiology and Immunology Halifax Canada tong&mdash;jun.lin&commat;dal.ca.
authors.forename: T J
authors.initials: TJ
authors.lastname: Lin
mesh_terms: D000818:Animals; D020170:Caspase 1 / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D005260:Female; D058847:Inflammasomes / Q000378:metabolism; D053583:Interleukin-1beta / Q000032:analysis / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016328:NF-kappa B / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000502:physiology; D011552:Pseudomonas Infections / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: C540422:Aim2 protein, mouse; D004268:DNA-Binding Proteins; D058847:Inflammasomes; D053583:Interleukin-1beta; D015850:Interleukin-6; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D020170:Caspase 1