title: TREM-1 promotes survival during Klebsiella pneumoniae liver abscess in mice.
abstract: Klebsiella pneumoniae liver abscess (KPLA) is prevalent in East Asia. Liver abscess can develop after translocation of K. pneumoniae from a patient's bowel into the liver via the portal circulation. TREM-1 (triggering receptor expressed on myeloid cells 1) amplifies inflammatory signaling during infection, but its role in KPLA is poorly understood. We used an animal study to characterize the role of TREM-1 in KPLA. We compared survival rates, bacterial burdens in tissues, inflammatory cytokine levels, and histology findings between wild-type and Trem-1 knockout (KO) mice after oral inoculation of capsular type K1 K. pneumoniae. Translocation of K. pneumoniae to mesenteric lymph nodes and liver was examined, and intestinal permeability, antimicrobial peptide expression, and the clearance of K. pneumoniae in the small intestine were determined. In the absence of TREM-1, KPLA model mice showed increased K. pneumoniae dissemination, enhanced liver and systemic inflammation, and reduced survival. Impaired bacterial clearance in the small intestine causes enhanced K. pneumoniae translocation, which renders Trem-1 KO mice more susceptible to K. pneumoniae oral infection. In conclusion, TREM-1-mediated bacterial clearance in the small intestine is an important immune response against K. pneumoniae. TREM-1 deficiency enhances K. pneumoniae translocation in the small intestine and increases mortality rates in mice with KPLA.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
authors.forename: Yi-Tsung
authors.initials: YT
authors.lastname: Lin
authors.forename: Kai-Yu
authors.initials: KY
authors.lastname: Tseng
authors.forename: Yi-Chen
authors.initials: YC
authors.lastname: Yeh
authors.forename: Fu-Chen
authors.initials: FC
authors.lastname: Yang
authors.forename: Chang-Phone
authors.initials: CP
authors.lastname: Fung
authors.forename: Nien-Jung
authors.initials: NJ
authors.lastname: Chen
mesh_terms: D000818:Animals; D018988:Bacterial Translocation / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D004195:Disease Models, Animal; D007249:Inflammation / Q000276:immunology / Q000382:microbiology; D007421:Intestine, Small / Q000276:immunology / Q000382:microbiology; D007710:Klebsiella Infections / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D007711:Klebsiella pneumoniae / Q000276:immunology*; D008099:Liver / Q000276:immunology / Q000382:microbiology; D008100:Liver Abscess / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology; D011971:Receptors, Immunologic / Q000235:genetics* / Q000276:immunology*; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D015854:Up-Regulation / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; C517262:TREM1 protein, mouse; D000073871:Triggering Receptor Expressed on Myeloid Cells-1