Author:
Lin Yi-Tsung,Tseng Kai-Yu,Yeh Yi-Chen,Yang Fu-Chen,Fung Chang-Phone,Chen Nien-Jung
Abstract
ABSTRACTKlebsiella pneumoniaeliver abscess (KPLA) is prevalent in East Asia. Liver abscess can develop after translocation ofK. pneumoniaefrom a patient's bowel into the liver via the portal circulation. TREM-1 (triggeringreceptorexpressed onmyeloid cells1) 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 andTrem-1knockout (KO) mice after oral inoculation of capsular type K1K. pneumoniae. Translocation ofK. pneumoniaeto mesenteric lymph nodes and liver was examined, and intestinal permeability, antimicrobial peptide expression, and the clearance ofK. pneumoniaein the small intestine were determined. In the absence of TREM-1, KPLA model mice showed increasedK. pneumoniaedissemination, enhanced liver and systemic inflammation, and reduced survival. Impaired bacterial clearance in the small intestine causes enhancedK. pneumoniaetranslocation, which rendersTrem-1KO mice more susceptible toK. pneumoniaeoral infection. In conclusion, TREM-1-mediated bacterial clearance in the small intestine is an important immune response againstK. pneumoniae. TREM-1 deficiency enhancesK. pneumoniaetranslocation in the small intestine and increases mortality rates in mice with KPLA.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
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