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International Journal of Clinical & Medical Microbiology Volume 1 (2016), Article ID 1:IJCMM-112, 5 pages
https://doi.org/10.15344/2456-4028/2016/112
Original Article
Contribution of Outer Membrane Porin (Omp) K36 to Klebsiella pneumoniae induced Liver Abscess

Junn-Liang Chang1,2, Wen-Cheng Tsai3 and Jiun-Han Chen4*

1Department of Pathology and Laboratory Medicine, Taoyuan Armed Forces General Hospital, Taoyuan City, Taiwan,
2Biomedical Engineering Department, Ming Chuan University, Taoyuan City, Taiwan
3Department of Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung City, Taiwan
4Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu, Taiwan
Prof. Jiun-Han Chen, Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu, Taiwan, 306, Yuanpei Street, Hsinchu, Taiwan; E-mail: jhchen@mail.ypu.edu.tw
26 August 2016; 29 September 2016; 01 October 2016
Chang JL, Tsai WC, Chen JH (2016) Contribution of Outer Membrane Porin (Omp) K36 to Klebsiella pneumoniae induced Liver Abscess. Int J Clin Med Microbiol 1: 112. doi: https://doi.org/10.15344/2456-4028/2016/112
This work was supported by grants from Zuoying Branch of Kaohsiung Armed Forces General Hospital (ZBH 102-02), Yuanpei University (101-COMP6011-10, 100-COMP6012-01), Taoyuan Armed Forces General Hospital (102-27).

Abstract

Introduction: Pyogenic liver abscess is usually caused by multiple bacterial infections. This disease can be caused by single microorganism, Klebsiella pneumoniae that has been reported in Asia, North America and Europe. Many virulence factors of K. pneumoniae have identified including capsular polysaccharide, lipopolysaccharide, serum resistance, adhesins and siderophores. Previously, we demonstrated the virulent effect of outer membrane porin (OMP) K 36 by a lethality study. However, the role of OmpK36 in liver abscess pathogenesis is still unclear.
Objective: In this study, a virulent K. pneumoniae strain NVT-1002 and OmpK36 deficient mutant (ΔOMPK) were used to examine the contribution of OmpK36 to liver abscess. Liver injuries and inflammatory cytokines expression were detected by tissue section and enzyme linked-immunosorbent assay respectively. The toxic effect of OmpK36 to human hepatoma cell (HepG2) was tested by bacterial infections and the treatment with OmpK36 recombinant protein.
Results: The Results demonstrated that the NVT-1002 induced sever liver injuries while little or no damage was found in mice injected with OmpK36. Expression of serum and liver cytokines including TNF-α, IL-1β, IL-6 and IL-10 were elevated after injection of NVT-1002, meanwhile, only IL-1β was transiently elevated in OmpK36 group. Interestingly, OmpK36 recombinant protein showed no toxic effect to HepG2 cells, and the virulence of OmpK36 mutant to HepG2 was not altered compared to NVT-1002 group.
Conclusion: In conclusion, OmpK36 contributes to the K. pneumoniae induced liver abscess and inflammatory responses. The virulent effect of OmpK36 is not mediated by the protein itself, but other uncertain mechanisms. OmpK36 may be a therapeutic target in K. pneumoniae infection.