Opisthorchis viverrini excretory/secretory products induce toll-like receptor 4 upregulation and production of interleukin 6 and 8 in cholangiocyte
Autor: | Puangrat Yongvanit, Kantima Ninlawan, Sasithorn Kaewkes, Arpa Surapaitoon, Steve P. O'Hara, Banchob Sripa, Nicholas F. LaRusso, Patrick L. Splinter |
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Rok vydání: | 2010 |
Předmět: |
Male
Chemokine Opisthorchiasis Article Cholangiocyte Cholangiocarcinoma Immune system Cricetinae parasitic diseases Animals Humans Interleukin 8 Opisthorchis viverrini Interleukin 6 Cell Line Transformed Toll-like receptor Mesocricetus biology Interleukin-6 Opisthorchis Interleukin-8 NF-kappa B Epithelial Cells Helminth Proteins biology.organism_classification Up-Regulation Toll-Like Receptor 4 Infectious Diseases Myeloid Differentiation Factor 88 Immunology biology.protein TLR4 Parasitology Bile Ducts |
Zdroj: | Parasitology International. 59:616-621 |
ISSN: | 1383-5769 |
DOI: | 10.1016/j.parint.2010.09.008 |
Popis: | Biliary tract infection with the Group I carcinogenic liver fluke Opisthorchis viverrini is associated with severe inflammation leading to cholangiocarcinoma – a major biliary cancer in Southeast Asia. However, mechanism(s) by which the liver fluke induces host mucosal immune/inflammatory responses are unclear. In the present study we address whether a normal immortalized human cholangiocyte cell line (H69 cells) recognizes and responds to O. viverrini excretory/secretory products (OVES). Expression of multiple TLRs, activation of NF-κB, and expression of proinflammatory cytokines were monitored in the presence and absence of OVES. Our results showed that OVES induced increased cholangiocyte TLR4 mRNA expression, induced IκB-α degradation in a MyD88-dependent manner, and activated NF-κB nuclear translocation. Moreover, OVES induced expression and secretion of the strong chemoattractant chemokine interleukin 8 (IL-8) and pro-inflammatory cytokine IL-6. These results demonstrate that secreted/excreted products of O. viverrini are recognized by human cholangiocytes and initiate innate mucosal immunity/inflammatory cascades, a primary event in the pathogenesis of opisthorchiasis and cholangiocarcinoma. |
Databáze: | OpenAIRE |
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