Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans

碩士 === 國立嘉義大學 === 微生物免疫與生物藥學系研究所 === 103 === Candida species is the most common opportunistic fungal pathogen of human. Candida albicans, one of Candida species, is a frequently fatal systemic pathogen. Compare the common body fluid of human including urine, sputum, blood and others, the Candida str...

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Main Author: 陳佩青
Other Authors: 劉怡文
Format: Others
Language:zh-TW
Online Access:http://ndltd.ncl.edu.tw/handle/19523725232042335565
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spelling ndltd-TW-103NCYU56030092017-04-26T04:33:31Z http://ndltd.ncl.edu.tw/handle/19523725232042335565 Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans 人類泌尿道上皮細胞與白色念珠菌共同培養後之發炎相關基因表現分析 陳佩青 碩士 國立嘉義大學 微生物免疫與生物藥學系研究所 103 Candida species is the most common opportunistic fungal pathogen of human. Candida albicans, one of Candida species, is a frequently fatal systemic pathogen. Compare the common body fluid of human including urine, sputum, blood and others, the Candida strains are isolated mostly from urine; therefore, bladder epithelia layer is an important barrier for defense of Candida strains’ invasion. So in this study, the host cellular response of urothelium infected by C. albicans was investigated. Currently, we found that C. albicans caused the urothelial morphology change, cell damage, cell de-attachment and inflammatory response including cyclooxygenase-2 (COX-2) gene and protein expression, prostaglandin E2 accumulation and interleukin-8 gene expression. Then the molecular mechanism of C. albicans-induced urothelial COX-2 gene expression was studied. The pathways potentially related to COX-2 expression were examined by Western blot. We observed the phosphorylation of ERK1/2, p38, and JNK were all increased after C. albicans infection for 12 h. The C. albicans-induced COX-2 protein expression was inhibited by the specific inhibitor of ERK and p38 (U0126 and SB203580), but not by the JNK inhibitor SP600125. We also observed increased amount of phosphorylation of RSK that is the mutual downstream molecule of ERK1/2 and p38. Furthermore, phosphorylation of RSK protein expression is decreased by the treatment of ERK or p38 inhibitors. Base on the data, it suggests that the urothelial COX-2 gene is induced majorly though ERK/p38-RSK pathway by C. albicans infection. And we found that transcription factor cAMP response element-binding protein-1 (CREB-1) was increased in binding to COX-2 gene promoter. Using receptor inhibitors including Toll-like receptors (TLRs)-MyD88 inhibitor (ST2825), Dectin-syk receptor inhibitor (syk inhibitor) and epidermal growth factor receptor (EGFR) inhibitor (PD168393) to identify which was the main receptor for C. albicans-induced COX-2 expression. We found that EGFR played an important mediator to activate ERK/p38-RSK pathway and induce COX-2 expression. 劉怡文 學位論文 ; thesis 82 zh-TW
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description 碩士 === 國立嘉義大學 === 微生物免疫與生物藥學系研究所 === 103 === Candida species is the most common opportunistic fungal pathogen of human. Candida albicans, one of Candida species, is a frequently fatal systemic pathogen. Compare the common body fluid of human including urine, sputum, blood and others, the Candida strains are isolated mostly from urine; therefore, bladder epithelia layer is an important barrier for defense of Candida strains’ invasion. So in this study, the host cellular response of urothelium infected by C. albicans was investigated. Currently, we found that C. albicans caused the urothelial morphology change, cell damage, cell de-attachment and inflammatory response including cyclooxygenase-2 (COX-2) gene and protein expression, prostaglandin E2 accumulation and interleukin-8 gene expression. Then the molecular mechanism of C. albicans-induced urothelial COX-2 gene expression was studied. The pathways potentially related to COX-2 expression were examined by Western blot. We observed the phosphorylation of ERK1/2, p38, and JNK were all increased after C. albicans infection for 12 h. The C. albicans-induced COX-2 protein expression was inhibited by the specific inhibitor of ERK and p38 (U0126 and SB203580), but not by the JNK inhibitor SP600125. We also observed increased amount of phosphorylation of RSK that is the mutual downstream molecule of ERK1/2 and p38. Furthermore, phosphorylation of RSK protein expression is decreased by the treatment of ERK or p38 inhibitors. Base on the data, it suggests that the urothelial COX-2 gene is induced majorly though ERK/p38-RSK pathway by C. albicans infection. And we found that transcription factor cAMP response element-binding protein-1 (CREB-1) was increased in binding to COX-2 gene promoter. Using receptor inhibitors including Toll-like receptors (TLRs)-MyD88 inhibitor (ST2825), Dectin-syk receptor inhibitor (syk inhibitor) and epidermal growth factor receptor (EGFR) inhibitor (PD168393) to identify which was the main receptor for C. albicans-induced COX-2 expression. We found that EGFR played an important mediator to activate ERK/p38-RSK pathway and induce COX-2 expression.
author2 劉怡文
author_facet 劉怡文
陳佩青
author 陳佩青
spellingShingle 陳佩青
Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
author_sort 陳佩青
title Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
title_short Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
title_full Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
title_fullStr Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
title_full_unstemmed Analysis of Proinflammatory Response and Mechanism in Human Urinary Epithelial Cells Infected by Candida albicans
title_sort analysis of proinflammatory response and mechanism in human urinary epithelial cells infected by candida albicans
url http://ndltd.ncl.edu.tw/handle/19523725232042335565
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