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A Host Defense Mechanism Involving CFTR-Mediated Bicarbonate Secretion in Bacterial Prostatitis
Xie, Chen1; Tang, Xiaoxiao1; Xu, Wenming2; Diao, Ruiying3; Cai, Zhiming3; Chan, Hsiao Chang1,2
刊名PLOS ONE
2010-12-07
DOI10.1371/journal.pone.0015255
5期:12
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]TRANSMEMBRANE CONDUCTANCE REGULATOR ; SOLUBLE ADENYLYL-CYCLASE ; CONGENITAL CHLORIDE DIARRHEA ; CYSTIC-FIBROSIS ; FERTILIZING-CAPACITY ; CL-/HCO3-EXCHANGE ; ESCHERICHIA-COLI ; MESSENGER-RNA ; FLUID ; PH
英文摘要

Background: Prostatitis is associated with a characteristic increase in prostatic fluid pH; however, the underlying mechanism and its physiological significance have not been elucidated.

Methodology/Principal Findings: In this study a primary culture of rat prostatic epithelial cells and a rat prostatitis model were used. Here we reported the involvement of CFTR, a cAMP-activated anion channel conducting both Cl(-) and O(3)(-), in mediating prostate HCO(3)(-) secretion and its possible role in bacterial killing. Upon Escherichia coli (E coli)-LPS challenge, the expression of CFTR and carbonic anhydrase II (CA II), along with several pro-inflammatory cytokines was up-regulated in the primary culture of rat prostate epithelial cells. Inhibiting CFTR function in vitro or in vivo resulted in reduced bacterial killing by prostate epithelial cells or the prostate. High HCO(3)(-) content (>50 mM), rather than alkaline pH, was found to be responsible for bacterial killing. The direct action of HCO(3)(-) on bacterial killing was confirmed by its ability to increase cAMP production and suppress bacterial initiation factors in E coli. The relevance of the CFTR-mediated HCO(3)(-) secretion in humans was demonstrated by the upregulated expression of CFTR and CAII in human prostatitis tissues.

Conclusions/Significance: The CFTR and its mediated HCO(3)(-) secretion may be up-regulated in prostatitis as a host defense mechanism.

语种英语
WOS记录号WOS:000285041800011
引用统计
被引频次:8[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54199
专题北京大学深圳医院
作者单位1.Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Epithelial Cell Biol Res Ctr, Hong Kong, Hong Kong, Peoples R China
2.Sichuan Univ, W China Univ Hosp 2, Chinese Univ Hong Kong Joint Lab Reprod Med, Hong Kong, Hong Kong, Peoples R China
3.Peking Univ, Shenzhen Hosp, Guangdong Key Lab Male Reprod & Genet, Shenzhen, Peoples R China
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GB/T 7714
Xie, Chen,Tang, Xiaoxiao,Xu, Wenming,et al. A Host Defense Mechanism Involving CFTR-Mediated Bicarbonate Secretion in Bacterial Prostatitis[J]. PLOS ONE,2010,5(12).
APA Xie, Chen,Tang, Xiaoxiao,Xu, Wenming,Diao, Ruiying,Cai, Zhiming,&Chan, Hsiao Chang.(2010).A Host Defense Mechanism Involving CFTR-Mediated Bicarbonate Secretion in Bacterial Prostatitis.PLOS ONE,5(12).
MLA Xie, Chen,et al."A Host Defense Mechanism Involving CFTR-Mediated Bicarbonate Secretion in Bacterial Prostatitis".PLOS ONE 5.12(2010).
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