Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis

被引:19
作者
Guseva, NV [1 ]
Dessus-Babus, SC [1 ]
Whittimore, JD [1 ]
Moore, CG [1 ]
Wyrick, PB [1 ]
机构
[1] E Tennessee State Univ, James H Quillen Coll Med, Dept Microbiol, Johnson City, TN 37614 USA
关键词
Chlamydia trachomatis; Chlamydia; hormone modulation; estrogen; cell lines; estrogen receptors;
D O I
10.1016/j.micinf.2005.05.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Chlamydial attachment and infectivity in vitro and ascending disease and sequelae in vivo have been reported to be enhanced/modulated by estrogen. Endometrial carcinoma cell lines Ishikawa and HEC-1B and the breast cancer lines MCF-7 and HCC-1806 were examined for Chlamydia trachomatis E infectivity. Estrogen receptor (ER) presence was confirmed by Western blot and qRT-PCR analyses. FACS analysis was used to determine the percent of plasma membrane-localized ERs (mERs), and their activity was tested by estrogen binding and competitive estrogen antagonists assays. Chlamydiae grew in all cell lines with HEC (90%) >> MCF-7 (57%) > Ishikawa (51%) >> HCC-1806 (20%). The cell line ER isoform composition was re-defined as: ER alpha + ER beta + for MCF-7, HCC-1806 and Ishikawa; and ER beta only for HEC-1B. HeLa cells were also tested and found to express ER beta, but not ER alpha. A small percentage of both ERs were surface-exposed and functionally active. The endometrium-predominant ER beta isoform was found in all cell lines, including those most representative of the common sites of C. trachomatis infection. Thus, the role of chlamydial attachment/infectivity will now be analyzed in ER beta + and-isogenic HEC-1B cells. (C) 2005 Elsevier SAS. All rights reserved.
引用
收藏
页码:1469 / 1481
页数:13
相关论文
共 49 条
[1]  
[Anonymous], GLOB PREV INC SEL CU
[2]   ESTROGEN ACTION VIA THE CAMP SIGNALING PATHWAY - STIMULATION OF ADENYLATE-CYCLASE AND CAMP-REGULATED GENE-TRANSCRIPTION [J].
ARONICA, SM ;
KRAUS, WL ;
KATZENELLENBOGEN, BS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (18) :8517-8521
[3]   Prospects for a vaccine against Chlamydia genital disease .1. Microbiology and pathogenesis [J].
Bavoil, PM ;
Hsia, RC ;
Rank, RG .
BULLETIN DE L INSTITUT PASTEUR, 1996, 94 (01) :5-54
[4]   ENHANCEMENT OF ADHERENCE AND GROWTH OF CHLAMYDIA-TRACHOMATIS BY ESTROGEN-TREATMENT OF HELA-CELLS [J].
BOSE, SK ;
GOSWAMI, PC .
INFECTION AND IMMUNITY, 1986, 53 (03) :646-650
[5]   ATYPICAL PELVIC INFLAMMATORY DISEASE - CAN WE IDENTIFY CLINICAL PREDICTORS [J].
CATES, W ;
JOESOEF, MR ;
GOLDMAN, MB .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1993, 169 (02) :341-346
[6]  
*CDCP, 2002, SEX TRANSM DIS SUR S
[7]   ERβ has nongenomic action in caveolae [J].
Chambliss, KL ;
Yuhanna, IS ;
Anderson, RGW ;
Mendelsohn, ME ;
Shaul, PW .
MOLECULAR ENDOCRINOLOGY, 2002, 16 (05) :938-946
[8]   Global analysis of ligand sensitivity of estrogen inducible and suppressible genes in MCF7/BUS breast cancer cells by DNA microarray [J].
Coser, KR ;
Chesnes, J ;
Hur, JY ;
Ray, S ;
Isselbacher, KJ ;
Shioda, T .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (24) :13994-13999
[9]   Hormonal factors and the laboratory detection of Chlamydia trachomatis in women: Implications for screening? [J].
Crowley, T ;
Horner, P ;
Hughes, A ;
Berry, J ;
Paul, I ;
Caul, O .
INTERNATIONAL JOURNAL OF STD & AIDS, 1997, 8 (01) :25-31
[10]   HORMONAL-CONTROL OF PROLIFERATION IN THE ISHIKAWA ENDOMETRIAL ADENOCARCINOMA CELL-LINE [J].
CROXTALL, JD ;
ELDER, MG ;
WHITE, JO .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1990, 35 (06) :665-669