2011
DOI: 10.1111/j.1462-5822.2011.01608.x
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The multifaceted role of oestrogen in enhancing Chlamydia trachomatis infection in polarized human endometrial epithelial cells

Abstract: The oestrogen receptor (ER) α-β+ HEC-1B and the ERα+β+ Ishikawa (IK) cell lines were investigated to dissect the effects of oestrogen exposure on several parameters of Chlamydia trachomatis infection. Antibody blockage of ERα or ERβ alone or simultaneously significantly decreased C. trachomatis infectivity (45-68%). Addition of the ERβ antagonist, tamoxifen, to IK or HEC-1B prior to or after chlamydial infection caused a 30-90% decrease in infectivity, the latter due to disrupted eukaryotic organelles. In vivo… Show more

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Cited by 27 publications
(33 citation statements)
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“…C. trachomatis development and replication in vivo may be subject to stresses imposed by nutritional requirements 142, innate and adaptive immune responses 143, host physiology via hormones 144145146 and even competition with commensals or co-pathogens 147148. Conditions that delay bacterial multiplication impair effectiveness of antibiotics in many microorganisms 149150151.…”
Section: Treatment and Preventionmentioning
confidence: 99%
“…C. trachomatis development and replication in vivo may be subject to stresses imposed by nutritional requirements 142, innate and adaptive immune responses 143, host physiology via hormones 144145146 and even competition with commensals or co-pathogens 147148. Conditions that delay bacterial multiplication impair effectiveness of antibiotics in many microorganisms 149150151.…”
Section: Treatment and Preventionmentioning
confidence: 99%
“…Clearance of C. trachomatis infection might be delayed by pathogen immune evasion strategies such as enhanced survival inside and outside host cells, reduced inflammatory and adaptive immune responses and ability to persist within host cells as AB [39]. Adding complexity, sex hormones modulate female genital tract immune responses 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 647 [40,41]. Women are more susceptible to chlamydial infection under the influence of estradiol, and estradiol enhances disease sequelae [40].…”
Section: Chlamydia Trachomatis: Genital Infectionsmentioning
confidence: 99%
“…Accordingly, estrogen and progesterone are important for the establishment of chlamydial infection. Furthermore, estrogen receptors have been involved in the internalization of CT [92,93]. Sex hormones affect the clinical outcome of chlamydial infections; thus, follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), progesterone (P4), and prolactin (PRL) are involved not only in the establishment of chlamydial infection but also in the development of sequelae on reproductive tissue [94,95].…”
Section: Age and Hormonal Statusmentioning
confidence: 99%