Abstract
The pathogenesis of inflammatory bowel diseases (IBD) seems to be associated with alterations of immunoregulation. Several lines of evidence suggest that estrogens play a role in the modulation of immune responses and may be related to the etiology of IBD. The purpose of this work was to examine the involvement of G protein-coupled estrogen receptor (GPER), estrogen receptor α (ERα), estrogen receptor β (ERβ) and ERα spliced variants ERα36 and ERα46 in Crohn’s disease (CD) and ulcerative colitis (UC). The studied group included 73 patients with IBD and 31 sex and age-related controls. No differences in serum levels of 17β-estradiol nor of CYP1A1 and SULT1E1 enzymes involved in estrogen catabolism were stated. The expression pattern of estrogen receptors in tissue samples was quantified using real-time PCR and Western blotting. Statistically significant up-regulation of GPER and ERα in both CD and UC as well as down-regulation of ERβ in CD patients was found. However, differences in the expression of estrogen receptors in CD and UC have been identified, depending on the sex and age of patients. In men, up-regulation of GPER, ERα and ERα46 expression was shown in CD and UC patients. In women under 50 years of age, GPER protein level increased in UC whereas ERβ expression tended to decrease in CD and UC patients. In turn, in women over 50 the protein level of ERα increased in UC while ERβ expression decreased in CD patients. Dysregulation of estrogen receptors in the intestinal mucosa of patients with CD and UC indicates that estrogen signaling may play a role in the local immune response and maintain epithelial homeostasis in a gender- and age-dependent manner.
Highlights
Crohn’s disease (CD) and ulcerative colitis (UC), the most commonly diagnosed types of inflammatory bowel diseases (IBD), are complex, immunologically mediated diseases of the gastrointestinal tract
Our analysis demonstrated no changes in tumor necrosis factor-α (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) mRNA level in colon samples obtained from IBD patients (Table 2)
There are a few main factors responsible for development of IBD, such as genetic and environmental factors which can lead to epithelial barrier dysfunction and dysregulation of immune response [23,24,25]
Summary
Crohn’s disease (CD) and ulcerative colitis (UC), the most commonly diagnosed types of inflammatory bowel diseases (IBD), are complex, immunologically mediated diseases of the gastrointestinal tract. There is evidence showing a higher prevalence of both IBD types with a relative risk of 1.65 for CD and 1.35 for UC in women [11]. A meta-analysis by Ortizo et al [12] indicated that OC users are characterized by a 24% and 30% higher risk for developing CD and UC, respectively. The positive relationship between OC use and risk of developing CD was noted in a large prospective cohort study [6]. An association between HRT and increased risk of UC was documented. It has been suggested that HRT has no effect on Crohn’s disease [8]. In case-control analysis a positive relationship between HRT and CD development was found [9]. Kane et al [10] documented a dose-dependent protective property of HRT on disease severity in IBD
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