Estradiol Has Differential Effects on Acute Colonic Inflammation in the Presence and Absence of Estrogen Receptor ß Expression.
Dig Dis Sci
; 62(8): 1977-1984, 2017 08.
Article
em En
| MEDLINE
| ID: mdl-28573506
ABSTRACT
BACKGROUND:
Inflammatory bowel disease (IBD) increases the risk of developing colon cancer. This risk is higher in men compared to women, implicating a role for female hormones in the protection against this disease. Studies from our laboratory demonstrated that estradiol (E2) protects against inflammation-associated colon tumor formation when administered following chemical carcinogen and induction of chronic colitis.AIM:
This study seeks to better understand the effect of E2 on acute colitis in the presence and absence of estrogen receptor ß (ERß).METHODS:
Inflammation was induced by 2,4,6-trinitrobenzenesulfonic acid in wild-type (WT) and ERß knockout (ERßKO) mice implanted with a control or E2-containing pellet and killed 5 days later. Inflammation and injury were scored by a pathologist. Apoptosis and proliferation were assessed by immunohistochemistry. Cytokines were measured by multiplex analysis.RESULTS:
E2 treatment reduced inflammation in the middle colon in WT mice and the distal colon in ERßKO mice compared to control mice. WT mice had reduced IL-6, IL-12, IL-17, GM-CSF, IFN-γ, MCP-1, MIP-1α, and TNF-α, and ERßKO had reduced IL-6 and IFN-γ expression in response to E2. Injury scores were lower in E2-treated ERßKO mice compared to control ERßKO mice. ERßKO mice had increased proliferation in the basal third of crypts in the distal colon and decreased apoptosis in the proximal colon.CONCLUSIONS:
These data suggest that E2 has differential protective effects against acute colitis in the presence or absence of ERß and provide insight into how E2 may protect against IBD.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Colite
/
Receptor beta de Estrogênio
/
Estradiol
/
Estrogênios
Limite:
Animals
Idioma:
En
Revista:
Dig Dis Sci
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Estados Unidos