Inflammatory bowel disease (IBD) is very common in Europe and USA. Its incidence in East Asia has been traditionally low, albeit the risk of IBD increases in Asian immigrants adopting western lifestyles, suggesting a strong role of environmental/dietary factors in IBD. A lifelong exposure to
phytoestrogen-rich diets has been associated with a decreased risk of developing
breast cancer and might also be protective against IBD. We studied the influence of in utero and postnatal exposure to a
phytoestrogen (PE)-rich diet on acute
inflammation in an animal model of TNBS-induced
colitis. Wistar rats were exposed in utero and postnatally to high (
genistein: 240 microg/g feed;
daidzein: 232 microg/g feed) or very low levels (
genistein and
daidzein <10 microg/g feed) of
phytoestrogen isoflavones fed to pregnant dams with the diet and throughout nursing. After weaning, the offspring had free access to these diets. At the age of 11 weeks,
colitis was induced with an
enema of TNBS. After 3 days, animals were sacrificed and tissues were collected for histological evaluation and analysis of molecular markers of
inflammation. Animals kept on a PE-rich diet (PRD) had higher colon weights than animals on low PE-levels (PDD), suggesting enhanced acute
inflammation by
phytoestrogens. This result was supported by histological findings and by analysis of
myeloperoxidase activity. Interestingly, relative
mRNA and
protein expression of
cyclooxygenase-2 (COX-2) were modulated in rats on PRD, providing evidence that COX-2, the inducible
isoform of the
enzyme, is involved in the management of colonic
inflammation. Our results suggest that early-in-life exposure to PE might not protect against the development of IBD but enhances the extent of acute
inflammation.