Abstract 1124
Poster Session IV, Tuesday, 5/4 (poster 238)
Some bacteria colonize the gut by adhering to a receptor on glycolipids or glycoprotein in microvillus membrane (MVM). Pathologic bacteria are defined in part by their expression of adhesions on their surface and the capacity of these adhesins to bind to the microvillus glycoconjugates in a lectin-like fasion. It seems that the specific glycosyltransferase activity adding sugar to MVM protein and lipids (glycosylation) is an important host determinant in bacterial colonization. We have previously reported that α2,6-sialyltransferase activity is increased in the immature rat intestine and α1,3-fucosyltransferase and β1,3-galactosyltransferase activity are decreased. To better understand the regulation of intestinal glycosylation, we have further studied the expression of these glycosyltransferases in different regions of mice intestine during postnatal development. The enzyme activities were assayed in the particulate fraction (105,000 × g pellet) of mucosa, scraped from different section of intestine. The results showed that α2,6-sialyltransferase activity was increased in the immature intestine of suckling mice, primarily in ileum and to a lesser extend in jejunum, but not in duodenum and colon; α1,3-fucosyltransferase activity was decreased in ileum and colon, but not in duodenum and jejunum compared to adults in the first 3 weeks of life, rapidly increased at 4 weeks; β1,3-galactosyltransferase activity was increased in the whole intestine (from duodenum to colon) during postnatal development. The injection of cortisone precociously induced a decreased α2,6-sialyltransferase activity in the whole small intestine, but not in colon, and an increased α1,3-fucosyltransferase activity in whole intestine, but not in colon, and an increased β1,3-galactosyltransferase activity in ileum and colon, but not in duodenum and jejunum in 2-week-old suckling mice. These results suggest that intestinal glycosyltransferases activities are under region-specific and developmental regulation and the ontogeny of these glycosyltransferases can be accelerated by the treatment of cortisone.
