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The role of indigenous microflora in the development of murine intestinal fucosyl‐ and sialyltransferases
Author(s) -
Nanda Nanthakumar N.,
Dai Dingwei,
Newburg David S.,
Allan Walker W.
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-0031fje
Subject(s) - glycosyltransferase , biology , glycoconjugate , fucosyltransferase , microbiology and biotechnology , disaccharidase , ontogeny , sialyltransferase , enzyme , endocrinology , biochemistry
ABSTRACT Most enteric bacteria use intestinal brushborder glycoconjugates as their target host cell receptors. It has been postulated that resident microbes regulate specific glycosyltransferases that are responsible for synthesizing brushborder glycoconjugates. To investigate this hypothesis, we measured glycosyltransferase enzyme activities in intestine from different regions of maturing conventional (CONV), germ‐free (GF), and ex‐germ‐free (XGF) mice and compared them to general enzyme markers of gut development, for example, disaccharidases. High α2,3/6‑Sialyltransferase (ST) activity and low α1,2‐fucosyltransferase (FT) activities were detected from duodenum to colon in suckling CONV mice, but the relative levels of these activities reversed during the third postnatal wk, rapidly reaching adult levels by the fourth wk. These age‐related enzyme changes were significantly attenuated in GF mice, maintaining an immature pattern well past 3 wk. Introduction of gut microflora in GF mice rapidly initiated maturation of glycosyltransferase activity but had no significant affect on developmental programming of dissacharidases. Therefore, in mice, intestinal glycosyltransferase activities are under tissue and developmental control and microflora play a major role in their specific ontogeny but not in overall development. These findings may help explain the regional specificity of commensal bacteria and of enteric pathogens and may also relate age‐related changes in microflora to susceptibility to enteropathogens.