Intestinal epithelial membrane changes in @entity35 immune to XXXX .

@entity3505 @entity8416 @entity3954 @entity1735 @entity281 @entity35
Establishment of @entity8416 infective larvae is blocked to a large degree in the immune @entity35 as compared with the nonimmune host. The rapidity with which this response occurs indicates that most worms are either prevented from penetrating the intestinal epithelium or are rejected immediately after cell entry. It is proposed that interference with larval infectivity is due to alterations in the epithelial cell apical or brush border membrane. Alterations may result from prior @entity281 or may reflect an acute change induced by @entity281 . In either case the establishment of normal populations of larvae in the mucosa is disturbed. Lectin binding capacity of brush border membranes was used to assess possible membrane alterations. This parameter in uninfected (control) @entity35 was compared with that in infected @entity35 , which acquire resistance to subsequent challenge, and in infected @entity35 immediately after a challenge inoculum. Enriched brush border membrane preparations were characterized for their binding of @entity3505 germ agglutinin, which attaches specifically to the @entity1735 , @entity3954 . Maximum specific binding of 125I-labeled @entity3505 germ agglutinin occurred within 20 min. The spontaneous rate of dissociation was negligible for 90 min. Highest specific binding resulted at 24 degrees C, pH 6.0 and with 75 micrograms brush border membrane protein per assay tube. Results suggested the existence of multiple binding sites. 1 mg of membrane protein from uninfected @entity35 and @entity35 immunized by @entity281 maximally bound 9.8 X 10(10) and 4.3 X 10(10) molecules of @entity3505 germ agglutinin, respectively. Binding for the 'immune' brush border membrane, as compared with the 'uninfected' brush border membrane was reduced during the first 3 weeks of @entity281 and remained low for at least 3 months. No further reduction in binding was observed for brush border membrane isolated within minutes after a secondary @entity281 . These results reveal the induction by a @entity281 of changes in brush border membrane structure and the persistence of these changes in the immune host. In view of the rapid turnover time of epithelial tissue the mechanism by which this change is perpetuated speculatively involves immune elements in the lamina propria.
