Immune-mediated alteration of the terminal sugars of goblet cell mucins in the small intestine of Nippostrongylus brasiliensis-infected rats.

Alteration of terminal sugars of goblet cell mucins in the small intestinal mucosa was examined by lectin histochemistry in rats infected with Nippostrongylus brasiliensis. To see whether alteration of the nature of mucins was regulated by the local immune system, adult worms were implanted intraduodenally into recipient rats of various immune status. When 7-day-old ('normal') adult worms were implanted into naive euthymic rats, about 60% remained until day 7 and then were expelled. The number of goblet cells transiently decreased on day 5 and then progressively increased from day 9 onwards. In parallel with the hyperplasia, mucins in and released from goblet cells strongly expressed terminal N-acetyl-D-galactosamine which was specifically recognized by Helix pomatia agglutinin (HPA). When 13-day-old ('damaged') adult worms were implanted into naive euthymic rats, they were rapidly expelled by day 9 in association with hastened goblet cell hyperplasia and the alteration of terminal sugars of the mucins. Hastened worm expulsion, goblet cell hyperplasia and alteration of terminal sugars of the mucins were also observed when 'normal' worms were implanted into immune recipients. On the other hand, after implantation of 'normal' worms into hypothymic (rnu/rnu) rats, goblet cell hyperplasia or the alteration of terminal sugars of the mucins was almost completely absent. These results suggest that alteration of sugar residues of goblet cell mucins, especially the strong expression of terminal N-acetyl-D-galactosamine, is regulated by the host's immune system and seems to be important in the expulsion of N. brasiliensis.