Biomedical subjects

E E Jarrett

Publications and source records attributed to E E Jarrett.

At least 37 records · Page 2Linked to original sources

PubMed1976

Time course studies on rat IgE production in N. Brasiliensis infection.

We present here a study of the relationship in time between the elevation of total serum IgE, the parasite-specific IgE response, and the potentiated IgE response to unrelated antigen which occurs in rats following infection with the worm parasite N. brasiliensis. During a first infection the potentiated IgE response (to egg albumin) and elevation of total IgE occur synchronously rising to a peak on days 12-14 after infection, with the fastest rate of increase occurring between days 8 and 10. N. brasiliensis-specific IgE rises to a peak some 2-3 weeks later when both total IgE and the potentiated response have largely declined. A strain difference is shown in that Wistar rats produce far lower levels of total and parasite-specific IgE than Hooded Listers. Events following reinfection differ in that total IgE rises more rapidly, very high levels being reached 6 days after reinfected together with a secondary specific IgE response to N. brasiliensis. The total IgE level, however, rises by a far greater factor than parasite-specific IgE and declines rapidly while the parasite-specific response declines slowly over many weeks. The egg albumin response is not repotentiated. It is proposed that the total IgE response and the potentiated IgE response which forms a small component of it results from the release of a non-specific IgE-stimulating factor produced by N. brasiliensis-specific T cells. In this scheme the same or similar cells are involved in the production of N. brasiliensis-specific IgE through a separate specific helper function.

Animals↗

PubMed1976

Rat IgE production. II. Primary and booster reaginic antibody responses following intradermal or oral immunization.

Primary and booster IgE antibody responses have been elicited in Hooded Lister rats by the intradermal injection or oral administration of very small quantities of egg albumin. Oral immunization was effected by giving antigen by stomach tube or in the drinking water. The minimum primary dose of antigen found to be effective was 1 mug intradermally and 10 mug orally, administered together with an intraperitoneal injection of B. pertussis adjuvant. In rats immunized with these doses secondary responses could be evoked by giving even smaller quantities of antigen, thus 1 ng intradermally or 1 mug orally without adjuvant. Smaller challenge doses were not tried. Large primary doses of antigen (greater than 100 mug) presented by these routes were, on the other hand, found to be inhibitory to the production of secondary IgE responses, this effect being similar to that observed in previously reported intraperitoneal immunization experiments. By contrast with previous experiments, however, tertiary responses could be obtained following immunization by these routes, and we believe this to be reflection of the absorption of smaller and therefore less inhibitory quantities of antigen. Our results are discussed in relation to the control of IgE antibody production, current concepts of the control of antigen absorption through mucosal barriers, and possible implications of the genesis of naturally occurring IgE responses in man.

Adjuvants, Immunologic↗

PubMed1975

Hypersensitivity reactions in small intestine. I Thymus dependence of experimental 'partial villous atrophy'.

Rats infected with the intestinal nematode Nippostrongylus brasiliensis have crypt hyperplasia with villous atrophy in affected areas of the small intestine. In thymus-deprived (B) rats the course of infection is prolonged but, despite the presence of many worms in the intestinal lumen, villi and crypts appear largely normal. This suggests that the tissue damaged associated with N. brasilliensis infection is caused, not by the worms, but by a local thymus-dependent immune reaction. There is some evidence to implicate lymphocytes rather than antibodies in this reaction. It is already know that T-cell-associated damage to the small intestine, such as occurs in allograft rejection, produces subtotal villous atrophy. The present findings suggest that when T cell react locally with helminth antigens a similar type of damage occurs. The presence of a local cell-mediated immune reaction may be the common factor which causes villous atrophy and crypt hyperplasia in many small intestinal diseases, eg, viral enteritis, giardiasis, cow's milk allergy, and coeliac disease.

Animals↗

PubMed1974