Worm kinetics and serum IgE in hooded lister rats infected with the acanthocephalan Moniliformis moniliformis and the nematode Nippostrongylus brasiliensis.

After infection with the intestinal helminths Moniliformis moniliformis or Nippostrongylus brasiliensis, worm-specific IgE first appeared in the serum rats between days 10 and 24 p.i., varying with host age, worm species and worm dose used. The rate of increase in specific IgE was comparable regardless of the worm species, infection dose or host age and a peak response was observed about 1 month after the sera turned positive. In the M. moniliformis infections, these events took place long before the beginning of worm expulsion on day 63 in high-dose (50 worms) infections, and potentiation of heterologous IgE was not observed. In contrast, IgE stimulation by N. brasiliensis infections was detected as potentiation of anti-ovalbumin IgE, anti-M. moniliformis IgE and total IgE. Most of the total IgE in the serum of M. moniliformis-infected rats was likely to be the worm-specific IgE. Anthelminthic removal of M. moniliformis revealed that the presence of residual worms was necessary to maintain worm-specific IgE production.

[Contribution to the knowledge of immunological relations between Moniliformis moniliformis Bremser, 1811 (Acanthocephala) and Rattus norvegicus Berkenhout, 1769, var. albinos (author's transl)]. / Contribution à la connaissance des relations immunologiques entre Moniliformis moniliformis Bremser, 1811 (acanthocephala) et Rattus norvegicus Berkenhout, 1769, var. albinos.

Cultured M. moniliformis (Acanthocephala) secrete and excrete antigenic substances. Immunoelectrophoretic analysis of these antigens revealed 14 lines of precipitation, 3 of which represent metabolic antigens. From the remaining 11 somatic antigens, 4 appear to be associated with the lemnisci. As shown by indirect immunofluorescence, specific antibodies predominantly bind to the lemnisci and to the worm's tegument. We therefore propose that metabolic antigens are either formed or stored in these tissues. Specific circulating antibodies have been demonstrated in rats infected with M. moniliformis using indirect immunofluorescence. Reinfection resulted in increased and prolonged antibody production (secondary response). Further immunofluorescence studies indicate that M. moniliformis is able to modify its antigenic set up, particularly between the 3rd and 5th weeks of infection. The immune reaction of the host against this parasite presumably leads to expulsion of worms starting 4 weeks after infection in females and 8 weeks after infection in males. Primary infection of rats with 30 worms elicits immunity. In fact, in preinfected rats only 26.6% of the transferred parasites could settle as compared to 66% following primary infection.

Evasion of the insect immune response by Moniliformis dubius (Acanthocephala): further observations on the origin of the envelope.

The envelope around larvae of Moniliformis dubius appears to protect the parasite against immune recognition and encapsulation by the insect host's haemocytes. The origin of this envelope has been the subject of controversy although most evidence suggests it is parasite-derived. If host-derived, the envelope would be expected to share surface properties with host tissue. Thus, experiments were undertaken, transplanting parasites and host tissue to other insects and using haemocytic encapsulation as an assay for immune recognition, in order to compare the response to host tissue and to the parasite's envelope. Parasites without their envelopes, and pieces of tissue (ventral nerve cord) from the experimental host (the locust Schistocerca gregaria) were recognized as foreign and encapsulated in the cockroach, Periplaneta americana. The majority of parasites with their envelopes were unencapsulated or only partially encapsulated on transfer to their normal host, P. americana, indicating that the envelope does not have surface similarity to locust tissue. Cockroach-derived parasites with or without envelopes were not encapsulated in S. gregaria, suggesting that the larva itself can evade or inhibit the locust's recognition mechanism. However, since larvae which develop in S. gregaria are enclosed in an envelope, the formation of the envelope would seem to be an inherent feature of the parasite's development.