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J A Clegg

Publications and source records attributed to J A Clegg.

At least 37 records · Page 2Linked to original sources
PubMed1984

Monoclonal antibodies demonstrate similarity of surface antigens on different clones of Schistosoma mansoni schistosomula.

Previous work has demonstrated wide variation in the susceptibility of different clones of Schistosoma mansoni to resistance in mice induced by a small schistosome infection. Eight monoclonal antibodies directed against individual surface antigens of juvenile schistosomes (schistosomula) were used to determine the distribution of these antigens among clones of schistosomula. All eight antigens were detected on the surface membranes of the 32 clones of schistosomula tested. This result implies that polymorphism of schistosomula surface antigens is very unlikely to be the cause of the variation in susceptibility of different clones to resistance in mice. Absence of heterogeneity among surface antigens of schistosomula may facilitate experimental vaccination aimed against these putative target antigens.

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PubMed1984

Schistosoma mansoni: decay of resistance induced by gamma irradiated cercariae in the mouse.

The level of resistance induced by a single percutaneous infection of cercariae which had been previously exposed to 20 kr of gamma irradiation was compared in two strains of mice. Challenge cercariae were given at several time intervals after the preliminary immunization either to the same skin site as that used for immunization or to a previously unexposed skin site. No significant difference in resistance to infection was observed when a different skin site was used for the challenge. A higher degree of resistance to challenge was observed in CBA/Ca mice than in BALB/c mice. Immunity in both strains declined to about two thirds of the original level after six months and could not be detected when challenge cercariae were given 70 weeks after the single immunizing dose of irradiated cercariae.

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PubMed1982

Passive immunization of mice against Schistosoma mansoni with an IgM monoclonal antibody.

Two hybridomas secreting monoclonal IgM antibody to Schistosoma mansoni have been isolated following fusion of spleen cells from Balb/c mice immunized with living S. mansoni and NS1 myeloma cells. One monoclonal IgM antibody (WP66.4) mediated about the same level of passive protection against a challenge infection as immune serum from mice with a chronic S. mansoni infection. The other monoclonal antibody (WP66.2) did not give a significant level of passive protection. This result indicates that the effective monoclonal antibody recognizes an antigen which may be a valuable candidate for experimental vaccination. In vitro one monoclonal antibody (WP66.4) caused a much higher level of complement-dependent cytotoxicity than the other (WP66.2), suggesting a possible mechanism for the effect observed in vivo. With indirect immunofluorescence both monoclonal antibodies reacted with surface determinants on living S. mansoni schistosomula, adult worms and miracidia but these determinants were not detected on cercariae or lung schistosomula. Neither monoclonal antibody cross-reacted with S. haematobium schistosomula or Fasciola hepatica metacercariae, indicating a possible use for these reagents in differential diagnosis of S. mansoni infections.

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PubMed1981

Improved culture of Fasciola hepatica in vitro.

Metacercariae of Fasciola hepatica were excysted in a simple system based on the stimuli determined by Dixon (1966). Reproducibly high levels of excystment (70-80%) were obtained within 3h. Equal volumes of human serum and medium RPMI 1640 with 2% washed human red blood cells supported better growth in vitro than human serum diluted with ELac or NCTC 135. Reduced rates of growth were observed with serum concentrations lower than 50%. During culture over a period of 14 weeks some organisms in every culture grew to a length of 3 mm at a linear rate approximately one quarter of the growth rate in vivo (mouse). A few parasites suddenly began to develop more rapidly after six weeks in culture and reached 6-7 mm in length, comparable to the size of sexually mature Fasciola grown in mice. These cultured worms showed extensive development of the uterus, vitellaria, and testes with spermatozoa. The ovary remained rudimentary and egg formation did not occur.

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PubMed1980

Surface proteins of Schistosoma mansoni and their expression during morphogenesis.

Surface components of Schistosoma mansoni have been identified by lactoperoxidasecatalyzed iodination. Cercariae have a simple labeling pattern in comparison to schistosomula. Transformation of cercariae to schistosomula results in the loss of a low molecular weight material which may be the glycocalyx, and the appearance of many more labeled proteins. Mechanical conversion of cercariae to schistosomula requires subsequent incubation at 37 degrees C for more than 1 h to give the full surface-labeling pattern of schistosomula. The majority of proteins found on schistosomula appear to be present throughout the remaining part of the developmental cycle, although adult male worms had only low levels of these antigens, and female worms had virtually no detectable surface antigens. The low level of expression of schistosome antigen could be caused by adsorbed host antigen, although no evidence for adsorbed host protein was found, or by a reduced level of antigens present on the worm surface. The low level of schistosome antigen could have a role in the resistance of adult worms to the host's immune response.

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PubMed1979

Different levels of immunity to Schistosoma mansoni in the mouse: the role of variant cercariae.

Very variable levels of immunity to a second infection with Schistosoma mansoni were recorded in 7 strains of mice, 12--15 weeks following a small primary infection. When 2 or more strains of mice were assayed at the same time, less variation occurred within the experiment than between different experiments. This evidence suggested variation between pools of cercariae as the main cause of variability in immunity. In direct experiments in one strain of mouse, 2 different pools of cercariae stimulated widely different levels of immunity to the same challenge. Conversely, challenge infections drawn from different pools showed different susceptibility to immunity stimulated by the same primary infection. Individual clones of cercariae, from snails infected with single miracidia, showed a high level of susceptibility to immunity stimulated by a small bisexual infection, or were not susceptible at all. Antigenic polymorphism is the most likely explanation for the differences observed between clones of cercariae. However, indirect immunofluorescence showed the presence of at least 1 common antigen on the surface of schistosomula derived from different clones of cercariae and clone-specific antigens have not been detected.

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PubMed1976

Different levels of acquired immunity to Schistosoma mansoni in two strains of hamster.

A primary infection with schistosoma mansoni, of 5 or more weeks duration, stimulated a high level of resistance to a challenge infection in the WO outbred strain of golden hamster. In sharp contrast, the LGN strain showed no statistically significant immunity to reinfection in most experiments and where detected the level of resistance was only about half that observed in the WO strain. Immunity to reinfection was assayed with the lung recovery method which assesses resistance a few days after challenge and with the conventional perfusion assay which measures immunity 6 weeks after challenge. Wide differences in the immune response to S. mansoni in different strains of the same host species have not been reported previously.

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PubMed1976

Cross-immunity to Schistosoma mansoni and S. haematobium in the hamster.

Hamsters (WO strain) with a primary infection of Schistosoma mansoni or S. haematobium rapidly developed immunity to homologous challenge judged by the lung recovery assay. Immunity was detected at 4-5 weeks and reached a plateau 6 weeks after infection. Using this information, hamsters with an 8-week primary infection with S. mansoni or S. haematobium were tested for resistance to homologous reinfection and resistance to a challenge with the other species of schistosome. Primary infection with S. mansoni or S. haematobium conferred a high level of immunity to reinfection with either species of schistosome judged by the perfusion assay, involving recovery of adult worms 6-10 weeks following challenge. Estimation of the level of immunity with the lung recovery assay, 5 days after challenge, indicated that immunity due to a primary infection with S. mansoni acted at or before migration of the challenge through the lungs but immunity stimulated by a primary S. haematobium infection was only partially effective at the lung stage and substantial destruction of challenging organisms occurred at a later stage of development. Antibodies in immune sera of hamsters with a primary S. mansoni or or S. haematobium infection were shown to bind to common antigens on the surface of young schistosomula of either species by u.v. microscopy using as detecting agent a fluorescein-labelled rabbit antiserum directed against hamster globulins.

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PubMed1976

Culture of Schistosoma haematobium in vivo and in vitro.

The maximum rate of development of Schistosoma haematobium in the hamster was determined by examination of the most advanced worms recovered at short intervals throughout the course of development. In culture S. haematobium developed at the same rate as in the hamster up to day 31 when pairing first occurs and male worms produce some spermatozoa. In vitro males formed some spermatozoa but pairing did not take place and, probably for this reason, females did not complete sexual maturation as occurs in the host between days 57-65. Somatic growth continued in vitro and at 70 days male worms had achieved almost the same length as in the hamster at this time. The culture medium, previously used for S. mansoni, consisted of equal volumes of serum and Earle's balanced saline with a final concentration of 0.25% lactalbumin hydrolysate, 100 units/ml penicillin, 100 mug/ml streptomycin and 1% rbc. The best culture results were obtained with one particular human serum; seven other human sera gave a wide range of growth support. The samples of baboon, rhesus monkey or foetal calf sera tested provided little or no growth support but prolonged survival was possible in all the sera.

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PubMed1976

Acquisition of human blood group antigens by Schistosoma mansoni.

Juvenile forms of Schistosoma mansoni (schistosomula) have been cultured in human blood of various specificities and tested for the presence of blood group substances on their surfaces. The tests employed were survival following transfer into rhesus monkeys immunized against human blood substances, mixed agglutination reactions, and immunofluorescence. A, B, H AND Lewisb+ antigens were expressed at the surface when the parasites were cultured in blood of appropriate specificities. Rhesus, M N S, AND Duffy antigens could not be detected on the parasite surface following culture. The evidence suggests that the expressed blood group antigens are of host origin and are acquired by the parasite during culture, probably in the form of glycolipids or megaloglycolipids. It is likely that these substances are also acquired by parasites in the bloodstream of man. They may serve to mask surface parasite antigens, and so enable schistosomes to evade parasite-specific humoral or cellular immune responses.

ABO Blood-Group System↗
PubMed1975

Acquisition of host antigens by young Schistosoma mansoni in mice: correlation with failure to bind antibody in vitro.

Young schistosomes collected after penetration through isolated mouse skin (3 h schistosomula) were cultured in medium containing immune rhesus monkey serum with a high titre of antibody known to kill schistosomula in the presence of complement. Morphological signs of damage in electron micrographs were confined to the surface tegument of the schistosomula. Antibodies in immune rhesus serum were shown to bind to the surface membrane of 3 h schistosomula using an antibody-enzyme bridge technique involving labelling with horseradish peroxidase and histochemical localization of the enzyme at the ultrastructural level. Schistosomula recovered from the lungs of mice 4 days after infection did not bind monkey antibodies at the surface and these 4-day schistosomula are not susceptible to damage by immune serum in vitro. Mouse erythrocyte antigens were detected on the surface of 4-day schistosomula using an appropriate antibody-enzyme bridge but these host antigens could not be found on 3 h schistosomula. This correlation between the presence of mouse host antigens on the surface of schistosomula and the inability of immune monkey antibodies to bind to the surface membrane is consistent with the hypothesis that host antigens are acquired by young schistosomes and serve to protect the surface membrane against antibody-mediated damage.

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