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At least 163 records · Page 9Linked to original sources
PubMed1990

Necator americanus in the mouse: histopathological changes associated with the passage of larvae through the lungs of mice exposed to primary and secondary infection.

The mouse/Necator americanus model was studied to assess the histopathological changes that occur in the lungs following primary and secondary exposure to infective larvae. Groups of BALB/c mice were infected percutaneously and killed on various days post infection. Parasite numbers were counted, the bronchoalveolar leukocyte response was quantified and histological sections of lung material were examined for evidence of host protective inflammatory reactions. An increase in the inflammatory infiltration was observed between days 5 and 9 in both primary and secondary infections but was considerably more intense in re-infected animals. This involved a marked change in the character of the infiltrate, particularly in the number of eosinophils that were recovered in lavage fluid. More worms were trapped in the lungs of challenged mice, as assessed through their inability to escape from lung material incubated in vitro. Overall, the results were found to be compatible with the development of acquired resistance to N. americanus and the expression of host protective immunity during the development of challenge-infection larvae in the lungs.

Animals↗
PubMed1995

Glutathione S-transferase (GST) expression in the human hookworm Necator americanus: potential roles for excretory-secretory forms of GST.

The difficulty in demonstrating protective immunity to human gastro-intestinal nematodes is thought to be a consequence of the expression of defences by the parasites directed against the toxic metabolites of leukocytes produced during inflammation (Brophy and Pritchard, 1992a). Parasite glutathione S-transferases (GSTs) may provide part of this defence by detoxifying the secondary products of lipid peroxidation produced via immune initiated free-radical attack on host or parasite membranes (Brophy and Pritchard, 1994; Taylor et al., 1988). Neutralisation of parasite immune defence components could tip the molecular balance in favour of the immune response during chronic infections. For example, GSTs have been extensively investigated from the digenean parasites Schistosoma and Fasciola hepatica and provide protection in animal-model systems (Mitchell, 1988; Wijffels et al., 1991). In contrast, although GSTs have been initially characterised in filarial nematodes (Salinas et al., 1994; Leibau et al., 1994; Jaffe and Lambert, 1986), there is limited information on GSTs from human gastro-intestinal nematode parasites. We were particularly interested in analysing the products of hookworms for evidence of the presence of excretory-secretory forms of this putative immune defence protein.

Animals↗
PubMed1992

Cross-reactivity between Necator americanus and Schistosoma mansoni in mice.

Poly-parasitism is common in endemic communities and reactivity of sera from hookworm-infected patients against schistosomular antigens has been reported. Protective cross-immunity between N. americanus and S. mansoni was investigated in NIH and BALB/c mice. Protective resistance to homologous challenge with both parasites was confirmed in this model, however, functional immunity to heterologous challenge was not demonstrated. Sera from animals which had received homologous challenge with N. americanus and from hookworm-infected mice, which had previously been exposed to radiation-attenuated S. mansoni, exhibited an enhanced IgGAM response to infective stage N. americanus somatic antigens. The implications of these results with respect to serodiagnosis are discussed.

Animals↗
PubMed1994

Resistance of the hookworms Ancylostoma ceylanicum and Necator americanus to intestinal inflammatory responses induced by heterologous infection.

Experiments were carried out to ascertain whether the acute inflammatory phase of the intestinal response of hamsters to infection with Trichinella spiralis would adversely affect hookworms in concurrently infected animals. The survival and growth of hookworms were unaffected. However, the presence of hookworms reduced the establishment of T. spiralis, the initial growth of female worms and their fecundity. The expulsion of T. spiralis was also significantly slower in concurrently infected animals and there was significant depression of the serum IgG antibody response to muscle stage and adult worm antigens of T. spiralis in concurrently infected animals. These results are discussed in relation to the chronicity of human hookworm infections.

Acute Disease↗