Relationship between Acquired Resistance, Portal Hypertension, and Lung Granulomas in Ten Strains of Mice Infected with Schistosoma Mansoni *

Dean, David A.; Bukowski, Maria A.; Cheever, Allen W.

doi:10.4269/ajtmh.1981.30.806

Cited by 54 publications

(27 citation statements)

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“…Mouse strain differences have been demonstrated with regard to S. mansoni pathology and resistance to reinfection, although our results do not reflect the lower resistance to reinfection shown earlier in C57BL/6 mice (Colley and Freeman, 1980; Dean et al, 1981). A proposed mechanism for resistance, the shunting of schistosomula from the liver back into the venous system, appears be a result of egg-induced pathology or mouse strain specific structure of hepatic-portal vasculature (reviewed in Wilson, 2009) rather than a specific immunological response to infection.…”

contrasting

confidence: 94%

Host Mouse Strain Is Not Selective for a Laboratory Adapted Strain of Schistosoma mansoni

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Liu

Prasad

et al. 2011

Journal of Parasitology

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We genotyped pooled adult worms of Schistosoma mansoni from infected CF1, C57BL/6, BALB/c, and BALB/c interferon gamma knockout mice in order to investigate if mouse strain differences selected for parasite genotypes. We also compared differentiation in eggs collected from liver and intestines to determine if there was differential distribution of parasite strains in the vertebrate host that might account for any genotype selection. We found that mouse strains with differing immune responses did not differ in resistance to infection and did not select for parasite genotypes. S. mansoni genotypes were also equally distributed in tissues and there was no difference between adult and egg allele frequencies. Differing immune responses in these mouse strains does not significantly affect the degree or the nature of host resistance to schistosomes.

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contrasting

confidence: 94%

Host Mouse Strain Is Not Selective for a Laboratory Adapted Strain of Schistosoma mansoni

Blank

Liu

Prasad

et al. 2011

Journal of Parasitology

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“…Marked differences in the proportion of S. mansoni cercariae which ultimately develop into adult worms have been noted among different mouse strains (Bickle et , Colley et al 1980, Dean et al 1981, Deelder et al 1978. This variability could be due to parasite factors such as heterogeneity in the capacity of cercariae to mature (Smith & Clegg 1979), host attributes which limit development of the helminth or to a combination of the two.…”

Section: Discussionmentioning

confidence: 99%

“…susceptibility to primary infection) is related to the genetic background of the host (Bickle et al 1980, Colley & Freeman 1980, Deelder, Class & DeVries 1978. Dean, Bukowski & Cheever (1981) recently measured the magnitude of the granulomatous reactions surrounding eggs deposited in the lungs and the level of portal hypertension (pathology) in several inbred lines of mice. These findings were then related to the reduction in expected adult worm burdens induced by previous exposure to S. mansoni (acquired resistance).…”

Section: Introductionmentioning

confidence: 99%

Genetic‐linked variation in susceptibility of mice to Schistosomiasis mansoni

Fanning

Kazura

1984

Parasite Immunology

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Genetic dependence of susceptibility to primary infection with Schistosoma mansoni was studied in inbred strains of mice. Eight weeks after the subcutaneous injection of 30 cercariae, C3H/HeJ (H-2k), DBA/1J (H-2q) and BALB/cJ (H-2d) had the highest number of adult worms per animal (8.0-9.8); DBA/2J (H-2d) and 129/J (H-2b) had an intermediate number (6.2-6.4); C57BL/6J (H-2b), BUB/BnJ (H-2q) and CBA/CaJ (H-2k) had the lowest number (3.4-4.0). Studies in congenic mice further suggested that genes within the major histocompatibility complex do not have a major influence on determining the ability of schistosomes to develop into mature adult worms. Results of experiments in which adult worm loads in the F1 generation of C57BL/6J X BALB/cJ were compared with F1 X C57BL/6J and F1 X BALB/cJ backcrosses are consistent with homozygosity for a polygenic phenomenon controlling susceptibility to primary S. mansoni infection. Strain associated differences in parasite development appeared to be related to host defense processes directed against maturing adult worms.

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“…A/J mice incur this complication early in infection and at low infection intensities (Dean et al 1981, Colley & Freeman 1983) while C57BL/6 and BALB/c mice are unusually resistant to death after infection. The mechanism of intestinal hemorrhage in mice is unrelated to gastrointestinal hemorrhage in humans with schistosomiasis.…”

Section: Causes Of Deathmentioning

confidence: 99%