Schistosoma mansoni: evidence that vascular abnormalities correlate with the 'non-permissive' trait in 129/Ola mice

A A Elsaghier1, D J McLaren

  • 1Division of Parasitology, National Institute for Medical Research, Mill Hill, London.

Parasitology
|December 1, 1989
PubMed

Insights

Vascular casting revealed distinct differences in mouse liver and lung vasculature. Some 129/Ola mice exhibited reduced peripheral vessels, a trait linked to Schistosoma mansoni infection susceptibility.

Area of Science:

  • Comparative anatomy
  • Immunology
  • Parasitology

Background:

  • The pulmonary and portal vasculature are critical for organ function and parasite migration.
  • Mouse strain differences can influence susceptibility to parasitic infections like Schistosoma mansoni.

Purpose of the Study:

  • To investigate the vascular anatomy of naïve mice from 129/Ola and CBA/Ca strains.
  • To correlate vascular differences with the 'non-permissive trait' observed in 129/Ola mice infected with Schistosoma mansoni.

Main Methods:

  • Vasculature casting technique using pigmented vinylite resin.
  • Tissue digestion with potassium hydroxide (KOH) to isolate vascular casts.
  • Analysis of cast morphology for vessel number, branching, and extent.
  • Correlation with Schistosoma mansoni infection status and pathology.

Main Results:

  • CBA/Ca mice displayed numerous, highly branched peripheral arterial and portal vessels.
  • 70-80% of naïve 129/Ola mice showed significantly reduced and truncated peripheral vessels.
  • The remaining 20-30% of 129/Ola mice had normal vasculature, similar to CBA/Ca mice.
  • Infected 129/Ola mice exhibited similar vascular segregation, correlating with the 'non-permissive trait' and Schistosoma mansoni infection.

Conclusions:

  • Significant vascular anatomical variations exist between 129/Ola and CBA/Ca mouse strains.
  • These vascular alterations in 'non-permissive' 129/Ola mice may facilitate abnormal parasite migration.
  • The findings provide insights into host-parasite interactions and disease pathogenesis.

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