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Genetic control of streptococcus-induced hepatic granulomatous lesions in mice

C Y Chen1, S A Cohen, M B Zaleski

  • 1Department of Microbiology, State University of New York, Buffalo 14214.

Immunogenetics
|January 1, 1992
PubMed

Insights

Mice with specific H-2 haplotypes show varying susceptibility to Streptococcus pyogenes-induced liver granulomas. Genetic mapping suggests a resistance gene near tumor necrosis factor (TNF) genes.

Area of Science:

  • Immunology
  • Genetics
  • Microbiology

Background:

  • Streptococcus pyogenes infections can lead to granulomatous inflammation.
  • Murine models are crucial for studying host-pathogen interactions and genetic influences on disease susceptibility.

Purpose of the Study:

  • To investigate the genetic basis of susceptibility and resistance to Streptococcus pyogenes-induced hepatic granulomas in mice.
  • To identify the chromosomal location of genes controlling this immune response.

Main Methods:

  • Induction of hepatic granulomas in mice using Streptococcus pyogenes cell-wall material.
  • Phenotypic analysis of granuloma formation across different H-2 haplotypes (H-2b, H-2k, H-2d).
  • Genetic analysis using backcross and H-2-recombinant mouse strains to map the responsible gene(s).

Main Results:

  • Mice with H-2b and H-2k haplotypes were highly susceptible, developing numerous granulomas.
  • Mice with the H-2d haplotype exhibited resistance, forming significantly fewer granulomas.
  • Resistance was inherited as a dominant trait and mapped to a region between the S and D regions of the H-2 complex, overlapping with TNF and lymphotoxin genes.

Conclusions:

  • The H-2 haplotype significantly influences the susceptibility to Streptococcus pyogenes-induced hepatic granulomas.
  • The genetic locus controlling this response is located near the tumor necrosis factor (TNF) gene cluster, suggesting a role for TNF in regulating granuloma formation.

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