Genetic control of eosinophilia. Mouse strain variation in response to antigens of parasite origin.

Strain variation in capacity to develop peripheral blood eosinophilia was observed in inbred NIH and C57BL/10 (B10) mice exposed to parasite antigens by infection or by parenteral injection in Freund's complete adjuvant. NIH mice were good responders, showing rapid development of high eosinophil counts, B10 mice were low responders. The difference in response phenotype was independent of the parasite used for infection (Trichinella spiralis or Nematospiroides dubius) and of the antigen used for injection (T. spiralis larval antigen or Limulus haemocyanin). Pre-treatment of T. spiralis infected mice with low doses of cyclophosphamide (150 mg/kg) or restriction of the duration of infection to 7 days by anthelmintic treatment did not enhance the response of B10 mice. Thus no evidence was found that the poor response phenotype of B10 during T. spiralis infection reflected any active suppressive mechanisms developed during the adult or muscle larval phases of infection. Demonstration that eosinophilia is induced primarily by the intestinal phase allows comparison with other parameters of the immune response induced by the adult worms, namely intestinal mastocytosis and worm expulsion. From this comparison it is concluded that the low eosinophil response phenotype of B10 mice may reflect a generalized deficiency in the response of bone marrow derived precursor cells to factors of T lymphocyte origin. The significance of genetically determined variation in eosinophil responsiveness is discussed in relation to the development of protective immune or pathological responses to parasite infection.