Modulation of cellular and humoral immunity, and disease manifestation during onset of patency in Brugia pahangi-infected dogs.
Recently, it has become possible to obtain as predicted disease manifestation in selectively bred dogs infected with the naturally occurring lymphatic nematode, Brugia pahangi. In this study, an attempt was made to correlate limb oedema with dynamic changes in immune cell responses occurring in the lymph node at the site of infection during onset of patency. Three litters of dogs were selectively bred; one for the expression of clinical disease, one for the lack of expression of clinical disease and one was of non-specific phenotype. Lymph node cells from 10 of 11 dogs showed a parasite-specific proliferative response at 4-6 weeks post-infection (p.i.), before the onset of patency. In six of 11 dogs, a loss of proliferative response to BpA in the infected node cells was detected around the time of onset of patency. In contrast, there was no reduction in the proliferative response to the mitogen phytohaemagglutinin (PHA). The proliferative response to BpA by unresponsive node cells could be restored by addition of substimulatory amounts of murine or human recombinant interleukin-2 (IL-2) to the culture medium. However, there was no correlation between the proliferative response of lymph node cells from infected limbs and the expression of clinical disease. Similarly, when in vitro parasite-specific antibody production by infected lymph node cells was examined, antibody production manifested by all dogs at 5 weeks p.i. was markedly changed at 8 weeks p.i., but these changes did not correlate with clinical disease. This lack of correlation indicates that the immune response to lymphatic filarial infection, as measured in this study, does not necessarily result directly in disease manifestation, and that other genetically determined factors may influence both the parasite-specific immune response and the clinical outcome of infection.
Schreuer
D
D
Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
Hammerberg
B
B
D000818:Animals; D000909:Antibodies, Helminth / Q000276:immunology; D017179:Brugia pahangi / Q000276:immunology*; D004283:Dog Diseases / Q000276:immunology* / Q000473:pathology; D004285:Dogs; D005260:Female; D005368:Filariasis / Q000276:immunology / Q000473:pathology / Q000662:veterinary*; D005434:Flow Cytometry; D007111:Immunity, Cellular; D007074:Immunoglobulin G / Q000096:biosynthesis; D007376:Interleukin-2 / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology / Q000473:pathology; D008297:Male; D008934:Mitogens
D000909:Antibodies, Helminth; D007074:Immunoglobulin G; D007376:Interleukin-2; D008934:Mitogens