Humoral immune responses to soluble somatic extracts of Dipetalonema viteae adult worms infected hamsters.

The present study examined the serum IgG1 and IgM antibody responses of infected hamsters to unfractionated and fractionated soluble somatic (SS) antigens of adult Dipetalonema viteae. Male and female adult worms were homogenized in a French pressure cell and the SS proteins extracted with 0.375 M Tris-glycine buffer. Serum IgG1 and IgM antibody responses in D. viteae infected with LVG, PD4 and CB hamster strains to the male and female unfractionated SS proteins were measured by an indirect enzyme linked immunosorbent assay (ELISA). Serum IgG1 antibody responses to the SS proteins were similar in all three strains of hamsters during the course of infection. There was no correlation between the level of IgG1 antibody and the onset of microfilariae clearance. The serum IgM antibody response was similar in both outbred LVG and inbred PD4 hamster strains. A lower IgM antibody response was found in CB hamsters and could be related to the failure of this hamster strain to eliminate microfilariae. The SS proteins of male and female adult worms were fractionated by preparative flat-bed isoelectric focusing on granulated gels (PIEF) to yield 8 and 7 fractions, respectively. The comparative antigenicity of the PIEF fractions from the SS proteins was measured by ELISA, using hyperimmune serum from LVG hamsters and rabbit antihamster IgG1-and IgM-alkaline phosphatase conjugates. No difference in ELISA reactivity was noted among the 8 and 7 PIEF fractions from male and female SS proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Lymphocyte response in mice infected with the Indonesian and Formosan strains of Schistosoma japonicum to concanavalin A, and to worm and egg antigens.

Cultures of splenocytes from mice infected with the Formosan and Indonesian strains of Schistosoma japonicum demonstrated a blastogenic response to concanavalin A (Con-A), adult worm antigen (SAA) and soluble egg antigen (SEA). The incorporation of tritiated thymidine was significantly greater for lymphocytes from mice infected with the pathogenic Indonesian strain than for lymphocytes from mice infected with the non-pathogenic Formosan strain in response to SAA; the responses also increased with duration of infection. The response to SEA, however, was only greater for the Indonesian strain, than that for the Formosan strain, at six weeks and the differences in response not statistically significant at five, seven, and nine weeks post-infection. The differences may have been associated with the number of worms developing in the mice since the adult worm recovery for the Indonesian strain was nearly twice that of recoveries from mice infected with the Formosan strain.