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The time course of biological and immunochemical allergy states induced by anisakis simplex larvae in rats
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Summary
Oral infection by Anisakis simplex third stage larvae (L3) frequently gives rise to an allergic response. To comprehend the allergic and immune responses induced by L3, we investigated the kinetics of specific antibody isotype expression and the time course of biological and immunochemical allergy states using sera prepared from rats orally infected with L3 twice, with an interval of 9 weeks between infections. Biological and immunochemical allergy states were analysed by RBL-2H3 exocytosis and by indirect ELISA for IgE, respectively. The peak IgM at reinfection (RI) was comparable or similar to that at primary infection (PI) both in levels analysed by indirect ELISA and in antigen recognition analysed by Western blot. IgG1 and IgG2a levels were higher and showed accelerated kinetics after RI vs. after PI. However, the level of IgG2b was substantially lower than that of IgG2a. Peak immunochemical and biological allergy states for RI were higher and were reached faster than those for PI. The peak biological allergy state was observed at 1 week postreinfection and this occurred sooner than that for the peak immunochemical allergy state found at 2 weeks postreinfection. Our analysis of the relationship between specific IgE avidity and biological allergy state did not show any meaningful correlation. These results suggest that the allergic response induced by L3 oral infection is predominantly caused by reinfection and that this is accompanied by an elevated IgM level, which further suggests that the biological allergy state might not be related to specific IgE avidity.
Title: The time course of biological and immunochemical allergy states induced by anisakis simplex larvae in rats
Description:
Summary
Oral infection by Anisakis simplex third stage larvae (L3) frequently gives rise to an allergic response.
To comprehend the allergic and immune responses induced by L3, we investigated the kinetics of specific antibody isotype expression and the time course of biological and immunochemical allergy states using sera prepared from rats orally infected with L3 twice, with an interval of 9 weeks between infections.
Biological and immunochemical allergy states were analysed by RBL-2H3 exocytosis and by indirect ELISA for IgE, respectively.
The peak IgM at reinfection (RI) was comparable or similar to that at primary infection (PI) both in levels analysed by indirect ELISA and in antigen recognition analysed by Western blot.
IgG1 and IgG2a levels were higher and showed accelerated kinetics after RI vs.
after PI.
However, the level of IgG2b was substantially lower than that of IgG2a.
Peak immunochemical and biological allergy states for RI were higher and were reached faster than those for PI.
The peak biological allergy state was observed at 1 week postreinfection and this occurred sooner than that for the peak immunochemical allergy state found at 2 weeks postreinfection.
Our analysis of the relationship between specific IgE avidity and biological allergy state did not show any meaningful correlation.
These results suggest that the allergic response induced by L3 oral infection is predominantly caused by reinfection and that this is accompanied by an elevated IgM level, which further suggests that the biological allergy state might not be related to specific IgE avidity.
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