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Influence of malaria on a pre-existing antibody response to heterologous antigens
Abstract:
Swiss mice were immunized with various antigens: polyvinylpyrrolidone (PVP), human serum transferrin (HST), bovine serum albumin (BSA) or tetanus toxoid (TT). Fifteen days after the last injection of antigen, the mice were infected with Plasmodium chabaudi AJ. Two weeks after the beginning of malarial infection, parasitaemia became latent and total gammaglobulin levels, as well as IgG and IgM levels, were significantly increased. At that period the antigen-binding capacity (ABC) and the total antigen-binding Sites (Abt) were determined for PVP, HST and BSA. It appeared that the ABC and Abt of anti-HST or anti-BSA antibodies were lower than those of corresponding uninfected controls. With regard to anti-PVP antibodies, only the Abt was modified after infection, but not the ABC. The evolution of anti-TT Ab levels determined by a solid-phase assay with 125I-TT was as above with a marked decrease on and after the 4th week of infection. Injection of low-density lipoproteins (LDL) from day-9-infected mice to TT-immunized mice significantly reduced anti-TT antibody levels. At similar doses, LDL from normal mice did not induce an inhibitory effect. At mouse-equivalent-dose, LDL from infected mice revealed an inhibitory effect compared to LDL from uninfected controls. Our results suggest that LDL from P. chabaudi-infected mice can exert an immunoregulatory role and thus could explain part of the immune impairment observed during the infective process. Moreover, from the present data it might be postulated that the hypergammaglobulinaemia of P. chabaudi infection does not result from a parasite-potentiating effect on a pre-existing antibody response.
Insights
Malaria infection in mice alters antibody responses and increases gammaglobulin levels. Low-density lipoproteins from Plasmodium chabaudi-infected mice suppress antibody production, suggesting an immunoregulatory role in malaria.
Area of Science:
- Immunology
- Parasitology
- Biochemistry
Background:
- Malaria infections are known to cause significant immune dysregulation.
- Understanding the mechanisms behind immune impairment during parasitic infections is crucial for developing effective treatments.
- The role of specific molecular factors in modulating immune responses during Plasmodium chabaudi infection requires further investigation.
Purpose of the Study:
- To investigate the impact of Plasmodium chabaudi infection on antibody responses in Swiss mice.
- To determine the effect of low-density lipoproteins (LDL) from infected mice on antibody production.
- To explore the potential immunoregulatory role of LDL during malaria.
Main Methods:
- Mice were immunized with various antigens (PVP, HST, BSA, TT) and subsequently infected with Plasmodium chabaudi AJ.
- Antibody levels, antigen-binding capacity (ABC), and total antigen-binding sites (Abt) were measured.
- The effect of LDL from infected and uninfected mice on antibody responses was assessed in vivo.
Main Results:
- Plasmodium chabaudi infection led to increased gammaglobulin, IgG, and IgM levels, with latent parasitemia.
- Antibody binding capacity and sites for anti-HST and anti-BSA were reduced post-infection.
- LDL from infected mice significantly suppressed anti-tetanus toxoid antibody levels, unlike LDL from normal mice.
Conclusions:
- Low-density lipoproteins from Plasmodium chabaudi-infected mice exhibit immunoregulatory properties.
- These LDL may contribute to the immune impairment observed during malaria infection.
- Hypergammaglobulinemia in P. chabaudi infection might not stem from a direct parasite-enhancing effect on antibody responses.