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Prophylactic and therapeutic immune reconstitution of SCID mice infected with Encephalitozoon cuniculi

J Hermánek1, B Koudela, Z Kucerová

  • 1Institute of Parasitology, Academy of Sciences of the Czech Republic, Ceské Budĕjovice.

Folia Parasitologica
|January 1, 1993
PubMed

Insights

Adoptive transfer of spleen cells confers resistance against Encephalitozoon cuniculi infection in severe combined immunodeficient (SCID) mice. This reconstitution restored protective immunity and humoral responses against opportunistic microsporidiosis.

Area of Science:

  • Immunology
  • Parasitology
  • Infectious Diseases

Background:

  • Severe combined immunodeficient (SCID) mice are susceptible to lethal Encephalitozoon cuniculi infections, mirroring opportunistic microsporidiosis in immunocompromised humans.
  • SCID mice lack adaptive immunity, making them a model to study the role of specific immune components in host defense.

Purpose of the Study:

  • To investigate the protective effects of adoptive immune cell transfer on E. cuniculi infection in SCID mice.
  • To evaluate the restoration of humoral immune responses following reconstitution with naive or immune spleen cells.

Main Methods:

  • SCID mice were reconstituted with naive or immune BALB/c spleen cells prior to or after infection with E. cuniculi.
  • Parasite load, clinical signs, survival rates, and parasite-specific antibody production (IgG) were assessed.

Main Results:

  • Complete resistance was observed in SCID mice reconstituted with naive spleen cells before infection.
  • Partial protection (40% survival) was achieved when SCID mice were reconstituted with immune lymphocytes after infection.
  • Reconstituted SCID mice exhibited restored humoral immune responses, including high levels of parasite-specific IgG antibodies, comparable to immunocompetent mice.

Conclusions:

  • Adoptive transfer of spleen cells can restore protective immunity against E. cuniculi in SCID mice.
  • Both naive and immune spleen cells can reconstitute humoral immunity, suggesting the importance of B cell function and antibody production in controlling microsporidiosis.

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