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Cell-mediated immune responses (CMIR) to Rhinosporidium seeberi in mice

S Jayasekera1, S N Arseculeratne, D N Atapattu

  • 1Animal Centre, Medical Research Institute, Colombo, Sri Lanka.

Mycopathologia
|January 5, 2002
PubMed

Insights

This study investigated cell-mediated immunity to Rhinosporidium seeberi, the cause of rhinosporidiosis. Researchers found that R. seeberi extracts induced a delayed-type hypersensitivity (DTH) response in mice, similar to other known antigens.

Area of Science:

  • Immunology
  • Parasitology
  • Mycology

Background:

  • Rhinosporidiosis is a fungal infection caused by Rhinosporidium seeberi.
  • There is a lack of data on cell-mediated immune responses to R. seeberi in experimental models.
  • Understanding the immune response is crucial for developing treatments and vaccines.

Purpose of the Study:

  • To investigate the cell-mediated immune response to Rhinosporidium seeberi in a mouse model.
  • To characterize the delayed-type hypersensitivity (DTH) response induced by R. seeberi antigens.
  • To determine the effect of pre-treatment duration on DTH reactivity.

Main Methods:

  • Quantitative mouse foot-pad model used to assay DTH response.
  • Histological examination to confirm DTH reactions.
  • Use of sonically disintegrated endospores and sporangia of R. seeberi as antigens.
  • Comparison with sheep red blood cells (SRBC) as a positive control.

Main Results:

  • Sonicated R. seeberi endospores/sporangia induced significant DTH responses in sensitized mice.
  • The DTH response intensity and histological profile were comparable to SRBC-induced responses.
  • Anti-rhinosporidial antibodies were induced.
  • Soluble antigens in filtrates failed to elicit a DTH response but induced antibody production.
  • Prolonged pre-treatment with R. seeberi antigens decreased DTH reactivity.

Conclusions:

  • R. seeberi antigens can induce a DTH cell-mediated immune response in mice.
  • Both cellular and humoral immune responses can be generated against R. seeberi.
  • The duration of antigen exposure influences DTH reactivity, with prolonged exposure potentially leading to suppression.

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