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Contact sensitivity responses in mice infected with Trypanosoma cruzi
Abstract:
Mechanisms of depression of contact sensitivity responses in C57BL/10 mice infected with Trypanosoma cruzi were studied. Cellular involvement during sensitization with oxazolone was investigated in mice acutely infected with T. cruzi. Contact sensitivity was not expressed in mice during the latter stages of the acute infection. Spleen cells from sensitized, infected mice which were unable to respond to oxazolone could confer contact sensitivity upon normal syngenic mice as effectively as spleen cells from uninfected, sensitized donors. The ability of mice infected with T. cruzi to respond to an eliciting dose of oxazolone was significantly improved when macrophages from normal syngenic donors were administered to them at the time of skin test. When either normal or infected mice were used as recipients of lymphocytes from sensitized donors, the normal mice responded significantly better than did infected mice after administration of an eliciting dose of oxazolone. An increase in pyroninophilic cells was observed in draining lymph nodes after application of a sensitizing dose of oxaxolone to the ears of either normal or acutely infected mice. These results indicate that suppression of contact sensitivity during acute T. cruzi infection is directed toward the efferent arm rather than the afferent arm of the response.
Insights
Trypanosoma cruzi infection suppresses contact sensitivity responses in mice. This immune suppression affects the efferent arm of the response, not the initial sensitization phase.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- Trypanosoma cruzi infection, the causative agent of Chagas disease, can modulate host immune responses.
- Contact sensitivity (CS) is a T-cell mediated immune response crucial for defense against certain antigens.
Purpose of the Study:
- To investigate the mechanisms underlying the depression of contact sensitivity responses during acute Trypanosoma cruzi infection.
- To determine whether the immune suppression affects the afferent (sensitization) or efferent (elicitation) phase of the contact sensitivity response.
Main Methods:
- Mice infected with Trypanosoma cruzi were sensitized and challenged with oxazolone to assess contact sensitivity.
- Spleen cells and lymphocytes from infected and uninfected mice were transferred to assess their functional capacity.
- Macrophage administration was used to evaluate its effect on elicitation of contact sensitivity.
Main Results:
- Contact sensitivity responses were significantly suppressed in mice during the acute phase of Trypanosoma cruzi infection.
- Spleen cells from sensitized, infected mice could still transfer contact sensitivity, indicating the afferent arm was intact.
- Administration of normal macrophages improved the elicitation of contact sensitivity in infected mice.
- Infected mice showed impaired elicitation of contact sensitivity compared to normal mice when receiving lymphocytes from sensitized donors.
Conclusions:
- The suppression of contact sensitivity during acute Trypanosoma cruzi infection is primarily directed at the efferent arm of the immune response.
- The findings suggest a defect in the elicitation phase, potentially involving macrophage or effector cell function, rather than a failure in sensitization.
