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INHIBITION OF CYCLOOXYGENASE-1 AND CYCLOOXYGENASE-2 IMPAIRS TRYPANOSOMA CRUZI ENTRY INTO CARDIAC CELLS AND PROMOTES DIFFERENTIAL MODULATION OF THE INFLAMMATORY RESPONSE
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Resumen en ingles
The intracellular protozoan parasite Trypanosoma cruzi is the etiologic agent of Chagas disease, a serious disorder that affects
millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite’s life
cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host’s cyclooxygenase
(COX) enzymes during T. cruzi invasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib)
caused marked inhibition of T. cruzi infection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory
drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO
and interleukin-1 and decreased production of transforming growth factor (TGF- ) by cells. Taken together, these results
indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruzi activity in cardiac cells, and they provide a
better understanding of the influence of TGF- -interfering therapies on the innate inflammatory response to T. cruzi infection
and may represent a very pertinent target for new therapeutic treatments of Chagas disease.
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