Late experimental amebic liver abscess in hamster is inhibited by cyclosporine and N-acetylcysteine.

During early experimental amebic liver abscess in hamsters (EALAH), acute inflammation is primarily responsible for tissue damage. However, during the late stages of this process, the relative contribution to tissue destruction of both parasite factors and host response is unknown. In the present work, the role of the cellular immune response in tissue damage during EALAH is explored by using the immunosuppressor drug cyclosporine A (CsA). CsA treatment inhibits tissue damage after 72 h (but not at 24 h). Also, many well-preserved parasite clusters with minimal or no leukocyte influx and with minimal or no tissue destruction characterize the late stage of the process (7 days). The same results are observed with the immunosuppressor tacrolimus, but not with sirolimus; the latter drug does not cause immunosuppression in hamsters. On the other hand, similar results are observed with the antioxidant and anti-inflammatory N-acetylcysteine, with minimal immunosuppression in hamsters. These results suggest that, as in the early EALAH (24 h), during the late stages of the process (7 days), inflammation is also primarily responsible for tissue damage. However, lysosomal and cationic proteins are responsible for the early lesions, whereas reactive oxygen and nitrogen species are primarily involved in late stages.