Association between Degree of Anaplasia and Degree of Inflammation with the Expression of COX-2 in Feline Injection Site Sarcomas.

Feline injection site sarcomas (FISSs) are mesenchymal neoplasms that develop at the sites of delivery of vaccines or other injectable products. Vaccine adjuvants can trigger an intense and persistent inflammatory response that may lead to neoplastic transformation. The proinflammatory role of cyclo-oxygenase (COX)-2 is well known and its overexpression has prognostic value in multiple neoplastic processes. One hundred and seventeen FISSs were evaluated for the degree of inflammation and anaplasia. Immunohistochemistry was used to determine the expression of COX-2 in these sarcomas. There was a significant association between the degree of inflammation and the expression of COX-2 by neoplastic cells. COX-2 expression was lower in tumours with higher degrees of anaplasia. These findings may be useful in predicting the sensitivity of FISSs to treatment with COX-2 inhibitors. The potential therapeutic use of such agents could then be restricted to tumours with lower degrees of anaplasia.

Mycotoxin T-2 and aflatoxin B1 as immunosuppressors in mice chronically infected with Toxoplasma gondii.

The aim of this study was to determine whether repeated ingestion of mycotoxin T-2 (T2) or aflatoxin B1 (AFL) at low doses could contribute to the activation of toxoplasmosis in experimentally infected mice. Mice were divided into two groups: Control (C) and Infected (I). The cyst-forming Beverley strain of Toxoplasma gondii was used to produce the infection one month before treatment with mycotoxins. Mycotoxins were given intragastrically for a 50-day period. The average weight gain was reduced in the groups treated with mycotoxins. Mice developed specific IgG to T. gondii. Histopathological studies showed severe encephalitis in all groups infected. The number of unruptured and ruptured cysts was established and the severity of the lesions was evaluated, the groups treated with mycotoxins being the most severely affected. Immunohistochemical studies of the brain showed free antigen in tissues surrounding ruptured cysts. It is suggested that low and repeated doses of mycotoxins, necessary to produce a subclinical intoxication, precipitate Toxoplasma cyst rupture and consequently the activation of chronic toxoplasmosis.