Reactivation Aggravating Cardiac Function Impairment in Mice.

Background: () reactivation is common, especially among immunocompromised individuals, such as AIDS patients. The cardiac involvement associated with toxoplasmosis, however, is usually obscured by neurological deterioration. The aim of this study was to observe the alterations in cardiac functions in various landmark periods after infection and to assess whether reactivation more seriously damages the heart.

Methods: We established three infection models in mice using TgCtwh6, a major strain of prevalent in China. The groups included an acute group, chronic latent group, and reactivation group. We evaluated the cardiac function impairment via H & E staining, Masson staining, echocardiography, myocardial enzyme profiles, and cardiac troponin, and detected the expression of inflammatory factors and antioxidant factors with Western blotting. Immunofluorescence was used to detect the expression of the macrophage marker F4/80.

Results: Our results showed that damage to the heart occurred in the acute and reactivation groups. Impaired cardiac function manifested as a decrease in heart rate and a compensatory increase in left ventricular systolic function. Serum levels of cardiac enzymes also increased dramatically. In the chronic phase, myocardial fibrosis developed, diastolic functions became severely impaired, inflammation persisted, and macrophage expression was slightly reduced. Ultimately, reactivation infection exacerbated damage to cardiac function in mice, potentially leading to diastolic heart failure. Macrophages were strongly activated, and myocardial fibrosis was increased. In addition, the antioxidant capacity of the heart was severely affected by the infection.

Conclusions: Taken together, these results suggested that the reactivation of infection could aggravate injury to the heart, which could be associated with a host-cell-mediated immune response and strong cytokine production by macrophages, thus representing a novel insight into the pathogenic mechanism of toxoplasmosis.