Correlation between interleukin-10 and in situ necrosis and fibrosis suggests a role for interleukin-10 in the resolution of the granulomatous response of tuberculous pleurisy patients.

In order to identify mediators involved in immune-mediated disease regression, the pleural cytokine and histopathological profile was evaluated in tuberculous pleurisy patients with varied disease duration and clinical presentation, previous to chemotherapy. Interleukin (IL)-10, interferon (IFN)-gamma and tumor necrosis factor (TNF) levels in pleural fluids were shown to decrease with disease time. IL-10 was positively correlated with IFN-gamma, TNF and necrosis area in pleural sections. To parallel these findings with disease regression, individuals showing fever, anorexia, and progressive exudate in the pleural cavity (active disease) were compared with patients without symptoms and with a decrease in exudate volume (regressive disease). IFN-gamma and TNF levels were lower in regressive disease, as well as reduced necrosis area in pleural sections. Our results indicate that tissue destruction and a prominent Th1 response mark the early phase of tuberculous pleurisy and suggest that down-modulation of this response, with the possible participation of IL-10, is associated with disease resolution.