Production of IFN-gamma is impaired in patients with paracoccidioidomycosis during active disease and is restored after clinical remission.

Abstract

Cellular immunity is usually suppressed during paracoccidioidomycosis (PCM) and is restored after treatment. In this study we evaluated the induction of a type 1 (interferon gamma (IFN-gamma)), a type 2 (interleukin (IL)-10) and a primarily macrophage derived cytokine (tumor necrosis factor (TNF)-alpha) in peripheral blood mononuclear cells (PBMC) from patients with PCM. Eight male patients with active PCM, nine male patients with clinical remission of the disease and 10 healthy control subjects were enrolled in the study. Cytokines were induced with non-specific stimuli --phytohaemagglutin (PHA) (induces IL-10 and IFN-gamma), Lipopolysaccharide (induces TNF-alpha)--and Paracoccidioides brasiliensis antigen (PbAg) (induces IL-10, IFN-gamma and TNF-alpha). Induction of IFN-gamma with PHA differed among the three groups (P < 0.01; Kruskal-Wallis test) and with PbAg was lower in patients with active disease compared to those in clinical remission (P = 0.05; Mann-Whitney). Induction of IL-10 and of TNF-alpha was similar in the three groups. The suppressed production of IFN-gamma in patients with active disease may underscore the cellular immune deficiency seen in these patients.