ABSTRACT
The effect of the intensity of infection (eggs per gram faeces, epg) on the production of interferon-gamma (INF-gamma), interleukin (IL)-10 and IL-13 by peripheral blood mononuclear cells (PBMCs) from individuals living in a Schistosoma mansoni-endemic area was evaluated. In vitro stimulation of PBMCs with soluble egg antigen (SEA) resulted in significantly higher secretion levels of IFN-gamma in egg-negative individuals compared with those with an intensity of infection of more than 100 epg. In contrast, the egg-positive group produced significantly higher amounts of IL-10. Levels of IL-13 did not differ significantly between egg-positive and egg-negative groups. These findings suggest that IL-10 is an important cytokine in the control of the T helper cell (Th) type 1 responses during human S. mansoni infection, shifting the immune response from Th0 in egg-negative individuals from an endemic area to a Th2 polarization in chronic infected individuals.
Subject(s)
Antigens, Helminth/immunology , Interferon-gamma/biosynthesis , Interleukin-10/biosynthesis , Interleukin-13/biosynthesis , Schistosomiasis mansoni/immunology , Adult , Age Factors , Animals , Brazil/epidemiology , Cells, Cultured , Disease Susceptibility/immunology , Endemic Diseases , Humans , Interferon-gamma/immunology , Interleukin-10/immunology , Interleukin-13/immunology , Leukocytes, Mononuclear/immunology , Schistosoma mansoni/immunology , Schistosomiasis mansoni/epidemiology , Severity of Illness IndexABSTRACT
Schistosomiasis mansoni remains a significant public health problem in many parts of the tropics and subtropics. Clinical manifestations range from the asymptomatic intestinal form through to the hepatosplenic form of the disease, a potentially lethal clinical condition in a subsection of the exposed population. In this study, we investigated the mechanisms by which interleukin (IL)-10 production could be differentially controlled in patients with the intestinal and hepatosplenic forms of the disease, as IL-10 may play a fundamental role in the development of the hepatosplenic disease state. It is reported that p38 mitogen-activated protein (MAP) kinase signalling, and in particular p38 MAPK activation, is central to IL-10 production of cells from patients with schistosomiasis. Furthermore, the difference in the levels of activated p38 MAPK and the activation transcription factor (ATF-2), may explain the difference in the amount of IL-10 produced by cells from intestinal and hepatosplenic patients. We suggest that the type of immune response triggered in patients with hepatosplenomegaly could be influenced by the levels of phosphorylated p38 MAPK.
