Monocyte-mediated killing of schistosomula of <i>Schistosoma mansoni</i>: alterations in human Schistosomiasis mansoni and tuberculosis.

Abstract

Abstract We studied the influence of schistosomiasis and tuberculosis on the capacity of human monocytes to kill the invasive larval stage of Schistosoma mansoni. The mean killing of schistosomula by monocytes from 12 uninfected controls incubated in autologous plasma was 12 ±1%; in control plasma it was 10 ± 1%, and in pooled immune plasma it was enhanced to 21 ± 1% (p &amp;lt; 0.001 ). Monocyte-mediated killing in 10 individuals with light S. mansoni infection (mean 197 eggs/g of stool) was 24 ± 3% (autologous), 12 ± 3% (control), and 23 ± 4% (immune plasma). Heavy infection, however, (mean 2276 eggs/g) in 9 subjects was associated with significant decrease in monocyte killing of 8 ± 3% (autologous), 4 ±1% (control), and 11 ±1% (immune plasma). The lack of reversal of this abnormality in allogeneic plasma suggested a primary cellular defect. Patients with hepatosplenic schistosomiasis also demonstrated defective monocyte effector function (2 ± 3% killing in control plasma). In contrast, monocytes from patients with tuberculosis demonstrated increased killing of schistosomula in all plasma pools. Furthermore, plasma from tuberculous patients with and without schistosomiasis enhanced killing by monocytes from control subjects by 187 and 75%, respectively. These results suggest an impairment in monocyte killing of schistosomula in subjects with heavy S. mansoni infection and hepatosplenic schistosomiasis, which may reflect their innate susceptibility or may be a consequence of infection. In persons with tuberculosis, increased killing of this multicellular parasite was observed that may be due to monocyte activation.