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Altered generation of interleukin 1 in chronic human schistosomiasis mansoni
K Zwingenberger1, J Richter, S Taupitz
1State Institute of Tropical Medicine, Berlin, FRG.
Insights
Chronic schistosomiasis mansoni impairs cell-mediated immunity. Interleukin-1 beta (IL-1) release by monocytes is reduced in patients but recovers after praziquantel therapy, indicating restored immune function.
Area of Science:
- Immunology
- Infectious Diseases
- Parasitology
Background:
- Chronic schistosomiasis mansoni is linked to diminished cell-mediated immune responsiveness (CMI).
- Interleukin-1 (IL-1) plays a crucial role in the induction phase of CMI.
- The role of IL-1 beta in severe granulomatous lesions in schistosomiasis requires investigation.
Purpose of the Study:
- To evaluate IL-1 concentration and monocyte function in patients with chronic schistosomiasis mansoni.
- To assess the impact of praziquantel therapy on IL-1 levels and immune cell function.
Main Methods:
- Sera and monocyte culture supernatants from schistosomiasis patients and controls were analyzed for IL-1 concentration.
- Monocyte surface antigens (IL-1, HLA-DP) and adherent cell oxidative-burst capacity were phenotyped.
- Patients were monitored before and after praziquantel treatment.
Main Results:
- Monocyte IL-1 beta release in vitro was significantly reduced in both intestinal and hepatosplenic schistosomiasis patients compared to controls.
- Circulating IL-1 beta levels were similar in untreated patients and controls.
- Three months post-therapy, serum IL-1 beta increased in intestinal schistosomiasis patients, and in vitro IL-1 release normalized by six months.
Conclusions:
- Reduced IL-1 beta production by monocytes is a feature of chronic schistosomiasis mansoni.
- Praziquantel therapy effectively restores IL-1 beta production, suggesting a recovery of immune function.
- IL-1 beta may be a relevant biomarker for monitoring treatment response in schistosomiasis.
Abstract:
Chronic schistosomiasis mansoni is associated with impaired cell-mediated immune responsiveness (CMI). To assess co-stimulatory factors essential in the induction phase of CMI, interleukin 1 (IL-1) concentration was determined in the sera and cell culture supernatants of Schistosoma mansoni-infected patients, and circulating monocytes were phenotyped, labelling membrane IL-1 and HLA-DP. In addition, adherent cell oxidative-burst capacity was investigated. Since involvement of IL-1 beta in the pathogenesis of severe granulomatous lesions could not be ruled out, 17 patients with intestinal schistosomiasis and 17 patients with hepatosplenic schistosomiasis were matched for intensity of infection and monitored 3-6 months after praziquantel therapy. Seventeen age- and sex-matched uninfected residents of the study area in Alagoas, Brazil, acted as controls. Whereas schistosomiasis patients and controls did not differ in the expression of monocyte surface antigens and the capacity of adherent cells to generate H2O2, IL-1 beta release by monocytes in vitro was significantly reduced in both intestinal and hepatosplenic patients. Low concentrations of circulating IL-1 beta were detected in comparable frequencies in untreated patients and controls. Three months after therapy, IL-1 beta was detectable in serum in an increased proportion of intestinal schistosomiasis patients. IL-1 release in vitro gradually increased in all patients and reached control values 6 months after therapy.
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