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Changes in complement C3 levels following treatment of patients with Brugia malayi infection
1Department of Genetics and Cellular Biology, University of Malaya, Kuala Lumpur, Malaysia.
Insights
Diethylcarbamizine citrate (DEC) treatment cleared Brugia malayi microfilariae rapidly. Complement C3 levels increased post-treatment, suggesting consumption during the immune response to microfilariae.
Area of Science:
- Immunology
- Parasitology
- Pharmacology
Background:
- Brugia malayi infection is a significant cause of lymphatic filariasis.
- Understanding the host immune response to infection and treatment is crucial for effective disease management.
Purpose of the Study:
- To investigate the impact of diethylcarbamizine citrate (DEC) on serum IgG and complement C3 levels in patients with Brugia malayi infection.
- To elucidate the role of complement C3 consumption in the context of microfilariae clearance.
Main Methods:
- Assay of serum IgG and complement C3 levels at multiple time points (Day 0, 1, 3-4, 7, 56-70) post-DEC treatment.
- Monitoring of microfilariae clearance and eosinophil counts in patients and healthy volunteers.
Main Results:
- DEC treatment rapidly cleared microfilariae within 24 hours.
- Eosinophil counts initially decreased then increased before returning to normal.
- Serum IgG levels showed transient fluctuations, returning to baseline.
- Complement C3 levels significantly increased over two months, particularly in patients with high initial microfilariae loads.
Conclusions:
- Brugia malayi infection likely stimulates high complement C3 synthesis, a process continuing post-treatment.
- DEC treatment does not decrease complement C3 levels despite microfilariae elimination.
- Complement C3 appears to be consumed upon antibody binding to microfilariae entering circulation.
Abstract:
Serum IgG levels and complement C3 levels were assayed on Day 0, 1, 3-4, 7 and 56-70 post-treatment with diethylcarbamizine citrate (DEC) in a series to 26 patients with Brugia malayi infection and 6 volunteers without infection. On treatment, the microfilariae were cleared from the blood within 24 hours. The eosinophils decreased dramatically on Day 1 post-treatment but increased rapidly by Day 4 to 7 and then dropped to normal levels in 45 days. The serum IgG mean levels decreased briefly following treatment with DEC but then returned to original levels. However, the complement C3 levels gradually increased over the 2 months period of study reaching statistical significance levels (p less than 0.01) in patients with initial high blood microfilariae. The observation suggests that Brugia malayi infection probably induces a high rate of synthesis of complement C3 and this process continued in the post-treatment phase. Since, DEC treatment did not cause a decrease in complement C3 with the elimination of blood microfilariae, it would appear that the complement C3 is consumed following antibody attachment to the microfilariae as they enter the blood circulation.