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Complement alterations in rodent malaria
Abstract:
In the course of rodent malaria, the ability of mouse serum to release immune complexes from lymphocytes (complex-release, or CRA), a complement dependent function, becomes profoundly altered. These alterations occur in parallel with changes in the serum levels of the third complement component (C3). A transitory but significant increase in CRA and C3 was noticed during the first 3 days after blood-induced Plasmodium berghei infection. This was followed by a progressive decrease in CRA, which was extremely low in the 2nd week after injection. At this time, C3 levels were about 25% of those found in normal mouse serum. Incubation of blood cells of malaria-infected animals with normal serum "in vitro" resulted in a significant inhibition of the CRA of the normal serum. This inhibition was shown to operate through the alternate complement pathway. In addition, a considerable proportion of hypocomplementemic malarious sera also had an inhibitory effect on the CRA of normal sera.
Insights
During rodent malaria, mouse serum
Area of Science:
- Immunology
- Parasitology
- Complement System
Background:
- Rodent malaria profoundly alters immune complex metabolism in mouse serum.
- These changes correlate with alterations in the third complement component (C3) levels.
Purpose of the Study:
- To investigate the dynamic changes in complex-release assay (CRA) and C3 levels during Plasmodium berghei infection in mice.
- To elucidate the mechanism of CRA inhibition observed in malaria-infected mouse serum.
Main Methods:
- Measurement of serum C3 levels and complex-release assay (CRA) in mice infected with Plasmodium berghei.
- In vitro incubation of blood cells from infected mice with normal serum to assess CRA inhibition.
- Investigation of the complement pathway involved in CRA inhibition.
Main Results:
- A transient increase in CRA and C3 occurred in the first 3 days post-infection, followed by a significant decrease.
- C3 levels dropped to approximately 25% of normal by the second week of infection.
- Infected mouse blood cells inhibited normal serum CRA via the alternate complement pathway.
Conclusions:
- Plasmodium berghei infection significantly impairs complement-dependent complex-release function in mouse serum.
- The alternate complement pathway plays a key role in the observed inhibition of CRA during malaria.
- Hypocomplementemic sera from infected mice can also inhibit normal serum CRA.