Abstract
BackgroundComplement (C) can be activated during malaria, C components consumed and inflammatory mediators produced. This has potential to impair host innate defence.MethodsIn a case-control study, C activation was assessed by measuring serum haemolytic activity (CH50), functional activity of each pathway and levels of C3a, C4a and C5a in children presenting at Kisumu District Hospital, western Kenya, with severe malarial anaemia (SMA) or uncomplicated malaria (UM).ResultsCH50 median titers for lysis of sensitized sheep erythrocytes in SMA (8.6 U/mL) were below normal (34–70 U/mL) and were one-fourth the level in UM (34.6 U/mL (P < 0.001). Plasma C3a median levels were 10 times higher than in normals forSMA (3,200 ng/ml) and for UM (3,500 ng/ml), indicating substantial C activation in both groups. Similar trends were obtained for C4a and C5a. The activities of all three C pathways were greatly reduced in SMA compared to UM (9.9% vs 83.4% for CP, 0.09% vs 30.7% for MBL and 36.8% vs 87.7% for AP respectively, P < 0.001).ConclusionThese results indicate that, while C activation occurs in both SMA and UM, C consumption is excessive in SMA. It is speculated that in SMA, consumption of C exceeds its regeneration.
Highlights
Complement (C) can be activated during malaria, C components consumed and inflammatory mediators produced
These results indicate that, while C activation occurs in both severe malarial anaemia (SMA) and uncomplicated malaria (UM), C consumption is excessive in SMA
There is ample evidence to indicate that malaria antigens, either on infected erythrocytes, or as free antigens released from schizont rupture, or as immune complexes formed from antibodies that target the antigens, can all activate complement (C) [1,2,3,4,5,6]
Summary
Complement (C) can be activated during malaria, C components consumed and inflammatory mediators produced. This has potential to impair host innate defence. Intravascular lysis of Plasmodium falciparum iE releases breakdown products such as haemoglobin and haematin, which have inflammatory properties and can activate C [7,8,9]. Low levels of C3, C4 and C1q in the sera of children with acute falciparum malaria have been demonstrated, implicating the classical pathway (CP). These studies have suggested that C activation may play a part in initiating (page number not for citation purposes). Other studies have shown that MBLdeficiency associated with MBL variant alleles that encode dysfunctional protein or decreased levels of the MBL can compromise the host's ability to fight malaria [11,12]
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