2014
DOI: 10.1179/2047773214y.0000000139
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Parasite virulence, co-infections and cytokine balance in malaria

Abstract: Strong early inflammatory responses followed by a timely production of regulatory cytokines are required to control malaria parasite multiplication without inducing major host pathology. Here, we briefly examine the homeostasis of inflammatory responses to malaria parasite species with varying virulence levels and discuss how co-infections with bacteria, viruses, and helminths can modulate inflammation, either aggravating or alleviating malaria-related morbidity.

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Cited by 32 publications
(34 citation statements)
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“…Immune responses are complex traits and vaccine development requires extensive knowledge of the processes and of the determinants that modulate immune responses in human populations. The effect of age, genetic factors, pathogen co-infection, and nutritional status have been more intensively explored and are recognized to influence anti-Plasmodium Ab responses and to have some association with malaria clinical protection [13][14][15].…”
mentioning
confidence: 99%
“…Immune responses are complex traits and vaccine development requires extensive knowledge of the processes and of the determinants that modulate immune responses in human populations. The effect of age, genetic factors, pathogen co-infection, and nutritional status have been more intensively explored and are recognized to influence anti-Plasmodium Ab responses and to have some association with malaria clinical protection [13][14][15].…”
mentioning
confidence: 99%
“…Induction of heme oxygenase-1 (HO-1) production following parasite-induced hemolysis is one of the putative mechanisms that impair neutrophil function and resistance to bacteria during acute malaria. 38 The induction of HO-1 is, indeed, essential to reduce heme-mediated tissue damage in hemolytic diseases such as malaria, but inhibits oxidative burst in granulocytes and favors bacterial survival within these cells; 3) malaria can increase the iron content in macrophages as a result of enhanced erythrophagocytosis, thus favoring the survival of iron-dependent bacteria such as non-typhi Salmonella within these cells. It can also increase the response to inflammatory stimuli from bacteria, contributing to overall disease severity 38 ; 4) accumulation of the hemozoin pigment in monocytes impairs the function of various macrophages, inhibiting expression of adhesion molecules-1, integrin CD11C, and major histocompatibility complex class II antigens and delaying differentiation into functional antigen-presenting cells and stimulatory proinflammatory cytokines and chemokines; each of these functions plays a significant role in antibacterial immunity 39 ; 5) finally, those children who are homozygous for β s -globin genes (HbSS) are common in malaria-endemic areas and are predisposed to bacterial invasive diseases.…”
Section: Discussionmentioning
confidence: 99%
“…Following infection, a Th1dependent immune response can develop in the mammalian host, aiding clearance of parasites via IFNc-dependent mechanisms. 14,15 IFNc production by antigen-specific CD4 + T cells during P. chabaudi chabaudi AS (PcAS) infection in mice has been reported, 16 and increased parasite growth was observed following IFNc neutralisation. 17 The relationship between IFNc production and control of parasite growth has also been reported in humans during blood stage Plasmodium falciparum (Pf) infection.…”
Section: Introductionmentioning
confidence: 99%