Abstract
BackgroundCo-infection with malaria and HIV increases the severity and mortality of both diseases, but the cytokine responses related to this co-infection are only partially characterised. The aim of this study was to explore cytokine responses in relation to severity and mortality in malaria patients with and without HIV co-infection.MethodsThis was a prospective cross-sectional study. Clinical data and blood samples were collected from adults in Mozambique. Plasma was analysed for 21 classical pro- and anti-inflammatory cytokines, including interleukins, interferons, and chemokines.ResultsWe included 212 in-patients with fever and/or suspected malaria and 56 healthy controls. Falciparum malaria was diagnosed in 131 patients, of whom 70 were co-infected with HIV-1. The malaria patients had marked increases in their cytokine responses compared with the healthy controls. Some of these changes, particularly interleukin 8 (IL-8) and interferon-γ-inducing protein 10 (IP-10) were strongly associated with falciparum malaria and disease severity. Both these chemokines were markedly increased in patients with falciparum malaria as compared with healthy controls, and raised levels of IL-8 and IP-10 were associated with increased disease severity, even after adjusting for relevant confounders. For IL-8, particularly high levels were found in malaria patients that were co-infected with HIV and in those who died during hospitalization.InterpretationsOur findings underscore the complex role of inflammation during infection with P. falciparum, and suggest a potential pathogenic role for IL-8 and IP-10. However, the correlations do not necessarily mean any causal relationship, and further both clinical and mechanistic research is necessary to elucidate the role of cytokines in pathogenesis and protection during falciparum malaria.
Highlights
Human Immunodeficiency Virus (HIV) 1 and Plasmodium falciparum malaria are two of the major lethal infectious diseases in sub-Saharan Africa, with 1.47 million and 1.13 million deaths, respectively, in 2010 [1, 2]
For interleukin 8 (IL-8), high levels were found in malaria patients that were co-infected with HIV and in those who died during hospitalization
The correlations do not necessarily mean any causal relationship, and further both clinical and mechanistic research is necessary to elucidate the role of cytokines in pathogenesis and protection during falciparum malaria
Summary
Human Immunodeficiency Virus (HIV) 1 and Plasmodium falciparum malaria are two of the major lethal infectious diseases in sub-Saharan Africa, with 1.47 million and 1.13 million deaths, respectively, in 2010 [1, 2]. Infection with P.falciparum is often associated with the activation of several inflammatory pathways, resulting in systemic and local inflammatory responses that involve the production of a wide range of cytokines,- from several cell types including leukocyte subsets, endothelial cells and various tissues cells such as macrophages This inflammatory response during malaria infection could activate anti-microbial responses in macrophages, T cells, granulocytes and endothelial cells and thereby be beneficial for the host [6]. The malaria patients had marked increases in their cytokine responses compared with the healthy controls Some of these changes, interleukin 8 (IL-8) and interferon-c-inducing protein 10 (IP-10) were strongly associated with falciparum malaria and disease severity. Interleukin 8 (IL-8) and interferon-c-inducing protein 10 (IP-10) were strongly associated with falciparum malaria and disease severity Both these chemokines were markedly increased in patients with falciparum malaria as compared with healthy controls, and raised levels of IL-8 and IP-10 were
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