Abstract
The intracellular pathogen Rickettsia felis causes flea-borne spotted fever and is increasingly recognized as an emerging cause of febrile illness in Africa, where co-infection with Plasmodium falciparum is common. Rickettsiae invade endothelial cells. Little is known, however, about the early immune responses to infection. In this study, we characterize for the first time the cytokine profile in the acute phase of illness caused by R. felis infection, as well as in plasmodial co-infection, using serum from 23 febrile children < 15 years of age and 20 age-matched healthy controls from Ghana. Levels of IL-8 (interleukin-8), IP-10 (interferon-γ-induced protein-10), MCP-1 (monocyte chemotactic protein-1), MIP-1α (macrophage inflammatory protein-1α) and VEGF (vascular endothelial growth factor) were significantly elevated in R. felis mono-infection; however, IL-8 and VEGF elevation was not observed in plasmodial co-infections. These results have important implications in understanding the early immune responses to R. felis and suggest a complex interplay in co-infections.
Highlights
Rickettsia felis causes flea-borne spotted fever (FBSF), an acute febrile illness commonly involving headache, myalgia and rash and potentially leading to severe neurological and respiratory complications [1]
We investigated serum cytokine responses in febrile children from Ghana with acute R. felis infection
Serum levels of IL-8, IP-10, MCP-1, MIP-1α and VEGF were significantly increased in R. felis mono-infections in comparison with healthy controls (Fig. 1; Table 1)
Summary
Rickettsia felis causes flea-borne spotted fever (FBSF), an acute febrile illness commonly involving headache, myalgia and rash and potentially leading to severe neurological and respiratory complications [1]. IFNγ (interferon-γ) and TNFα have protective properties during rickettsial infection of susceptible mouse strains [24,25,26,27,28,29]. IFNγ and TNFα activate intracellular bactericidal mechanisms; it was shown that IFNγ inhibits the growth of rickettsia in various host cells [28,29,30,31,32,33]. In humans, the early host immune responses have not been well-characterized. We investigated serum cytokine responses in febrile children from Ghana with acute R. felis infection
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