Serum cytokine responses in Rickettsia felis infected febrile children, Ghana

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.

Keywords: Cytokine; Flea-borne spotted fever; Rickettsia felis; Rickettsiosis.

Fig. 1

Cytokine and chemokine levels in sera from children during the first week of R. felis infection. 15 sera from R. felis infected children, 8 sera from P. falciparum co-infected children and 20 sera from healthy children without rickettsial disease or malaria were analyzed in parallel by bead-based LEGENDplex assay. Data are expressed as mean ± SD. Statistical analyses was performed with 1 way ANOVA and subsequent Tukey’s multiple comparisons test. Asterisks indicate statistically significant differences (*p < 0.05, **p < 0.01, ***p < 0.001)