Malaria primes the innate immune response due to interferon-gamma induced enhancement of toll-like receptor expression and function.

ABSTRACT: Malaria-induced sepsis is associated with an intense proinflammatory cytokinemia for which the underlying mechanisms are poorly understood. It has been demonstrated that experimental infection of humans with Plasmodium falciparum primes Toll-like receptor (TLR)-mediated proinflammatory responses. Nevertheless, the relevance of this phenomenon during natural infection and, more importantly, the mechanisms by which malaria mediates TLR hyperresponsiveness are unclear. Here we show that TLR responses are boosted in febrile patients during natural infection with P. falciparum. Microarray analyses demonstrated that an extraordinary percentage of the up-regulated genes, including genes involving TLR signaling, had sites for IFN-inducible transcription factors. To further define the mechanism inv

SUBMITTER: Franklin BS 

PROVIDER: S-EPMC2657593 | biostudies-literature | 2009 Apr

REPOSITORIES: biostudies-literature