Abstract
SUMMARYToxoplasmosis affects a third of the global population and is of particular concern for immunologically compromised individuals. Toxoplasmosis induces host physiological events ranging from immunological to metabolic responses across multiple biological compartments. To understand the sequence of host responses during acute and chronicToxoplasma gondiiinfection, eight male BALB/c mice were infected with 2000T. gondiiME49 tachyzoites with a further eight uninfected mice used as controls. Plasma cytokines status, urinary metabolic profiling and fecal microbial profiles were characterized to monitor temporal variation related toT. gondiiinfection. The results showed elevated serum interferon-γ(IFN-γ), interleukin-12p40 and necrosis factor-αduring acute phase of infection with concomitant perturbation in host energy metabolism and host-gut microbiome co-metabolism of phenolics and a shift in microbial composition. However, the differences were less pronounced during the putative chronic phase of infection with elevated IFN-γ, differences in urinaryN-acetyls andO-acetyls of glycoproteins with no shift in gut microbial composition. Structural equation modelling on the current data showed host immune responses as the main driver for changes observed in urinary metabolites and gut microbial composition. Such an approach can be applied to other models of infectious diseases to aid understanding of host–pathogen interactions and potential biomarker discovery.
Highlights
Toxoplasmosis, one of the most common parasitic diseases worldwide, is caused by the protozoan Toxoplasma gondii
Pattern in overall host immune responses derived from cytokine multiplex
The systems biology approach used here to understand the effect of T. gondii infection in mammalian host sheds new light into host metabolic as well as host gut microbe responses to infection
Summary
Toxoplasmosis, one of the most common parasitic diseases worldwide, is caused by the protozoan Toxoplasma gondii It is a parasite with no specific host and has more than one obligatory host in its life cycle (Tenter et al 2000). Metabolic profiling strategy has been used to investigate other rodent host–parasite models including Schistosoma japonicum-hamster (Wang et al 2006), and Trypanosoma brucei brucei-mouse (Wang et al 2008) with the aim of characterizing the metabolic responses of hosts to these parasites at the molecular level Such single matrix/platform approach allowed for comprehensive characterization of hostparasite interaction from the metabolic perspective, a combination of different sample matrices, analysed using different platforms, will enable a more holistic understanding of such complex biological interactions involving multiple levels of biological complexities
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