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Systemic metabolic reprogramming induced by infection exerts profound, pathogen-specific effects on infection outcome. Here, we detail the host immune and metabolic response during sickness and recovery in a mouse model of malaria. We describe extensive alterations in metabolism during acute infection, and identify increases in host-derived metabolites that signal through the aryl hydrocarbon receptor (AHR), a transcription factor with immunomodulatory functions. We find that  Ahr -/-   mice are more susceptible to malaria and develop high plasma heme and acute kidney injury. This phenotype is dependent on AHR in  Tek -expressing radioresistant cells. Our findings identify a role for AHR in limiting tissue damage during malaria. Furthermore, this work demonstrates the critical role of host metabolism in surviving infection.

Metabolic profiling during malaria reveals the role of the aryl hydrocarbon receptor in regulating kidney injury