Dietary alterations could impact the odds of Plasmodium infection and disease

Researchers from the University of Lisbon (Lisbon, Portugal) have revealed that dietary alterations, particularly a high-fat diet (HFD), could impact the susceptibility of Plasmodium infection and disease outcome in mice.

Prior research from this team has shown that Plasmodium parasites rely on the scavenging of host and environmental lipids. Thus, the replication of Plasmodium parasites is said to heavily rely on a high demand of lipids.

Recently, the same team published a study in Nature Microbiology that evaluated the impact of dietary lipids in mice and their susceptibility to Plasmodium infection. Mice were subjected to a HFD prior to Plasmodium berghei infection. When the researchers compared these mice to normal mice consuming a normal diet, they demonstrated that there was a significant reduction of the parasite count in the liver of HFD-fed mice.

The researchers also observed that there was a delay in the onset of parasitaemia in HFD-fed mice and that there were no circulating parasites even 20 days after infection.

The mechanism utilized by the host in order to eliminate the parasite is revealed in the study, which goes into depth about the relationship between oxidative stress genes and a HFD. This research may contribute to explain how certain genetic alterations associate to high levels of oxidative stress, such as sickle cell anaemia or beta thalassemia, and have been selected in the population due to their protective effect against malaria.

In the paper the researchers commented: “Our data clearly establish that acute and transient disruption of host metabolic homeostasis can dramatically change host susceptibility to infection and determine the outcome of the disease. It is therefore our conviction that the strategies aiming to control infectious diseases must take into account alterations in populations’ dietary habits.”

Sources: Zuzarte-Luis V, Mello-Vieira J, Marreiros IM et al. Dietary alterations modulate susceptibility to Plasmodium infection. Nat. Microbiol. doi:10.1038/s41564-017-0025-2 (2017) (Epub ahead of print);


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