Researchers have found that the host's susceptibility to develop malaria depends on his or her metabolic state, which can be easily manipulated through external stimuli such as dietary patterns.
The progression and development of an infectious disease is directly dependent not only on the characteristics of the causing infectious agent but also on the genetic characteristics of the host, which also dictate the efficiency of the infection.
During the last years scientific discoveries have suggested that external factors independent of the host-parasite dichotomy, such as eating habits, can impact in the establishment, progression and endpoint of infections.
The team, manipulated the diet fed to lab mice for very short periods of time and evaluated the level of infection caused by the malaria parasite. Administration of a high-fat diet to mice for a period as short as 4 days impairs Plasmodium liver infection by over 90%. Plasmodium sporozoites can successfully invade and initiate replication but die inside hepatocytes, thereby are unable to cause severe disease.
Transcriptional analyses combined with genetic and chemical approaches reveal that this impairment of infection is mediated by oxidative stress. Authors show that reactive oxygen species, probably spawned from fatty acid β-oxidation, directly impact Plasmodium survival inside hepatocytes, and parasite load can be rescued by exogenous administration of the antioxidant N-acetylcysteine or the β-oxidation inhibitor etomoxir. The results, were published in the journal Nature Microbiology,
The mechanism used by the host to eliminate the malaria parasite, now revealed in this study, may contribute to explain how certain genetic alterations associate to high levels of oxidative stress, such as sickle-cell anaemia or beta thalassemia, have been selected in the population due to their protective effect against malaria.
Metabolism directly impacts the odds of developing malaria
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