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02 Feb 2015

Lead authors Pedro Mejia and J. Humberto Trevino-Villarreal, both researchers at Harvard T.H. Chan School of Public Health, found that leptin--a hormone secreted from fat tissue with roles in suppressing appetite, but also in activating adaptive immune and inflammatory responses--is increased upon infection in a mouse model of cerebral malaria, and turns out to be a major bad actor in promoting neurological symptoms and death. Remarkably, Mejia, Trevino-Villarreal and colleagues showed that reducing leptin using a variety of means, either genetically, pharmacologically, or nutritionally by reducing food intake during the first two days of infection, protected against cerebral malaria. The researchers also found that leptin acted primarily on cytotoxic T cells by turning on the well-studied mTOR protein, for which pharmacologic inhibitors are readily available. In their animal model, treating mice with the mTOR inhibitor rapamycin protected them against the neurological complications of cerebral malaria. Protection was due in part to a preservation of the blood brain barrier, which prevented the entry of blood cells carrying the parasites into the brain. As rapamycin is already FDA-approved for use in humans, trials in humans for cerebral malaria treatment with this drug may be possible, according to the researchers.
For the original version including any supplementary images or video, visit http://www.sciencedaily.com/releases/2015/01/150130082100.htm


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