Keto Diet Activates Protective γδ T Cell Responses Against Influenza Virus Infection
From the study:
Given that BHB serves as the primary energy substrate during glucose deprivation and KD feeding (27), we next tested whether BHB itself was responsible for the γδ T cell increase in the lungs after IAV infection. To test this possibility, we fed mice 1,3-butanediol (BD), which increases circulating BHB levels without the requirement for mitochondrial fatty acid oxidation, a necessary metabolic switch induced by KD. Although BD efficiently elevated blood BHB to levels comparable with KD-fed mice, it failed to induce γδ T cell expansion or to protect Mx1 mice from IAV-induced weight loss (Fig. 3, A and B), indicating that BHB is not sufficient to mediate this phenotype. These data indicate that metabolic adaptation favoring enhanced fatty acid oxidation during KD feeding (28), rather than a simple increase in BHB levels, is required for the expansion of protective γδ T cells in the lung and the maintenance of body weight during IAV infection.
Interesting that adaptation was necessary to offer protection, and feeding exogenous ketones did nothing.
