Previous research has shown that biotin deficiency increases inflammation but since there are so many causes of inflammation – physiologically speaking – the actual metabolic pathways between biotin deficiency and inflammation are unclear. In this study, researchers subjected human immune cells to biotin deficiency and compared the result to human immune cells living in a biotin-rich environment. Biotin, also known as vitamin B7, is a key vitamin necessary for proper cellular metabolism. It is a cofactor to cellular energy production and therefore important to cellular health at a fundamental level.
When the human immune cells were biotin deficient, expression of inflammatory proteins increased. Specifically, CD4+T cells were used, which are also known as T-helper cells because they are a type of white blood cell that directs the function of other immune cells. In other words, T-helper cells supervise immune cells, sending signals to attack viruses and bacteria, for example. In biotin deficiency, the number of these regulatory immune cells (CD4+T) decreased. At the same time, biotin deficiency caused an increase in the metabolic pathway (called mTOR) that regulates cell growth. mTOR (mammalian target of rapamycin) is a protein that senses the nutrient and energy status of cells and regulates their metabolism accordingly. A decrease in mTOR is generally good and can lead to a longer lifespan. An increase in mTOR is generally bad and can lead to tumors or cancerous growths.
The results of this study – both in vivo and in vitro – showed that biotin deficiency increased the mTOR pathway, which then resulted in an increase in several inflammatory compounds. This, combined with the fact that biotin deficiency decreased the number of T-helper cells, meaning fewer immune cells were around to regulate everything, ultimately induced the increase in inflammation seen in biotin deficiency.
(Journal of Immunology, April 2018)
LINK to ABSTRACT Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway.