Antimicrobial activity inactivation and toxic immune reactions induce Epilepsy in human
Abstract
The calorie sensitive gene Sirtuin 1 (Sirt 1) determines nitric oxide (NO) homeostasis and immunosenescence relevant to the induction of various chronic diseases in human and other species. Appetite control is essential to Sirt 1 function for preventing adipose tissue transformation (adipocytokine release), non alcoholic fatty liver disease (NAFLD) and the development of epilepsy. Sirt 1 repression by bacterial lipopolysaccharides (LPS) leads to delayed hepatic clearance of anti-microbial drugs with relevance to mitophagy, neuron apoptosis and interference with antimicrobial/antiepileptic drug therapy. Increased absorption of LPS from food/water induces magnesium deficiency with inactivation of antimicrobial/antiepileptic drug therapy. Heat and cold stress alters Sirt 1’s role in cell cholesterol dyshomeostasis associated with increased heat shock proteins (HSP) involved with inactivation of antimicrobial proteins and promotion of the cytotoxic immune response. The genetics of immunity that determines immune competence changes over a human’s life span and involves the gene Sirt 1 that has antimicrobial properties by its regulation of NO metabolism connected to the immune system, mitophagy and epilepsy.
Document Type
Journal Article
Location of the Work
United States
School
School of Medical and Health Sciences
RAS ID
26267
Copyright
free_to_read
Publisher
Publons
Comments
Martins, I. J. (2017). Antimicrobial activity inactivation and toxic immune reactions induce Epilepsy in human. Journal of Medical Discovery, 2(4), 1-7. Available here.