Vitamin D Deficiency Reduces the Immune Response, Phagocytosis Rate, and Intracellular Killing Rate of Microglial Cells

• DOI: 10.1128/iai.01814-14
• Publication Date: 2014-04-01T04:23:04Z
• Authors: Marija Djukic; Marie Luise Onken; Sandra Schütze; Sandra Redlich; Alexander Götz; Uwe-Karsten Hanisch; Thomas Bertsch; Sandra Ribes; Andrea Hanenberg; Simon Schneider; Cornelius Bollheimer; Cornel Sieber; Roland Nau
• Keywords: Lipopolysaccharides; 0301 basic medicine; Analysis of Variance; Meningitis, Escherichia coli; Cell Survival; Toll-Like Receptors; Colony Count, Microbial; Nitric Oxide; Immunity, Innate; 3. Good health; Mice, Inbred C57BL; Disease Models, Animal; Mice; 03 medical and health sciences; Phagocytosis; Escherichia coli; Animals; Cytokines; Microglia; Chemokines; Vitamin D; Cells, Cultured; Calcifediol

Meningitis and meningoencephalitis caused by Escherichia coli are associated with high rates of mortality neurological sequelae. A prevalence disorders has been observed in geriatric populations at risk hypovitaminosis D. Vitamin D potent effects on human immunity, including induction antimicrobial peptides (AMPs) suppression T-cell proliferation, but its influence microglial cells is unknown. The purpose the present study was to determine vitamin deficiency phagocytosis rate, intracellular killing, immune response murine cultures after stimulation Toll-like receptor (TLR) agonists tripalmitoyl-S-glyceryl-cysteine (TLR1/2), poly(I·C) (TLR3), lipopolysaccharide (TLR4), CpG oligodeoxynucleotide (TLR9). Upon concentrations TLR agonists, release tumor necrosis factor alpha (TNF-α) interleukin 6 (IL-6) decreased D-deficient compared that D-sufficient cultures. Phagocytosis E. K1 TLR3, -4, -9 killing all were lower than respective control cells. Our observations suggest may impair resistance brain against bacterial infections.