Abstract
Vitamin D deficiency is a common health problem with consequences not limited to bone and calcium hemostasis. Low levels have also been linked to tuberculosis and other respiratory infections as well as autoimmune diseases. We have previously shown that supplementation with vitamin D can induce the antimicrobial peptide cathelicidin during ex vivo infection of human urinary bladder. In rodents, however, cathelicidin expression is not linked to vitamin D and therefore this vitamin D-related effect fighting bacterial invasion is not relevant. To determine if vitamin D had further protective mechanisms during urinary tract infections, we therefore used a mouse model. In vitamin D-deficient mice, we detected more intracellular bacterial communities in the urinary bladder, higher degree of bacterial spread to the upper urinary tract and a skewed cytokine response. Furthermore, we show that the vitamin D receptor was upregulated in the urinary bladder and translocated into the cell nucleus after E. coli infection. This study supports a more general role for vitamin D as a local immune response mediator in the urinary tract.
Highlights
Urinary tract infection (UTI) is one of the most common bacterial infections in humans, mainly affecting women and children [1]
We have demonstrated that the antimicrobial peptide cathelicidin protects the urinary tract against severe UTI in mice and that the same mechanisms are of importance during E. coli UTI in humans [7]
Mice were infected with E. coli and after 24 hours bladders and kidneys were analysed for the presence of bacteria (Fig 1C and 1D)
Summary
Urinary tract infection (UTI) is one of the most common bacterial infections in humans, mainly affecting women and children [1]. For UTI to occur, bacteria enter the urinary tract, proceed against the flow of urine, adhere and invade superficial facet cells of the uroepithelium They rapidly multiply and may form intracellular bacterial communities (IBC) [4, 5], tightly packed bacteria surrounded by a biofilm-like substance, which enable them to hide from eradication by the host innate immune defense. Bacteria released from such IBCs can re-activate the infection, spread to other parts of the urinary tract or can invade nearby cells where they may enter a dormant stage [6]. The host on the other hand has developed different mechanisms to respond
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