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VITAMIN D — PROTECTIVE MECHANISMS 
IN ETIOPATHOGENESIS AND SANOGENESIS 
OF COVID19 DISEASE
Knez N., M.D., student, demonstrator
Department of Pathophysiology, School of Medicine University of Zagreb, 
University Hospital Centre, KBC Rebro, 
Zagreb, Croatia
Acad. Supervisor: Prof. Z. Kovač, M.D., Ph.D., Chairman of Dept.
Introduction. 
Vitamin D, „sunshine“ vitamin, has a major role in 
calcium/bone homeostasis. In addition. vitamin D has extra-skeletal 
immunomodulatory actions. 1-alpha hydroxylase, enzyme that forms 
calcitrol — active form of vitamin D, is expressed in macrophages and 
dendritic cells. The effect on innate immunity is based on preserving 
the structural integrity of the epithelial barrier which serves as the first 
line of defence. Vitamin D increases gene expression of proteins that 
form intercellular connections such as claudins, e-cadherins, occludins. 
Furthermore, it also stimulates synthesis of antimicrobial peptides such as 
cathelicidin and β-defensin, and thus increases the resistance of epithelial 
surfaces to microbial colonization. In acquired immune response vitamin 
D induces Th2 and Treg cell phenotypes while simultaneously suppressing 
Th1response and antigen presenting cells (APC) resulting in suppression 
of pro-inflammatory cytokine and enhancement of anti-inflammatory 
cytokine production. Patients that develop cytokine storm tend to have 
more severe clinical pictures and poor prognosis in infectious diseases. 
This review will discuss vitamin D deficiency in patients with COVID19 
as a risk factor for worse outcome.
Methods and materials. 
PubMed and Google Scholar were used as 
a literature source from December 2020 to March 2021. Retrospectively 
analysed studies were focused on immunomodulatory effects of vitamin 
D in immune response, as well as studies with hypothesis that people with 
vitamin D deficency suffer from more severe forms of COVID19 disease.