Vitamin D status and expression of vitamin D receptor and LL-37 in patients with spontaneous bacterial peritonitis
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Published on: May 4, 2018
Chong Zhang1, Lianrong Zhao, Li Ma
1Department of Infectious Diseases, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, China.
Background:
Vitamin D, which exerts its effect through vitamin D receptor (VDR), and LL-37, a vitamin D-dependent antimicrobial peptide, are involved in many infectious diseases.
Aim:
The objective of this study was to evaluate whether vitamin D status and expressions of VDR and LL-37 are involved in the pathogenesis of spontaneous bacterial peritonitis (SBP).
Methods:
Serum and ascitic fluid 25-dihydroxyvitamin D [25(OH)D] concentrations and levels of VDR and LL-37 in peritoneal leukocytes were measured by ELISA and real-time PCR methods in cirrhotic patients with SBP (n = 19) and cirrhotic patients with simple ascites (n = 28). The correlations between these levels and clinical variables were evaluated.
Results:
Cirrhotic patients with ascites showed low vitamin D concentrations in both serum and ascitic fluid. Lower serum vitamin D concentrations were observed in cirrhotic patients with Child-Pugh C class. 25(OH)D concentrations in ascitic fluid were positive correlated with that in serum (r = 0.74, P < 0.001). The SBP group showed significantly higher levels of both VDR and LL-37 mRNA expressions in peritoneal leukocytes than the simple ascites group (P = 0.005 and P = 0.003, respectively). In the SBP group, VDR and LL-37 expressions in peritoneal leukocytes were positively correlated (r = 0.70, P = 0.001).
Conclusions:
Vitamin D insufficiency was universal among cirrhotic patients with ascites, and the situation was more severe with more serious cirrhosis. Expressions of peritoneal leukocytes VDR and LL-37 genes were simultaneously up-regulated in cirrhotic patients with SBP when compared with cirrhotic patients with simple ascites. It is indicated that the vitamin D-VDR system and its downstream gene, LL-37, are involved in the pathogenesis and antibacterial immune response to SBP.
