Published online before print August 14, 2008

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(Journal of Leukocyte Biology. 2008;84:1279-1286.)
© 2008 by Society for Leukocyte Biology

Vitamin D₃ induces pro-LL-37 expression in myeloid precursors from patients with severe congenital neutropenia

Jenny Karlsson^*,1, Göran Carlsson, Olivia Larne^*, Mats Andersson^* and Katrin Pütsep^*

^* Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; and
Childhood Cancer Research Unit, Department of Woman and Child Health, Karolinska University Hospital Solna, Stockholm, Sweden

¹ Correspondence: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden. E-mail: jenny.karlsson{at}ki.se

ABSTRACT

The innate immune system produces a number of effector molecules that are important for protection against bacterial infections. Neutrophils and antimicrobial peptides are major components of innate defense with the capacity of rapid bacterial killing. Patients with severe congenital neutropenia (SCN) experience recurrent and chronic infections despite recombinant G-CSF-mobilized neutrophils. We have shown previously that these neutrophils are deficient in that they lack the antimicrobial peptide LL-37. Here, we show that pro-LL-37 mRNA is not expressed in neutrophil precursors from patients with SCN, although the gene and promoter region for pro-LL-37, CAMP, does not display any mutations. The hormonal form of vitamin D₃ [1,25(OH)₂D₃] induced the expression of pro-LL-37 in isolated neutrophil progenitors and in EBV-transformed B cells from patients with SCN, whereas all-trans retinoic acid only induced expression in transformed B cells. These results demonstrate that myeloid cells of patients with SCN can produce pro-LL-37, suggesting that other pathways are impaired.

Key Words: 1.25(OH)₂D₃ • Kostmann syndrome • hCAP18 • all-trans retinoic acid

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