DOI: 10.4049/jimmunol.178.11.7190. IFN-γ- and TNF-Independent Vitamin D-Inducible Human Suppression of Mycobacteria: The Role of Cathelicidin LL-37

IFN-γ- and TNF-Independent Vitamin D-Inducible Human Suppression of Mycobacteria: The Role of Cathelicidin LL-37

10.4049/jimmunol.178.11.7190

Crossref journal-article

Oxford University Press (OUP)

The Journal of Immunology (286)

Abstract

Abstract Vitamin D deficiency is associated with susceptibility to tuberculosis, and its biologically active metabolite, 1α,25 dihydroxyvitamin D3 (1α,25(OH)2D3), has pleiotropic immune effects. The mechanisms by which 1α,25(OH)2D3 protects against tuberculosis are incompletely understood. 1α,25(OH)2D3 reduced the growth of mycobacteria in infected human PBMC cultures in a dose-dependent fashion. Coculture with agonists or antagonists of the membrane or nuclear vitamin D receptors indicated that these effects were primarily mediated by the nuclear vitamin D receptors. 1α,25(OH)2D3 reduced transcription and secretion of protective IFN-γ, IL-12p40, and TNF in infected PBMC and macrophages, indicating that 1α,25(OH)2D3 does not mediate protection via these cytokines. Although NOS2A was up-regulated by 1α,25(OH)2D3, inhibition of NO formation marginally affected the suppressive effect of 1α,25(OH)2D3 on bacillus Calmette Guérin in infected cells. By contrast, 1α,25(OH)2D3 strongly up-regulated the cathelicidin hCAP-18 gene, and some hCAP-18 polypeptide colocalized with CD14 in 1α,25(OH)2D3 stimulated PBMC, although no detectable LL-37 peptide was found in supernatants from similar 1α,25(OH)2D3-stimulated PBMC cultures. A total of 200 μg/ml of the active peptide LL-37, in turn, reduced the growth of Mycobacterium tuberculosis in culture by 75.7%. These findings suggest that vitamin D contributes to protection against TB by “nonclassical” mechanisms that include the induction of antimicrobial peptides.

Bibliography

Martineau, A. R., Wilkinson, K. A., Newton, S. M., Floto, R. A., Norman, A. W., Skolimowska, K., Davidson, R. N., SÃ¸rensen, O. E., Kampmann, B., Griffiths, C. J., & Wilkinson, R. J. (2007). IFN-Î³- and TNF-Independent Vitamin D-Inducible Human Suppression of Mycobacteria: The Role of Cathelicidin LL-37. The Journal of Immunology, 178(11), 7190â7198.

Authors 11

Adrian R Martineau (first)
Katalin A Wilkinson (additional)
Sandra M Newton (additional)
R Andres Floto (additional)
Anthony W Norman (additional)
Keira Skolimowska (additional)
Robert N Davidson (additional)
Ole E Sørensen (additional)
Beate Kampmann (additional)
Christopher J Griffiths (additional)
Robert J Wilkinson (additional)

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Dates

Type	When
Created	11 years, 4 months ago (April 18, 2014, 7:24 p.m.)
Deposited	5 months ago (March 30, 2025, 12:18 a.m.)
Indexed	4 weeks, 1 day ago (Aug. 6, 2025, 8:03 a.m.)
Issued	18 years, 3 months ago (June 1, 2007)
Published	18 years, 3 months ago (June 1, 2007)
Published Online	18 years, 3 months ago (June 1, 2007)
Published Print	18 years, 3 months ago (June 1, 2007)

Funders 0

None

BibTeX

@article{Martineau_2007, title={IFN-γ- and TNF-Independent Vitamin D-Inducible Human Suppression of Mycobacteria: The Role of Cathelicidin LL-37}, volume={178}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.178.11.7190}, DOI={10.4049/jimmunol.178.11.7190}, number={11}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Martineau, Adrian R and Wilkinson, Katalin A and Newton, Sandra M and Floto, R Andres and Norman, Anthony W and Skolimowska, Keira and Davidson, Robert N and Sørensen, Ole E and Kampmann, Beate and Griffiths, Christopher J and Wilkinson, Robert J}, year={2007}, month=jun, pages={7190–7198} }

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  "abstract": "<jats:title>Abstract</jats:title>\n               <jats:p>Vitamin D deficiency is associated with susceptibility to tuberculosis, and its biologically active metabolite, 1\u03b1,25 dihydroxyvitamin D3 (1\u03b1,25(OH)2D3), has pleiotropic immune effects. The mechanisms by which 1\u03b1,25(OH)2D3 protects against tuberculosis are incompletely understood. 1\u03b1,25(OH)2D3 reduced the growth of mycobacteria in infected human PBMC cultures in a dose-dependent fashion. Coculture with agonists or antagonists of the membrane or nuclear vitamin D receptors indicated that these effects were primarily mediated by the nuclear vitamin D receptors. 1\u03b1,25(OH)2D3 reduced transcription and secretion of protective IFN-\u03b3, IL-12p40, and TNF in infected PBMC and macrophages, indicating that 1\u03b1,25(OH)2D3 does not mediate protection via these cytokines. Although NOS2A was up-regulated by 1\u03b1,25(OH)2D3, inhibition of NO formation marginally affected the suppressive effect of 1\u03b1,25(OH)2D3 on bacillus Calmette Gue\u0301rin in infected cells. By contrast, 1\u03b1,25(OH)2D3 strongly up-regulated the cathelicidin hCAP-18 gene, and some hCAP-18 polypeptide colocalized with CD14 in 1\u03b1,25(OH)2D3 stimulated PBMC, although no detectable LL-37 peptide was found in supernatants from similar 1\u03b1,25(OH)2D3-stimulated PBMC cultures. A total of 200 \u03bcg/ml of the active peptide LL-37, in turn, reduced the growth of Mycobacterium tuberculosis in culture by 75.7%. These findings suggest that vitamin D contributes to protection against TB by \u201cnonclassical\u201d mechanisms that include the induction of antimicrobial peptides.</jats:p>",
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