Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response-Reference-Cited by-同舟云学术

Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response

Published:2006-03-24 Issue:5768 Volume:311 Page:1770-1773
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Liu Philip T.¹²³⁴⁵,Stenger Steffen¹²³⁴⁵,Li Huiying¹²³⁴⁵,Wenzel Linda¹²³⁴⁵,Tan Belinda H.¹²³⁴⁵,Krutzik Stephan R.¹²³⁴⁵,Ochoa Maria Teresa¹²³⁴⁵,Schauber Jürgen¹²³⁴⁵,Wu Kent¹²³⁴⁵,Meinken Christoph¹²³⁴⁵,Kamen Diane L.¹²³⁴⁵,Wagner Manfred¹²³⁴⁵,Bals Robert¹²³⁴⁵,Steinmeyer Andreas¹²³⁴⁵,Zügel Ulrich¹²³⁴⁵,Gallo Richard L.¹²³⁴⁵,Eisenberg David¹²³⁴⁵,Hewison Martin¹²³⁴⁵,Hollis Bruce W.¹²³⁴⁵,Adams John S.¹²³⁴⁵,Bloom Barry R.¹²³⁴⁵,Modlin Robert L.¹²³⁴⁵

Affiliation:

1. Department of Microbiology, Immunology, and Molecular Genetics; University of California at Los Angeles, Los Angeles, CA 90095, USA.

2. Division of Dermatology, Department of Medicine, David Geffen School of Medicine; University of California at Los Angeles, Los Angeles, CA 90095, USA.

3. Department of Chemistry and Biological Chemistry, Howard Hughes Medical Institute; and Department of Energy Institute of Genomics and Proteomics, University of California at Los Angeles, Los Angeles, CA 90095, USA.

4. Institut für Klinische Mikrobiologie, Immunologie, und Hygiene, Universität Erlangen, D-91054 Erlangen, Germany.

5. Division of Dermatology, University of California at San Diego, and Veterans Affairs San Diego Healthcare Center, San Diego, CA 92161, USA.

Abstract

In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1–hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis . We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D–mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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