Evidence map›Paper›PMID 29965969›Full record

ArticlePLoS neglected tropical diseases2018

Vitamin D status contributes to the antimicrobial activity of macrophages against Mycobacterium leprae.

Elliot W Kim, Rosane M B Teles, Salem Haile, Philip T Liu, Robert L Modlin

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  16. Bovine Immunity and Vitamin DMicroorganisms · 2022
    Review
  17. Vitamin D and the Kidney: Two Players, One Console.International journal of molecular sciences · 2022
    Review
  18. The Immunomodulatory Properties of Vitamin D.Mediterranean journal of rheumatology · 2022
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Elliot W KimMolecular Biology Institute, University of California, Los Angeles, Los Angeles, California, United States of America.
Rosane M B TelesDivision of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America.ORCID 0000-0003-2908-3244
Salem HaileDepartment of Hematology and Oncology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, United States of America.ORCID 0000-0003-0484-7930
Philip T LiuDivision of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America.
Robert L ModlinMolecular Biology Institute, University of California, Los Angeles, Los Angeles, California, United States of America.ORCID 0000-0003-4720-031X
University of California, Los Angeles · US

Funding

Molecular Analysis of the Host Immune Response in LeprosyR01AI022553 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROBERT L MODLIN · 1989 to 2026
$15.7M
TCR GAMMA/DELTA LYMPHOCYTES IN HUMAN SKIN LESIONSR01AR040312 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MODLIN, ROBERT L · 1990 to 2025
$10.4M
Anti-TB sterilizing immunity in immune and HIV+ individualsR01HL129887 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHEN, ZHENG W · 2015 to 2018
$2.1M
Role of Vitamin D Prohormone 25-OHD in the Immune Response to TuberculosisR01HL119068 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LIU, PHILIP T., MODLIN, ROBERT L · 2014 to 2017
$1.5M
NHLBI NIH HHS R01 HL119068NHLBI NIH HHS R01 HL129887NIAID NIH HHS R01 AI022553NIAMS NIH HHS R01 AR040312NIH HHS AI022553NIH HHS AR40312NIH HHS HL119068
6 · The paper itself

Abstract

backgroundThe immune system depends on effector pathways to eliminate invading pathogens from the host in vivo. Macrophages (MΦ) of the innate immune system are armed with vitamin D-dependent antimicrobial responses to kill intracellular microbes. However, how the physiological levels of vitamin D during MΦ differentiation affect phenotype and function is unknown. METHODOLOGY/PRINCIPAL: The human innate immune system consists of divergent MΦ subsets that serve distinct functions in vivo. Both IL-15 and IL-10 induce MΦ differentiation, but IL-15 induces primary human monocytes to differentiate into antimicrobial MΦ (IL-15 MΦ) that robustly express the vitamin D pathway. However, how vitamin D status alters IL-15 MΦ phenotype and function is unknown. In this study, we found that adding 25-hydroxyvitamin D3 (25D3) during the IL-15 induced differentiation of monocytes into MΦ increased the expression of the antimicrobial peptide cathelicidin, including both CAMP mRNA and the encoded protein cathelicidin in a dose-dependent manner. The presence of physiological levels of 25D during differentiation of IL-15 MΦ led to a significant vitamin D-dependent antimicrobial response against intracellular Mycobacterium leprae but did not change the phenotype or phagocytic function of these MΦ. These data suggest that activation of the vitamin D pathway during IL-15 MΦ differentiation augments the antimicrobial response against M. leprae infection. CONCLUSIONS/SIGNIFICANCE: Our data demonstrates that the presence of vitamin D during MΦ differentiation bestows the capacity to mount an antimicrobial response against M. leprae.

Indexed as

Cell DifferentiationHumansInterleukin-10Interleukin-15LeprosyMacrophagesMycobacterium lepraeVitamin DInterleukin-10Interleukin-15Vitamin D

Identifiers

PMID29965969
PMCPMC6044553
OpenAlexW2810887536

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.