CD209 genetic polymorphism and tuberculosis disease.

<h4>Background</h4>Tuberculosis causes significant morbidity and mortality worldwide, especially in sub-Saharan Africa. DC-SIGN, encoded by CD209, is a receptor capable of binding and internalizing Mycobacterium tuberculosis. Previous studies have reported that the CD209 promoter single...

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Main Authors: Fredrik O Vannberg, Stephen J Chapman, Chiea C Khor, Kerrie Tosh, Sian Floyd, Dolly Jackson-Sillah, Amelia Crampin, Lifted Sichali, Boubacar Bah, Per Gustafson, Peter Aaby, Keith P W J McAdam, Oumou Bah-Sow, Christian Lienhardt, Giorgio Sirugo, Paul Fine, Adrian V S Hill
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2008-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0001388&type=printable
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author Fredrik O Vannberg
Stephen J Chapman
Chiea C Khor
Kerrie Tosh
Sian Floyd
Dolly Jackson-Sillah
Amelia Crampin
Lifted Sichali
Boubacar Bah
Per Gustafson
Peter Aaby
Keith P W J McAdam
Oumou Bah-Sow
Christian Lienhardt
Giorgio Sirugo
Paul Fine
Adrian V S Hill
author_facet Fredrik O Vannberg
Stephen J Chapman
Chiea C Khor
Kerrie Tosh
Sian Floyd
Dolly Jackson-Sillah
Amelia Crampin
Lifted Sichali
Boubacar Bah
Per Gustafson
Peter Aaby
Keith P W J McAdam
Oumou Bah-Sow
Christian Lienhardt
Giorgio Sirugo
Paul Fine
Adrian V S Hill
author_sort Fredrik O Vannberg
collection DOAJ
description <h4>Background</h4>Tuberculosis causes significant morbidity and mortality worldwide, especially in sub-Saharan Africa. DC-SIGN, encoded by CD209, is a receptor capable of binding and internalizing Mycobacterium tuberculosis. Previous studies have reported that the CD209 promoter single nucleotide polymorphism (SNP)-336A/G exerts an effect on CD209 expression and is associated with human susceptibility to dengue, HIV-1 and tuberculosis in humans. The present study investigates the role of the CD209 -336A/G variant in susceptibility to tuberculosis in a large sample of individuals from sub-Saharan Africa.<h4>Methods and findings</h4>A total of 2,176 individuals enrolled in tuberculosis case-control studies from four sub-Saharan Africa countries were genotyped for the CD209 -336A/G SNP (rs4804803). Significant overall protection against pulmonary tuberculosis was observed with the -336G allele when the study groups were combined (n = 914 controls vs. 1262 cases, Mantel-Haenszel 2 x 2 chi(2) = 7.47, P = 0.006, odds ratio = 0.86, 95%CI 0.77-0.96). In addition, the patients with -336GG were associated with a decreased risk of cavitory tuberculosis, a severe form of tuberculosis disease (n = 557, Pearson's 2x2 chi(2) = 17.34, P = 0.00003, odds ratio = 0.42, 95%CI 0.27-0.65). This direction of association is opposite to a previously observed result in a smaller study of susceptibility to tuberculosis in a South African Coloured population, but entirely in keeping with the previously observed protective effect of the -336G allele.<h4>Conclusion</h4>This study finds that the CD209 -336G variant allele is associated with significant protection against tuberculosis in individuals from sub-Saharan Africa and, furthermore, cases with -336GG were significantly less likely to develop tuberculosis-induced lung cavitation. Previous in vitro work demonstrated that the promoter variant -336G allele causes down-regulation of CD209 mRNA expression. Our present work suggests that decreased levels of the DC-SIGN receptor may therefore be protective against both clinical tuberculosis in general and cavitory tuberculosis disease in particular. This is consistent with evidence that Mycobacteria can utilize DC-SIGN binding to suppress the protective pro-inflammatory immune response.
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spelling doaj-art-3bf431da418046018b6816ba4cdf67fc2025-08-20T02:00:47ZengPublic Library of Science (PLoS)PLoS ONE1932-62032008-01-0131e138810.1371/journal.pone.0001388CD209 genetic polymorphism and tuberculosis disease.Fredrik O VannbergStephen J ChapmanChiea C KhorKerrie ToshSian FloydDolly Jackson-SillahAmelia CrampinLifted SichaliBoubacar BahPer GustafsonPeter AabyKeith P W J McAdamOumou Bah-SowChristian LienhardtGiorgio SirugoPaul FineAdrian V S Hill<h4>Background</h4>Tuberculosis causes significant morbidity and mortality worldwide, especially in sub-Saharan Africa. DC-SIGN, encoded by CD209, is a receptor capable of binding and internalizing Mycobacterium tuberculosis. Previous studies have reported that the CD209 promoter single nucleotide polymorphism (SNP)-336A/G exerts an effect on CD209 expression and is associated with human susceptibility to dengue, HIV-1 and tuberculosis in humans. The present study investigates the role of the CD209 -336A/G variant in susceptibility to tuberculosis in a large sample of individuals from sub-Saharan Africa.<h4>Methods and findings</h4>A total of 2,176 individuals enrolled in tuberculosis case-control studies from four sub-Saharan Africa countries were genotyped for the CD209 -336A/G SNP (rs4804803). Significant overall protection against pulmonary tuberculosis was observed with the -336G allele when the study groups were combined (n = 914 controls vs. 1262 cases, Mantel-Haenszel 2 x 2 chi(2) = 7.47, P = 0.006, odds ratio = 0.86, 95%CI 0.77-0.96). In addition, the patients with -336GG were associated with a decreased risk of cavitory tuberculosis, a severe form of tuberculosis disease (n = 557, Pearson's 2x2 chi(2) = 17.34, P = 0.00003, odds ratio = 0.42, 95%CI 0.27-0.65). This direction of association is opposite to a previously observed result in a smaller study of susceptibility to tuberculosis in a South African Coloured population, but entirely in keeping with the previously observed protective effect of the -336G allele.<h4>Conclusion</h4>This study finds that the CD209 -336G variant allele is associated with significant protection against tuberculosis in individuals from sub-Saharan Africa and, furthermore, cases with -336GG were significantly less likely to develop tuberculosis-induced lung cavitation. Previous in vitro work demonstrated that the promoter variant -336G allele causes down-regulation of CD209 mRNA expression. Our present work suggests that decreased levels of the DC-SIGN receptor may therefore be protective against both clinical tuberculosis in general and cavitory tuberculosis disease in particular. This is consistent with evidence that Mycobacteria can utilize DC-SIGN binding to suppress the protective pro-inflammatory immune response.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0001388&type=printable
spellingShingle Fredrik O Vannberg
Stephen J Chapman
Chiea C Khor
Kerrie Tosh
Sian Floyd
Dolly Jackson-Sillah
Amelia Crampin
Lifted Sichali
Boubacar Bah
Per Gustafson
Peter Aaby
Keith P W J McAdam
Oumou Bah-Sow
Christian Lienhardt
Giorgio Sirugo
Paul Fine
Adrian V S Hill
CD209 genetic polymorphism and tuberculosis disease.
PLoS ONE
title CD209 genetic polymorphism and tuberculosis disease.
title_full CD209 genetic polymorphism and tuberculosis disease.
title_fullStr CD209 genetic polymorphism and tuberculosis disease.
title_full_unstemmed CD209 genetic polymorphism and tuberculosis disease.
title_short CD209 genetic polymorphism and tuberculosis disease.
title_sort cd209 genetic polymorphism and tuberculosis disease
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0001388&type=printable
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