PMID- 18940815
OWN - NLM
STAT- MEDLINE
DCOM- 20090203
LR  - 20220317
IS  - 1460-2083 (Electronic)
IS  - 0964-6906 (Print)
IS  - 0964-6906 (Linking)
VI  - 18
IP  - 2
DP  - 2009 Jan 15
TI  - MCP-1 promoter variant -362C associated with protection from pulmonary 
      tuberculosis in Ghana, West Africa.
PG  - 381-8
LID - 10.1093/hmg/ddn352 [doi]
AB  - Current endeavour focuses on human genetic factors that contribute to 
      susceptibility to or protection from tuberculosis (TB). Monocytes are crucial in 
      containing Mycobacterium tuberculosis infection, and the monocyte chemoattractant 
      protein-1 (MCP-1) cytokine plays a role in their recruitment to the site of 
      infection. The G allele of the MCP-1 promoter polymorphism at position -2581 
      relative to the ATG transcription start codon has been described to be associated 
      in Mexican and Korean TB patients with increased susceptibility to TB. We 
      genotyped this and additional MCP-1 variants in sample collections comprising 
      more than 2000 cases with pulmonary TB and more than 2300 healthy controls and 
      332 affected nuclear families from Ghana, West Africa, and more than 1400 TB 
      patients and more than 1500 controls from Russia. In striking contrast to 
      previous reports, MCP-1 -2581G was significantly associated with resistance to TB 
      in cases versus controls [odds ratio (OR) 0.81, corrected P-value (P(corr)) = 
      0.0012] and nuclear families (OR 0.72, P(corr) = 0.04) and not with disease 
      susceptibility, whereas in the Russian sample no evidence of association was 
      found (P = 0.86). Our and other results do not support an association of MCP-1 
      -2581 with TB. In the Ghanaian population, eight additional MCP-1 polymorphisms 
      were genotyped. MCP-1 -362C was associated with resistance to TB in the 
      case-control collection (OR 0.83, P(corr) = 0.00017) and in the affected families 
      (OR 0.7, P(corr) = 0.004). Linkage disequilibrium (LD) and logistic regression 
      analyses indicate that, in Ghanaians, the effect results exclusively from the 
      MCP-1 -362 variant, whereas the effect of -2581 may in part be explained by its 
      LD with -362.
FAU - Thye, Thorsten
AU  - Thye T
AD  - Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, 
      Hamburg, Germany.
FAU - Nejentsev, Sergey
AU  - Nejentsev S
FAU - Intemann, Christopher D
AU  - Intemann CD
FAU - Browne, Edmund N
AU  - Browne EN
FAU - Chinbuah, Margaret Amanua
AU  - Chinbuah MA
FAU - Gyapong, John
AU  - Gyapong J
FAU - Osei, Ivy
AU  - Osei I
FAU - Owusu-Dabo, Ellis
AU  - Owusu-Dabo E
FAU - Zeitels, Lauren R
AU  - Zeitels LR
FAU - Herb, Florian
AU  - Herb F
FAU - Horstmann, Rolf D
AU  - Horstmann RD
FAU - Meyer, Christian G
AU  - Meyer CG
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081020
PL  - England
TA  - Hum Mol Genet
JT  - Human molecular genetics
JID - 9208958
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Adult
MH  - Case-Control Studies
MH  - Chemokine CCL2/*genetics
MH  - Female
MH  - *Genetic Predisposition to Disease
MH  - Ghana/epidemiology
MH  - Humans
MH  - Male
MH  - Polymorphism, Genetic
MH  - *Promoter Regions, Genetic
MH  - Russia/epidemiology
MH  - Tuberculosis, Pulmonary/epidemiology/*genetics
PMC - PMC2638774
EDAT- 2008/10/23 09:00
MHDA- 2009/02/04 09:00
PMCR- 2010/01/15
CRDT- 2008/10/23 09:00
PHST- 2008/10/23 09:00 [pubmed]
PHST- 2009/02/04 09:00 [medline]
PHST- 2008/10/23 09:00 [entrez]
PHST- 2010/01/15 00:00 [pmc-release]
AID - ddn352 [pii]
AID - 10.1093/hmg/ddn352 [doi]
PST - ppublish
SO  - Hum Mol Genet. 2009 Jan 15;18(2):381-8. doi: 10.1093/hmg/ddn352. Epub 2008 Oct 
      20.