PMID- 16352737
OWN - NLM
STAT- MEDLINE
DCOM- 20060523
LR  - 20240326
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 202
IP  - 12
DP  - 2005 Dec 19
TI  - A functional promoter polymorphism in monocyte chemoattractant protein-1 is 
      associated with increased susceptibility to pulmonary tuberculosis.
PG  - 1649-58
AB  - We examined the distribution of single nucleotide polymorphisms (SNPs) in nitric 
      oxide synthase 2A, monocyte chemoattractant protein-1 (MCP-1), regulated on 
      activation, normal T cell expressed and secreted, and macrophage inflammatory 
      protein-1alpha genes in tuberculosis patients and healthy controls from Mexico. 
      The odds of developing tuberculosis were 2.3- and 5.4-fold higher in carriers of 
      MCP-1 genotypes AG and GG than in homozygous AA. Cases of homozygous GG had the 
      highest plasma levels of MCP-1 and the lowest plasma levels of IL-12p40, and 
      these values were negatively correlated. Furthermore, stimulation of monocytes 
      from healthy carriers of the genotype GG with Mycobacterium tuberculosis antigens 
      yielded higher MCP-1 and lower IL-12p40 concentrations than parallel experiments 
      with monocytes from homozygous AA. Addition of anti-MCP-1 increased IL-12p40 
      levels in cultures of M. tuberculosis-stimulated monocytes from homozygous GG, 
      and addition of exogenous MCP-1 reduced IL-12p40 production by M. 
      tuberculosis-stimulated monocytes from homozygous AA. Furthermore, we could 
      replicate our results in Korean subjects, in whom the odds of developing 
      tuberculosis were 2.8- and 6.9-fold higher in carriers of MCP-1 genotypes AG and 
      GG than in homozygous AA. Our findings suggest that persons bearing the MCP-1 
      genotype GG produce high concentrations of MCP-1, which inhibits production of 
      IL-12p40 in response to M. tuberculosis and increases the likelihood that M. 
      tuberculosis infection will progress to active pulmonary tuberculosis.
FAU - Flores-Villanueva, Pedro O
AU  - Flores-Villanueva PO
AD  - Center for Biomedical Research, University of Texas Health Center at Tyler, 
      Tyler, TX 75708, USA. pedro.flores@UTHCT.edu
FAU - Ruiz-Morales, Jorge A
AU  - Ruiz-Morales JA
FAU - Song, Chang-Hwa
AU  - Song CH
FAU - Flores, Ludmila M
AU  - Flores LM
FAU - Jo, Eun-Kyeong
AU  - Jo EK
FAU - Montano, Marta
AU  - Montano M
FAU - Barnes, Peter F
AU  - Barnes PF
FAU - Selman, Moises
AU  - Selman M
FAU - Granados, Julio
AU  - Granados J
LA  - eng
GR  - K30 HL004095/HL/NHLBI NIH HHS/United States
GR  - R21 HL072177/HL/NHLBI NIH HHS/United States
GR  - HL04095-04/HL/NHLBI NIH HHS/United States
GR  - R21 HL72177/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20051213
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (DNA Primers)
RN  - 0 (Interleukin-12 Subunit p40)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Protein Subunits)
RN  - 187348-17-0 (Interleukin-12)
RN  - EC 1.14.13.39 (NOS2 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Chemokine CCL2/blood/*genetics/*metabolism
MH  - Chemokine CCL4
MH  - DNA Primers
MH  - Enzyme-Linked Immunosorbent Assay
MH  - *Epistasis, Genetic
MH  - *Genetic Predisposition to Disease
MH  - Humans
MH  - Interleukin-12/blood/*metabolism
MH  - Interleukin-12 Subunit p40
MH  - Korea
MH  - Macrophage Inflammatory Proteins/genetics
MH  - Mexico
MH  - Middle Aged
MH  - Nitric Oxide Synthase Type II/genetics
MH  - Polymorphism, Single Nucleotide/genetics
MH  - Promoter Regions, Genetic/genetics
MH  - Protein Subunits/blood/*metabolism
MH  - Tuberculosis, Pulmonary/*genetics
PMC - PMC2212957
EDAT- 2005/12/15 09:00
MHDA- 2006/05/24 09:00
PMCR- 2006/06/19
CRDT- 2005/12/15 09:00
PHST- 2005/12/15 09:00 [pubmed]
PHST- 2006/05/24 09:00 [medline]
PHST- 2005/12/15 09:00 [entrez]
PHST- 2006/06/19 00:00 [pmc-release]
AID - jem.20050126 [pii]
AID - 20050126 [pii]
AID - 10.1084/jem.20050126 [doi]
PST - ppublish
SO  - J Exp Med. 2005 Dec 19;202(12):1649-58. doi: 10.1084/jem.20050126. Epub 2005 Dec 
      13.