PMID- 16988194
OWN - NLM
STAT- MEDLINE
DCOM- 20070515
LR  - 20081121
IS  - 0031-3998 (Print)
IS  - 0031-3998 (Linking)
VI  - 60
IP  - 5
DP  - 2006 Nov
TI  - Involvement of TNFalpha -308A promoter polymorphism in the development of asthma 
      in children infected with Chlamydophila pneumoniae.
PG  - 543-8
AB  - Several data indicate a connection between Chlamydophila pneumoniae infection and 
      asthma. Although C. pneumoniae is a common cause of infection, not all infected 
      patients develop asthma. This suggests that certain individuals may be 
      genetically predisposed to the chronic effects of C. pneumoniae infection on 
      airway functions. We investigated the possible modifying effect of different 
      polymorphisms on C. pneumoniae infection and on the susceptibility to asthma in 
      318 children, among those 144 had asthma and 174 had no asthmatic symptoms. C. 
      pneumoniae-specific antibodies were measured by ELISA. Tumor necrosis 
      factor-alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), and RANTES 
      (regulated on activation normal T cell expressed and secreted) genotypes were 
      determined by PCR-restriction fragment length polymorphism (RFLP). There were no 
      significant differences in the percentage of children positive for C. 
      pneumoniae-specific antibodies between cases and controls. None of the genotypes 
      was associated with altered susceptibility to C. pneumoniae infection. Among 
      asthmatic children carrying the TNFalpha -308A allele, there were significantly 
      more patients positive for C. pneumoniae-specific IgG, than among control 
      children carrying the same allele (20.1% versus 9.2% of asthmatic versus control 
      children, respectively; p = 0.002; odds ratio = 3.52 (1.52-7.53); p = 0.005). 
      This study indicates the possible roles of polymorphisms in the immune system in 
      the susceptibility to asthma in children infected with C. pneumoniae.
FAU - Tolgyesi, Gergely
AU  - Tolgyesi G
AD  - Department of Genetics, Cell and Immunobiology, Semmelweis University, H-1089, 
      Budapest, Hungary.
FAU - Keszei, Marton
AU  - Keszei M
FAU - Ungvari, Ildiko
AU  - Ungvari I
FAU - Nagy, Adrienne
AU  - Nagy A
FAU - Falus, Andras
AU  - Falus A
FAU - Szalai, Csaba
AU  - Szalai C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060920
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Antibodies)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adolescent
MH  - Antibodies/blood
MH  - *Asthma/etiology/genetics/immunology
MH  - Chemokine CCL2/genetics/metabolism
MH  - Chemokine CCL5/genetics/metabolism
MH  - Child
MH  - Child, Preschool
MH  - *Chlamydophila Infections/complications/immunology
MH  - Chlamydophila pneumoniae/*immunology
MH  - Disease Susceptibility
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Male
MH  - *Polymorphism, Genetic
MH  - *Promoter Regions, Genetic
MH  - Regression Analysis
MH  - Tumor Necrosis Factor-alpha/*genetics/metabolism
EDAT- 2006/09/22 09:00
MHDA- 2007/05/16 09:00
CRDT- 2006/09/22 09:00
PHST- 2006/09/22 09:00 [pubmed]
PHST- 2007/05/16 09:00 [medline]
PHST- 2006/09/22 09:00 [entrez]
AID - 01.pdr.0000242298.24089.52 [pii]
AID - 10.1203/01.pdr.0000242298.24089.52 [doi]
PST - ppublish
SO  - Pediatr Res. 2006 Nov;60(5):543-8. doi: 10.1203/01.pdr.0000242298.24089.52. Epub 
      2006 Sep 20.