PMID- 23269628
OWN - NLM
STAT- MEDLINE
DCOM- 20131203
LR  - 20211021
IS  - 1573-4978 (Electronic)
IS  - 0301-4851 (Linking)
VI  - 40
IP  - 6
DP  - 2013 Jun
TI  - Association of interleukin-18 gene variants with susceptibility to visceral 
      leishmaniasis in Iranian population.
PG  - 4009-14
LID - 10.1007/s11033-012-2479-x [doi]
AB  - Host resistance to Leishmania infection is mediated by cellular immune responses 
      leading to macrophage activation and parasite killing. Interleukin-18 (IL-18) 
      known as interferon-gamma (IFN-gamma) inducing factor, stimulates IFN-gamma production by T 
      cells. Taking into account the important role of IL-18 in the defense against 
      visceral leishmaniasis (VL) and the known effect of IL-18 gene polymorphisms on 
      its production, the aim of this study was to investigate the probable 
      relationship between IL-18 gene polymorphisms and the susceptibility to VL. The 
      study groups included 118 pediatric patients who suffered from VL and 156 
      non-relative healthy people as the controls from the same endemic area. IL-18 
      gene polymorphisms at the positions -656 G/T, -137 G/C and +105A/C (codon 35/3) 
      were analyzed by polymerase chain reaction-restricted fragment length 
      polymorphism (PCR-RFLP). The results showed that the frequency of T allele at the 
      position -656 was significantly higher in the controls, compared with that in the 
      patients (P = 0.047), but it couldn't tolerate Bonferroni correction. Regarding 
      the IL-18 genotypes, there was no significant difference between the patients and 
      controls. Although the frequencies of ATG single haplotype and AGG/ATG double 
      haplotype were significantly higher in the controls (P = 0.043) and the patients 
      (P = 0.044), respectively, the two P values couldn't tolerate Bonferroni 
      correction. Furthermore, a strong linkage disequilibrium was observed among the 
      -656, -137 and +105 single nucleotide polymorphisms of IL-18 gene (all Ps < 
      0.001). In conclusion, this study suggests that the inheritance of T allele at 
      the position -656 may be considered as a genetic factor for resistance to VL.
FAU - Moravej, Ali
AU  - Moravej A
AD  - Department of Immunology, Fasa University of Medical Sciences, Fasa, Fars, Iran.
FAU - Rasouli, Manoochehr
AU  - Rasouli M
FAU - Asaei, Sadaf
AU  - Asaei S
FAU - Kalani, Mehdi
AU  - Kalani M
FAU - Mansoori, Yaser
AU  - Mansoori Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121227
PL  - Netherlands
TA  - Mol Biol Rep
JT  - Molecular biology reports
JID - 0403234
RN  - 0 (Interleukin-18)
SB  - IM
MH  - Adolescent
MH  - Case-Control Studies
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - Gene Frequency/genetics
MH  - *Genetic Association Studies
MH  - *Genetic Predisposition to Disease
MH  - Haplotypes/genetics
MH  - Humans
MH  - Infant
MH  - Interleukin-18/*genetics
MH  - Iran
MH  - Leishmaniasis, Visceral/*genetics
MH  - Linkage Disequilibrium/genetics
MH  - Male
MH  - Polymorphism, Single Nucleotide/*genetics
EDAT- 2012/12/28 06:00
MHDA- 2013/12/16 06:00
CRDT- 2012/12/28 06:00
PHST- 2012/08/18 00:00 [received]
PHST- 2012/12/18 00:00 [accepted]
PHST- 2012/12/28 06:00 [entrez]
PHST- 2012/12/28 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - 10.1007/s11033-012-2479-x [doi]
PST - ppublish
SO  - Mol Biol Rep. 2013 Jun;40(6):4009-14. doi: 10.1007/s11033-012-2479-x. Epub 2012 
      Dec 27.