Association of interleukin-18 gene variants with susceptibility to visceral leishmaniasis in Iranian population
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-γ (IFN-γ) inducing factor, stimulates IFN-γ production by T cells. Taking into account the important role of IL-18 in the...
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| creator | Moravej, Ali Rasouli, Manoochehr Asaei, Sadaf Kalani, Mehdi Mansoori, Yaser |
| description | 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-γ (IFN-γ) inducing factor, stimulates IFN-γ 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
P
s |
| doi_str_mv | 10.1007/s11033-012-2479-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1367487212</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2983844001</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-dc24c1deeabc64eab083c5f99f163d6491d2e9ab72533dc4ca149b253a824ff3</originalsourceid><addsrcrecordid>eNqNkU9vFiEQxonR2Ld_PoAXQ-LFC8oAu8Cxaapt0sRL74Rl2Za6L6zA1vbby-tbG9PExAtkht88M8OD0Dugn4BS-bkAUM4JBUaYkJo8vEIb6CQnQkv1Gm0op0CE6uAAHZZyRykVILu36IBx1uueqQ1Kp6UkF2wNKeI04RCrz7Nfv4dIQOEbHz2-tznYWAv-GeotLmtxfqlhCHOoj7gmfB9aJtsZzz6U262NwZZQmhS-zLsg4iUt6_y7xzF6M9m5-JOn-whdfzm_PrsgV9--Xp6dXhEnaFfJ6JhwMHpvB9eLdlLFXTdpPUHPx15oGJnXdpCs43x0wlkQemiBVUxMEz9CH_eyS04_Vl-q2e6GnGcbfVqLAd5LoSQD9h9o-03KlRIN_fACvUtrjm2PRnW90kr0slGwp1xOpWQ_mSWHrc2PBqjZ-Wb2vpnmm9n5Zh5azfsn5XXY-vG54o9RDWB7oLSneOPzX63_qfoLlEqlIw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1356898467</pqid></control><display><type>article</type><title>Association of interleukin-18 gene variants with susceptibility to visceral leishmaniasis in Iranian population</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Moravej, Ali ; Rasouli, Manoochehr ; Asaei, Sadaf ; Kalani, Mehdi ; Mansoori, Yaser</creator><creatorcontrib>Moravej, Ali ; Rasouli, Manoochehr ; Asaei, Sadaf ; Kalani, Mehdi ; Mansoori, Yaser</creatorcontrib><description>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-γ (IFN-γ) inducing factor, stimulates IFN-γ 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
P
s < 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.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-012-2479-x</identifier><identifier>PMID: 23269628</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adolescent ; Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Gene Frequency - genetics ; Genes ; Genetic Association Studies ; Genetic Predisposition to Disease ; Haplotypes - genetics ; Histology ; Humans ; Infant ; Interleukin-18 - genetics ; Iran ; Leishmania ; Leishmaniasis, Visceral - genetics ; Life Sciences ; Linkage Disequilibrium - genetics ; Male ; Morphology ; Polymerase chain reaction ; Polymorphism, Single Nucleotide - genetics ; Population genetics</subject><ispartof>Molecular biology reports, 2013-06, Vol.40 (6), p.4009-4014</ispartof><rights>Springer Science+Business Media Dordrecht 2012</rights><rights>Springer Science+Business Media Dordrecht 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-dc24c1deeabc64eab083c5f99f163d6491d2e9ab72533dc4ca149b253a824ff3</citedby><cites>FETCH-LOGICAL-c405t-dc24c1deeabc64eab083c5f99f163d6491d2e9ab72533dc4ca149b253a824ff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-012-2479-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-012-2479-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23269628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moravej, Ali</creatorcontrib><creatorcontrib>Rasouli, Manoochehr</creatorcontrib><creatorcontrib>Asaei, Sadaf</creatorcontrib><creatorcontrib>Kalani, Mehdi</creatorcontrib><creatorcontrib>Mansoori, Yaser</creatorcontrib><title>Association of interleukin-18 gene variants with susceptibility to visceral leishmaniasis in Iranian population</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>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-γ (IFN-γ) inducing factor, stimulates IFN-γ 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
P
s < 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.</description><subject>Adolescent</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Female</subject><subject>Gene Frequency - genetics</subject><subject>Genes</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Haplotypes - genetics</subject><subject>Histology</subject><subject>Humans</subject><subject>Infant</subject><subject>Interleukin-18 - genetics</subject><subject>Iran</subject><subject>Leishmania</subject><subject>Leishmaniasis, Visceral - genetics</subject><subject>Life Sciences</subject><subject>Linkage Disequilibrium - genetics</subject><subject>Male</subject><subject>Morphology</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Single Nucleotide - 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genetics</topic><topic>Genes</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Haplotypes - genetics</topic><topic>Histology</topic><topic>Humans</topic><topic>Infant</topic><topic>Interleukin-18 - genetics</topic><topic>Iran</topic><topic>Leishmania</topic><topic>Leishmaniasis, Visceral - genetics</topic><topic>Life Sciences</topic><topic>Linkage Disequilibrium - genetics</topic><topic>Male</topic><topic>Morphology</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Population genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moravej, Ali</creatorcontrib><creatorcontrib>Rasouli, Manoochehr</creatorcontrib><creatorcontrib>Asaei, Sadaf</creatorcontrib><creatorcontrib>Kalani, Mehdi</creatorcontrib><creatorcontrib>Mansoori, Yaser</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moravej, Ali</au><au>Rasouli, Manoochehr</au><au>Asaei, Sadaf</au><au>Kalani, Mehdi</au><au>Mansoori, Yaser</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of interleukin-18 gene variants with susceptibility to visceral leishmaniasis in Iranian population</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>40</volume><issue>6</issue><spage>4009</spage><epage>4014</epage><pages>4009-4014</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>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-γ (IFN-γ) inducing factor, stimulates IFN-γ 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
P
s < 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.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>23269628</pmid><doi>10.1007/s11033-012-2479-x</doi><tpages>6</tpages></addata></record> |
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| subjects | Adolescent Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Case-Control Studies Child Child, Preschool Female Gene Frequency - genetics Genes Genetic Association Studies Genetic Predisposition to Disease Haplotypes - genetics Histology Humans Infant Interleukin-18 - genetics Iran Leishmania Leishmaniasis, Visceral - genetics Life Sciences Linkage Disequilibrium - genetics Male Morphology Polymerase chain reaction Polymorphism, Single Nucleotide - genetics Population genetics |
| title | Association of interleukin-18 gene variants with susceptibility to visceral leishmaniasis in Iranian population |
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