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Relationship between γ-interferon gene polymorphisms and susceptibility to brucellosis infection

ABSTRACT Interferon‐gamma (IFN‐γ) is a pro‐inflammatory cytokine that plays a pivotal role in the defense mechanism against Brucella infection. It was hypothesized that the IFN‐γ in (+874 A/T in intron 1) TT and +5644 T/A, TT genotypes, which are reportedly associated with high IFN production, are a...

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Published in:Microbiology and immunology 2013-11, Vol.57 (11), p.785-791
Main Authors: Eskandari-Nasab, Ebrahim, Moghadampour, Mehdi, Hasani, Seyed-Shahaboddin, Hadadi-fishani, Mehdi, Mirghanizadeh-Bafghi, Seyyed-Ali, Asadi-Saghandi, Abolghasem, Zare, Fateme, Sadeghi-Kalani, Behrooz, Ghazali-bina, Mehran
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cited_by cdi_FETCH-LOGICAL-c4463-89e41fdae7c4669d3ec3efeb05f48192762d50b488312ddfdc999258f5d096403
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container_issue 11
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container_title Microbiology and immunology
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creator Eskandari-Nasab, Ebrahim
Moghadampour, Mehdi
Hasani, Seyed-Shahaboddin
Hadadi-fishani, Mehdi
Mirghanizadeh-Bafghi, Seyyed-Ali
Asadi-Saghandi, Abolghasem
Zare, Fateme
Sadeghi-Kalani, Behrooz
Ghazali-bina, Mehran
description ABSTRACT Interferon‐gamma (IFN‐γ) is a pro‐inflammatory cytokine that plays a pivotal role in the defense mechanism against Brucella infection. It was hypothesized that the IFN‐γ in (+874 A/T in intron 1) TT and +5644 T/A, TT genotypes, which are reportedly associated with high IFN production, are associated with susceptibility to brucellosis in Iranian subjects. Genotyping of these IFN‐γ variants by an allele‐specific polymerase chain reaction method was performed in 281 subjects, comprising 153 patients with active brucellosis and 128 healthy controls. It was found that the +874 minor allele (A) and homozygote genotype (AA) were significantly more frequently present in brucellosis patients than in controls (OR = 2.588; 95% CI, 1.313–5.104; P = 0.006 for the AA genotype; OR = 1.575; 95% CI, 1.124–2.216; P = 0.010 for the A allele). However, the allelic and genotypic distribution of the IFN‐γ polymorphism at position UTR5644 A>T did not differ significantly between patients and controls (P > 0.05). The distribution of haplotypes in this study suggests that the T/A haplotype (+874/UTR5644), which was present more frequently in controls than in patients, may protect subjects against Brucella infection. It is suggested that IFN‐γ +874 AA genotype and A allele are risk factors for developing brucellosis infection in Iranian subjects.
doi_str_mv 10.1111/1348-0421.12093
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It was hypothesized that the IFN‐γ in (+874 A/T in intron 1) TT and +5644 T/A, TT genotypes, which are reportedly associated with high IFN production, are associated with susceptibility to brucellosis in Iranian subjects. Genotyping of these IFN‐γ variants by an allele‐specific polymerase chain reaction method was performed in 281 subjects, comprising 153 patients with active brucellosis and 128 healthy controls. It was found that the +874 minor allele (A) and homozygote genotype (AA) were significantly more frequently present in brucellosis patients than in controls (OR = 2.588; 95% CI, 1.313–5.104; P = 0.006 for the AA genotype; OR = 1.575; 95% CI, 1.124–2.216; P = 0.010 for the A allele). However, the allelic and genotypic distribution of the IFN‐γ polymorphism at position UTR5644 A&gt;T did not differ significantly between patients and controls (P &gt; 0.05). The distribution of haplotypes in this study suggests that the T/A haplotype (+874/UTR5644), which was present more frequently in controls than in patients, may protect subjects against Brucella infection. 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The distribution of haplotypes in this study suggests that the T/A haplotype (+874/UTR5644), which was present more frequently in controls than in patients, may protect subjects against Brucella infection. It is suggested that IFN‐γ +874 AA genotype and A allele are risk factors for developing brucellosis infection in Iranian subjects.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Brucella - physiology</subject><subject>Brucellosis</subject><subject>Brucellosis - genetics</subject><subject>Brucellosis - microbiology</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Female</subject><subject>gene polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>interferon-gamma</subject><subject>Interferon-gamma - genetics</subject><subject>Iran</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Young Adult</subject><issn>0385-5600</issn><issn>1348-0421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFkMtu1DAUhi1ERaeFNTvkJZu0vsdewgBtpZkicRFLK4mPqSGJUztRmefqe_BMJEw723pzJOv7P53zI_SakjM6v3PKhS6IYPSMMmL4M7Q6_DxHK8K1LKQi5Bid5PyLEFYyLV6gYyYI50LpFaq-QFuNIfb5Jgy4hvEOoMd_74vQj5A8pNjjn9ADHmK762IabkLuMq56h_OUGxjGUIc2jDs8RlynqYG2jTlkHHoPzSJ-iY581WZ49TBP0fdPH7-tL4vN54ur9btN0QiheKENCOpdBWUjlDKOQ8PBQ02kF5oaVirmJKmF1pwy57xrjDFMai8dMWq-5xS93XuHFG8nyKPtQl7WqXqIU7ZUSEOlkKWa0fM92qSYcwJvhxS6Ku0sJXbp1S4t2qVF-7_XOfHmQT7VHbgD_1jkDMg9cBda2D3ls9ur7aO42OdCHuHPIVel31aVvJT2x_WFXX99_2GzNVu74f8APIqTpg</recordid><startdate>201311</startdate><enddate>201311</enddate><creator>Eskandari-Nasab, Ebrahim</creator><creator>Moghadampour, Mehdi</creator><creator>Hasani, Seyed-Shahaboddin</creator><creator>Hadadi-fishani, Mehdi</creator><creator>Mirghanizadeh-Bafghi, Seyyed-Ali</creator><creator>Asadi-Saghandi, Abolghasem</creator><creator>Zare, Fateme</creator><creator>Sadeghi-Kalani, Behrooz</creator><creator>Ghazali-bina, Mehran</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201311</creationdate><title>Relationship between γ-interferon gene polymorphisms and susceptibility to brucellosis infection</title><author>Eskandari-Nasab, Ebrahim ; Moghadampour, Mehdi ; Hasani, Seyed-Shahaboddin ; Hadadi-fishani, Mehdi ; Mirghanizadeh-Bafghi, Seyyed-Ali ; Asadi-Saghandi, Abolghasem ; Zare, Fateme ; Sadeghi-Kalani, Behrooz ; Ghazali-bina, Mehran</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4463-89e41fdae7c4669d3ec3efeb05f48192762d50b488312ddfdc999258f5d096403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Brucella - physiology</topic><topic>Brucellosis</topic><topic>Brucellosis - genetics</topic><topic>Brucellosis - microbiology</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Female</topic><topic>gene polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>interferon-gamma</topic><topic>Interferon-gamma - genetics</topic><topic>Iran</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eskandari-Nasab, Ebrahim</creatorcontrib><creatorcontrib>Moghadampour, Mehdi</creatorcontrib><creatorcontrib>Hasani, Seyed-Shahaboddin</creatorcontrib><creatorcontrib>Hadadi-fishani, Mehdi</creatorcontrib><creatorcontrib>Mirghanizadeh-Bafghi, Seyyed-Ali</creatorcontrib><creatorcontrib>Asadi-Saghandi, Abolghasem</creatorcontrib><creatorcontrib>Zare, Fateme</creatorcontrib><creatorcontrib>Sadeghi-Kalani, Behrooz</creatorcontrib><creatorcontrib>Ghazali-bina, Mehran</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Microbiology and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eskandari-Nasab, Ebrahim</au><au>Moghadampour, Mehdi</au><au>Hasani, Seyed-Shahaboddin</au><au>Hadadi-fishani, Mehdi</au><au>Mirghanizadeh-Bafghi, Seyyed-Ali</au><au>Asadi-Saghandi, Abolghasem</au><au>Zare, Fateme</au><au>Sadeghi-Kalani, Behrooz</au><au>Ghazali-bina, Mehran</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship between γ-interferon gene polymorphisms and susceptibility to brucellosis infection</atitle><jtitle>Microbiology and immunology</jtitle><addtitle>Microbiol Immunol</addtitle><date>2013-11</date><risdate>2013</risdate><volume>57</volume><issue>11</issue><spage>785</spage><epage>791</epage><pages>785-791</pages><issn>0385-5600</issn><eissn>1348-0421</eissn><abstract>ABSTRACT Interferon‐gamma (IFN‐γ) is a pro‐inflammatory cytokine that plays a pivotal role in the defense mechanism against Brucella infection. It was hypothesized that the IFN‐γ in (+874 A/T in intron 1) TT and +5644 T/A, TT genotypes, which are reportedly associated with high IFN production, are associated with susceptibility to brucellosis in Iranian subjects. Genotyping of these IFN‐γ variants by an allele‐specific polymerase chain reaction method was performed in 281 subjects, comprising 153 patients with active brucellosis and 128 healthy controls. It was found that the +874 minor allele (A) and homozygote genotype (AA) were significantly more frequently present in brucellosis patients than in controls (OR = 2.588; 95% CI, 1.313–5.104; P = 0.006 for the AA genotype; OR = 1.575; 95% CI, 1.124–2.216; P = 0.010 for the A allele). However, the allelic and genotypic distribution of the IFN‐γ polymorphism at position UTR5644 A&gt;T did not differ significantly between patients and controls (P &gt; 0.05). The distribution of haplotypes in this study suggests that the T/A haplotype (+874/UTR5644), which was present more frequently in controls than in patients, may protect subjects against Brucella infection. It is suggested that IFN‐γ +874 AA genotype and A allele are risk factors for developing brucellosis infection in Iranian subjects.</abstract><cop>Australia</cop><pub>Blackwell Publishing Ltd</pub><pmid>24033468</pmid><doi>10.1111/1348-0421.12093</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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ispartof Microbiology and immunology, 2013-11, Vol.57 (11), p.785-791
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1348-0421
language eng
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source Wiley-Blackwell Read & Publish Collection; Alma/SFX Local Collection
subjects Adolescent
Adult
Aged
Brucella - physiology
Brucellosis
Brucellosis - genetics
Brucellosis - microbiology
Case-Control Studies
Child
European Continental Ancestry Group - genetics
Female
gene polymorphism
Genetic Predisposition to Disease
Genotype
Humans
interferon-gamma
Interferon-gamma - genetics
Iran
Male
Middle Aged
Polymorphism, Single Nucleotide
Young Adult
title Relationship between γ-interferon gene polymorphisms and susceptibility to brucellosis infection
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