BACKGROUND: Factors conferring susceptibility to chronic rhinosinusitis remain unknown. However, advances in genomics offer powerful tools to explore this disorder. Tumour necrosis factor (TNF) is a crucial proinflammatory cytokine that exerts inflammatory and immunomodulatory activities important in host defense. Our objective was to determine whether polymorphisms in genes in the TNF superfamily (TNF, TNF-alpha-induced protein 3, TNF-alpha-induced protein 6) were associated with chronic rhinosinusitis. METHODS: Deoxyribonucleic acid (DNA) extracted from a population of 206 patients with severe chronic rhinosinusitis and 196 postal code-matched controls was used. Three candidate genes related to the TNF inflammatory pathway were assessed. For each gene, an informative set of single nucleotide polymorphisms was genotyped. RESULTS: Thirty-five single nucleotide polymorphisms were genotyped. Two polymorphisms located within the TNF-alpha-induced protein 3 gene (TNFAIP3) reached the nominal p value threshold (p < .05) for association with chronic rhinosinusitis. However, none of these polymorphisms resist multiple testing adjustments. CONCLUSIONS: Our data suggest that two polymorphisms in TNFAIP3 are weakly associated with severe chronic rhinosinusitis but do not support an association with genetic variants in TNF or TNF-alpha-induced protein 6. Although these results do not support correction for multiple testing and have to be validated in a second population, they nevertheless suggest that further studies of the role of TNFAIP3 in the pathogenesis of disease are warranted.
BACKGROUND: Factors conferring susceptibility to chronic rhinosinusitis remain unknown. However, advances in genomics offer powerful tools to explore this disorder. Tumour necrosis factor (TNF) is a crucial proinflammatory cytokine that exerts inflammatory and immunomodulatory activities important in host defense. Our objective was to determine whether polymorphisms in genes in the TNF superfamily (TNF, TNF-alpha-induced protein 3, TNF-alpha-induced protein 6) were associated with chronic rhinosinusitis. METHODS: Deoxyribonucleic acid (DNA) extracted from a population of 206 patients with severe chronic rhinosinusitis and 196 postal code-matched controls was used. Three candidate genes related to the TNF inflammatory pathway were assessed. For each gene, an informative set of single nucleotide polymorphisms was genotyped. RESULTS: Thirty-five single nucleotide polymorphisms were genotyped. Two polymorphisms located within the TNF-alpha-induced protein 3 gene (TNFAIP3) reached the nominal p value threshold (p < .05) for association with chronic rhinosinusitis. However, none of these polymorphisms resist multiple testing adjustments. CONCLUSIONS: Our data suggest that two polymorphisms in TNFAIP3 are weakly associated with severe chronic rhinosinusitis but do not support an association with genetic variants in TNF or TNF-alpha-induced protein 6. Although these results do not support correction for multiple testing and have to be validated in a second population, they nevertheless suggest that further studies of the role of TNFAIP3 in the pathogenesis of disease are warranted.
Authors: Joy Hsu; Pedro C Avila; Robert C Kern; M Geoffrey Hayes; Robert P Schleimer; Jayant M Pinto Journal: J Allergy Clin Immunol Date: 2013-04 Impact factor: 10.793
Authors: Tarik Ghadban; Magdalena Schmidt-Yang; Magdalena Smif; Faik G Uzunoglu; Daniel R Perez; Tung Y Tsui; Alexander T El Gammal; Peter J Erbes; Veacheslav Zilbermints; Ulrich Wellner; Klaus Pantel; Jakob R Izbicki; Yogesh K Vashist Journal: J Hum Genet Date: 2014-10-30 Impact factor: 3.172
Authors: Soo Jung Cho; Ghislaine C Echevarria; Sophia Kwon; Bushra Naveed; Edward J Schenck; Jun Tsukiji; William N Rom; David J Prezant; Anna Nolan; Michael D Weiden Journal: Respir Med Date: 2013-11-13 Impact factor: 3.415
Authors: Trilokraj Tejasvi; Philip E Stuart; Vinod Chandran; John J Voorhees; Dafna D Gladman; Proton Rahman; James T Elder; Rajan P Nair Journal: J Invest Dermatol Date: 2011-11-24 Impact factor: 8.551