Implication of BIRC5 in asthma pathogenesisCitation formats

  • External authors:
  • I. Ungvári
  • É. Hadadi
  • V. Virág
  • A. Nagy
  • T.F. Semsei
  • G. Gálffy
  • L. Tamási
  • I. Horváth
  • C. Szalai

Standard

Implication of BIRC5 in asthma pathogenesis. / Ungvári, I.; Hadadi, É.; Virág, V.; Bikov, A.; Nagy, A.; Semsei, T.F.; Gálffy, G.; Tamási, L.; Horváth, I.; Szalai, C.

In: International immunology, Vol. 24, No. 5, 2012, p. 293-301.

Research output: Contribution to journalArticle

Harvard

Ungvári, I, Hadadi, É, Virág, V, Bikov, A, Nagy, A, Semsei, TF, Gálffy, G, Tamási, L, Horváth, I & Szalai, C 2012, 'Implication of BIRC5 in asthma pathogenesis', International immunology, vol. 24, no. 5, pp. 293-301. https://doi.org/10.1093/intimm/dxs007

APA

Ungvári, I., Hadadi, É., Virág, V., Bikov, A., Nagy, A., Semsei, T. F., ... Szalai, C. (2012). Implication of BIRC5 in asthma pathogenesis. International immunology, 24(5), 293-301. https://doi.org/10.1093/intimm/dxs007

Vancouver

Ungvári I, Hadadi É, Virág V, Bikov A, Nagy A, Semsei TF et al. Implication of BIRC5 in asthma pathogenesis. International immunology. 2012;24(5):293-301. https://doi.org/10.1093/intimm/dxs007

Author

Ungvári, I. ; Hadadi, É. ; Virág, V. ; Bikov, A. ; Nagy, A. ; Semsei, T.F. ; Gálffy, G. ; Tamási, L. ; Horváth, I. ; Szalai, C. / Implication of BIRC5 in asthma pathogenesis. In: International immunology. 2012 ; Vol. 24, No. 5. pp. 293-301.

Bibtex

@article{7c7f53b33dd64699a2897a980616af50,
title = "Implication of BIRC5 in asthma pathogenesis",
abstract = "In the last few years, it has been recognized that the unbalanced regulation of survival and apoptosis of bronchial inflammatory cells is a key component in the development of asthma. Baculoviral IAP repeat containing 5 (BIRC5) (also known as survivin) is an important anti-apoptotic protein that has been implicated in many cancer types, and recent studies provide evidence for its role in controlling inflammatory disorders as well. Our aim was to investigate at both genetic and transcriptional levels if BIRC5 has an impact on asthma development. We found that induced sputum samples of patients with bronchial asthma contained elevated levels of BIRC5 mRNA compared with healthy subjects and its level was in correlation with sputum eosinophil percentages. Furthermore, in a case-control study examining single nucleotide polymorphisms (SNPs) in the BIRC5 regulatory regions, the minor alleles of rs8073903 and rs8073069 were found to be significantly associated with asthma and especially non-allergic asthma phenotypes, which associations were more prominent among women. Two marker haplotype analyses further strengthen the impact of these two polymorphisms on both asthma and non-allergic asthma. In the female cohort, rs1508147 was also significantly associated with increased risk of non-allergic asthma. Additionally, with linear regression analysis, we showed that rs9904341 was significantly correlated with both absolute and relative serum eosinophil levels. In conclusion, our results suggest that possibly by inhibition of the eosinophil apoptosis, BIRC5 might be an important regulator of the asthmatic processes and we provide some evidence that its effect might be affected by SNPs located in the gene regulatory regions. {\circledC} The Japanese Society for Immunology. 2012. All rights reserved.",
keywords = "Apoptosis, Expression, mRNA, Non-allergic asthma, SNP, Survivin, biological marker, messenger RNA, survivin, adult, allele, apoptosis, article, asthma, Birc5 gene, bronchus, cell survival, cohort analysis, controlled study, eosinophil, female, gene, gene location, genetic transcription, genetic variability, haplotype, human, inflammatory cell, major clinical study, male, pathogenesis, phenotype, priority journal, single nucleotide polymorphism, sputum analysis, Adult, Alleles, Asthma, Case-Control Studies, Female, Haplotypes, Humans, Inhibitor of Apoptosis Proteins, Linear Models, Male, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, RNA, Messenger, Young Adult",
author = "I. Ungv{\'a}ri and {\'E}. Hadadi and V. Vir{\'a}g and A. Bikov and A. Nagy and T.F. Semsei and G. G{\'a}lffy and L. Tam{\'a}si and I. Horv{\'a}th and C. Szalai",
note = "Cited By :15 Export Date: 20 February 2019 CODEN: INIME Correspondence Address: Szalai, C.; Heim P{\'a}l Children's Hospital, PO Box 66, H-1958, Budapest, Hungary; email: genomika.cs@gmail.com Chemicals/CAS: survivin, 195263-98-0; BIRC5 protein, human; Inhibitor of Apoptosis Proteins; RNA, Messenger Funding details: Eg{\'e}szs{\'e}g{\"u}gyi Tudom{\'a}nyos Tan{\'a}cs, ETT, 415/2009 Funding details: Orsz{\'a}gos Tudom{\'a}nyos Kutat{\'a}si Alapprogramok, OTKA, OTKA Funding details: Orsz{\'a}gos Tudom{\'a}nyos Kutat{\'a}si Alapprogramok, OTKA, K81941 Funding details: Nemzeti Kutat{\'a}si {\'e}s Technol{\'o}giai Hivatal, NKTH, TECH_08-A1/2-2008-0120 Funding text 1: Hungarian Scientific Research Fund (OTKA) (K81941); Scientific Committee of the Hungarian Ministry of Health (ETT) (415/2009); National Office of Research and Technology (NKTH) (TECH_08-A1/2-2008-0120). References: Vignola, A.M., Chanez, P., Chiappara, G., Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis (1999) J. Allergy Clin. Immunol., 103, p. 563; Walsh, G.M., Eosinophil apoptosis: mechanisms and clinical relevance in asthmatic and allergic inflammation (2000) Br. J. Haematol., 111, p. 61; Woolley, K.L., Gibson, P.G., Carty, K., Wilson, A.J., Twaddell, S.H., Woolley, M.J., Eosinophil apoptosis and the resolution of airway inflammation in asthma (1996) Am. J. Respir. Crit. Care Med., 154, p. 237; Kankaanranta, H., Lindsay, M.A., Giembycz, M.A., Zhang, X., Moilanen, E., Barnes, P.J., Delayed eosinophil apoptosis in asthma (2000) J. Allergy Clin. Immunol., 106, p. 77; Duncan, C.J., Lawrie, A., Blaylock, M.G., Douglas, J.G., Walsh, G.M., Reduced eosinophil apoptosis in induced sputum correlates with asthma severity (2003) Eur. Respir. J., 22, p. 484; Ambrosini, G., Adida, C., Altieri, D.C., A novel antiapoptosis gene, survivin, expressed in cancer and lymphoma (1997) Nat. Med., 3, p. 917; Li, F., Ambrosini, G., Chu, E.Y., Control of apoptosis and mitotic spindle checkpoint by survivin (1998) Nature, 396, p. 580; Tamm, I., Wang, Y., Sausville, E., IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs (1998) Cancer Res, 58, p. 5315; Ambrosini, G., Adida, C., Sirugo, G., Altieri, D.C., Induction of apoptosis and inhibition of cell proliferation by survivin gene targeting (1998) J. Biol. Chem., 273, p. 11177; Liu, T., Brouha, B., Grossman, D., Rapid induction of mitochondrial events and caspase-independent apoptosis in survivin-targeted melanoma cells (2004) Oncogene, 23, p. 39; Adida, C., Berrebi, D., Peuchmaur, M., Reyes-Mugica, M., Altieri, D.C., Anti-apoptosis gene, survivin, and prognosis of neuroblastoma (1998) Lancet, 351, p. 882; Mita, A.C., Mita, M.M., Nawrocki, S.T., Giles, F.J., Survivin: key regulator of mitosis and apoptosis and novel target for cancer therapeutics (2008) Clin. Cancer Res., 14, p. 5000; Altznauer, F., Martinelli, S., Yousefi, S., Inflammationassociated cell cycle-independent block of apoptosis by survivin in terminally differentiated neutrophils (2004) J. Exp. Med., 199, p. 1343; Vassina, E.M., Yousefi, S., Simon, D., Zwicky, C., Conus, S., Simon, H.U., cIAP-2 and survivin contribute to cytokinemediated delayed eosinophil apoptosis (2006) Eur. J. Immunol., 36, p. 1975; Tolgyesi, G., Molnar, V., Semsei, A.F., Gene expression profiling of experimental asthma reveals a possible role of paraoxonase-1 in the disease (2009) Int. Immunol., 21, p. 967; Tumes, D.J., Connolly, A., Dent, L.A., Expression of survivin in lung eosinophils is associated with pathology in a mouse model of allergic asthma (2009) Int. Immunol., 21, p. 633; Di Valentin, E., Crahay, C., Garbacki, N., New asthma biomarkers: lessons from murine models of acute and chronic asthma (2009) Am. J. Physiol. Lung Cell. Mol. Physiol., 296, pp. L185; Nathan, R.A., Sorkness, C.A., Kosinski, M., Development of the asthma control test: a survey for assessing asthma control (2004) J. Allergy Clin. Immunol., 113, p. 59; Green, R.H., Brightling, C.E., McKenna, S., Asthma exacerbations and sputum eosinophil counts: a randomised controlled trial (2002) Lancet, 360, p. 1715; Jayaram, L., Pizzichini, M.M., Cook, R.J., Determining asthma treatment by monitoring sputum cell counts: effect on exacerbations (2006) Eur. Respir. J., 27, p. 483; Schleich, F.N., Seidel, L., Sele, J., Exhaled nitric oxide thresholds associated with a sputum eosinophil count >/=3{\%} in a cohort of unselected patients with asthma (2010) Thorax, 65, p. 1039; Virchow Jr., J.C., Kroegel, C., Walker, C., Matthys, H., Inflammatory determinants of asthma severity: mediator and cellular changes in bronchoalveolar lavage fluid of patients with severe asthma (1996) J. Allergy Clin. Immunol., 98, pp. S27; Yang, X., Xiong, G., Chen, X., Survivin expression in esophageal cancer: correlation with p. 53 mutations and promoter polymorphism (2009) Dis. Esophagus, 22, p. 223; Han, C.H., Wei, Q., Lu, K.K., Liu, Z., Mills, G.B., Wang, L.E., Polymorphisms in the survivin promoter are associated with age of onset of ovarian cancer (2009) Int. J. Clin. Exp. Med., 2, p. 289; Dixon, A.L., Liang, L., Moffatt, M.F., A genome-wide association study of global gene expression (2007) Nat. Genet., 39, p. 1202; A haplotype map of the human genome (2005) Nature, 437, p. 1299. , The International HapMap Consortium; Krepela, E., Dankova, P., Moravcikova, E., Increased expression of inhibitor of apoptosis proteins, survivin and XIAP, in non-small cell lung carcinoma (2009) Int. J. Oncol., 35, p. 1449; Hmeljak, J., Erculj, N., Dolzan, V., Kern, I., Cor, A., BIRC5 promoter SNPs do not affect nuclear survivin expression and survival of malignant pleural mesothelioma patients (2011) J Cancer Res. Clin. Oncol., 137, p. 1641; Cheng, Z.J., Hu, L.H., Huang, S.J., Correlation of -31G/C polymorphisms of survivin promoter to tumorigenesis of gastric carcinoma (2008) Ai Zheng, 27, p. 258; Srivastava, K., Srivastava, A., Mittal, B., Survivin promoter -31G/C (rs9904341) polymorphism and cancer susceptibility: a meta-analysis (2012) Mol. Biol. Report., 39, p. 1509; Boidot, R., Vegran, F., Jacob, D., The expression of BIRC5 is correlated with loss of specific chromosomal regions in breast carcinomas (2008) Genes Chromosomes Cancer, 47, p. 299",
year = "2012",
doi = "10.1093/intimm/dxs007",
language = "English",
volume = "24",
pages = "293--301",
journal = "International immunology",
issn = "0953-8178",
publisher = "Oxford University Press",
number = "5",

}

RIS

TY - JOUR

T1 - Implication of BIRC5 in asthma pathogenesis

AU - Ungvári, I.

AU - Hadadi, É.

AU - Virág, V.

AU - Bikov, A.

AU - Nagy, A.

AU - Semsei, T.F.

AU - Gálffy, G.

AU - Tamási, L.

AU - Horváth, I.

AU - Szalai, C.

N1 - Cited By :15 Export Date: 20 February 2019 CODEN: INIME Correspondence Address: Szalai, C.; Heim Pál Children's Hospital, PO Box 66, H-1958, Budapest, Hungary; email: genomika.cs@gmail.com Chemicals/CAS: survivin, 195263-98-0; BIRC5 protein, human; Inhibitor of Apoptosis Proteins; RNA, Messenger Funding details: Egészségügyi Tudományos Tanács, ETT, 415/2009 Funding details: Országos Tudományos Kutatási Alapprogramok, OTKA, OTKA Funding details: Országos Tudományos Kutatási Alapprogramok, OTKA, K81941 Funding details: Nemzeti Kutatási és Technológiai Hivatal, NKTH, TECH_08-A1/2-2008-0120 Funding text 1: Hungarian Scientific Research Fund (OTKA) (K81941); Scientific Committee of the Hungarian Ministry of Health (ETT) (415/2009); National Office of Research and Technology (NKTH) (TECH_08-A1/2-2008-0120). References: Vignola, A.M., Chanez, P., Chiappara, G., Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis (1999) J. Allergy Clin. Immunol., 103, p. 563; Walsh, G.M., Eosinophil apoptosis: mechanisms and clinical relevance in asthmatic and allergic inflammation (2000) Br. J. Haematol., 111, p. 61; Woolley, K.L., Gibson, P.G., Carty, K., Wilson, A.J., Twaddell, S.H., Woolley, M.J., Eosinophil apoptosis and the resolution of airway inflammation in asthma (1996) Am. J. Respir. Crit. Care Med., 154, p. 237; Kankaanranta, H., Lindsay, M.A., Giembycz, M.A., Zhang, X., Moilanen, E., Barnes, P.J., Delayed eosinophil apoptosis in asthma (2000) J. Allergy Clin. Immunol., 106, p. 77; Duncan, C.J., Lawrie, A., Blaylock, M.G., Douglas, J.G., Walsh, G.M., Reduced eosinophil apoptosis in induced sputum correlates with asthma severity (2003) Eur. Respir. J., 22, p. 484; Ambrosini, G., Adida, C., Altieri, D.C., A novel antiapoptosis gene, survivin, expressed in cancer and lymphoma (1997) Nat. Med., 3, p. 917; Li, F., Ambrosini, G., Chu, E.Y., Control of apoptosis and mitotic spindle checkpoint by survivin (1998) Nature, 396, p. 580; Tamm, I., Wang, Y., Sausville, E., IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs (1998) Cancer Res, 58, p. 5315; Ambrosini, G., Adida, C., Sirugo, G., Altieri, D.C., Induction of apoptosis and inhibition of cell proliferation by survivin gene targeting (1998) J. Biol. Chem., 273, p. 11177; Liu, T., Brouha, B., Grossman, D., Rapid induction of mitochondrial events and caspase-independent apoptosis in survivin-targeted melanoma cells (2004) Oncogene, 23, p. 39; Adida, C., Berrebi, D., Peuchmaur, M., Reyes-Mugica, M., Altieri, D.C., Anti-apoptosis gene, survivin, and prognosis of neuroblastoma (1998) Lancet, 351, p. 882; Mita, A.C., Mita, M.M., Nawrocki, S.T., Giles, F.J., Survivin: key regulator of mitosis and apoptosis and novel target for cancer therapeutics (2008) Clin. Cancer Res., 14, p. 5000; Altznauer, F., Martinelli, S., Yousefi, S., Inflammationassociated cell cycle-independent block of apoptosis by survivin in terminally differentiated neutrophils (2004) J. Exp. Med., 199, p. 1343; Vassina, E.M., Yousefi, S., Simon, D., Zwicky, C., Conus, S., Simon, H.U., cIAP-2 and survivin contribute to cytokinemediated delayed eosinophil apoptosis (2006) Eur. J. Immunol., 36, p. 1975; Tolgyesi, G., Molnar, V., Semsei, A.F., Gene expression profiling of experimental asthma reveals a possible role of paraoxonase-1 in the disease (2009) Int. Immunol., 21, p. 967; Tumes, D.J., Connolly, A., Dent, L.A., Expression of survivin in lung eosinophils is associated with pathology in a mouse model of allergic asthma (2009) Int. Immunol., 21, p. 633; Di Valentin, E., Crahay, C., Garbacki, N., New asthma biomarkers: lessons from murine models of acute and chronic asthma (2009) Am. J. Physiol. Lung Cell. Mol. Physiol., 296, pp. L185; Nathan, R.A., Sorkness, C.A., Kosinski, M., Development of the asthma control test: a survey for assessing asthma control (2004) J. Allergy Clin. Immunol., 113, p. 59; Green, R.H., Brightling, C.E., McKenna, S., Asthma exacerbations and sputum eosinophil counts: a randomised controlled trial (2002) Lancet, 360, p. 1715; Jayaram, L., Pizzichini, M.M., Cook, R.J., Determining asthma treatment by monitoring sputum cell counts: effect on exacerbations (2006) Eur. Respir. J., 27, p. 483; Schleich, F.N., Seidel, L., Sele, J., Exhaled nitric oxide thresholds associated with a sputum eosinophil count >/=3% in a cohort of unselected patients with asthma (2010) Thorax, 65, p. 1039; Virchow Jr., J.C., Kroegel, C., Walker, C., Matthys, H., Inflammatory determinants of asthma severity: mediator and cellular changes in bronchoalveolar lavage fluid of patients with severe asthma (1996) J. Allergy Clin. Immunol., 98, pp. S27; Yang, X., Xiong, G., Chen, X., Survivin expression in esophageal cancer: correlation with p. 53 mutations and promoter polymorphism (2009) Dis. Esophagus, 22, p. 223; Han, C.H., Wei, Q., Lu, K.K., Liu, Z., Mills, G.B., Wang, L.E., Polymorphisms in the survivin promoter are associated with age of onset of ovarian cancer (2009) Int. J. Clin. Exp. Med., 2, p. 289; Dixon, A.L., Liang, L., Moffatt, M.F., A genome-wide association study of global gene expression (2007) Nat. Genet., 39, p. 1202; A haplotype map of the human genome (2005) Nature, 437, p. 1299. , The International HapMap Consortium; Krepela, E., Dankova, P., Moravcikova, E., Increased expression of inhibitor of apoptosis proteins, survivin and XIAP, in non-small cell lung carcinoma (2009) Int. J. Oncol., 35, p. 1449; Hmeljak, J., Erculj, N., Dolzan, V., Kern, I., Cor, A., BIRC5 promoter SNPs do not affect nuclear survivin expression and survival of malignant pleural mesothelioma patients (2011) J Cancer Res. Clin. Oncol., 137, p. 1641; Cheng, Z.J., Hu, L.H., Huang, S.J., Correlation of -31G/C polymorphisms of survivin promoter to tumorigenesis of gastric carcinoma (2008) Ai Zheng, 27, p. 258; Srivastava, K., Srivastava, A., Mittal, B., Survivin promoter -31G/C (rs9904341) polymorphism and cancer susceptibility: a meta-analysis (2012) Mol. Biol. Report., 39, p. 1509; Boidot, R., Vegran, F., Jacob, D., The expression of BIRC5 is correlated with loss of specific chromosomal regions in breast carcinomas (2008) Genes Chromosomes Cancer, 47, p. 299

PY - 2012

Y1 - 2012

N2 - In the last few years, it has been recognized that the unbalanced regulation of survival and apoptosis of bronchial inflammatory cells is a key component in the development of asthma. Baculoviral IAP repeat containing 5 (BIRC5) (also known as survivin) is an important anti-apoptotic protein that has been implicated in many cancer types, and recent studies provide evidence for its role in controlling inflammatory disorders as well. Our aim was to investigate at both genetic and transcriptional levels if BIRC5 has an impact on asthma development. We found that induced sputum samples of patients with bronchial asthma contained elevated levels of BIRC5 mRNA compared with healthy subjects and its level was in correlation with sputum eosinophil percentages. Furthermore, in a case-control study examining single nucleotide polymorphisms (SNPs) in the BIRC5 regulatory regions, the minor alleles of rs8073903 and rs8073069 were found to be significantly associated with asthma and especially non-allergic asthma phenotypes, which associations were more prominent among women. Two marker haplotype analyses further strengthen the impact of these two polymorphisms on both asthma and non-allergic asthma. In the female cohort, rs1508147 was also significantly associated with increased risk of non-allergic asthma. Additionally, with linear regression analysis, we showed that rs9904341 was significantly correlated with both absolute and relative serum eosinophil levels. In conclusion, our results suggest that possibly by inhibition of the eosinophil apoptosis, BIRC5 might be an important regulator of the asthmatic processes and we provide some evidence that its effect might be affected by SNPs located in the gene regulatory regions. © The Japanese Society for Immunology. 2012. All rights reserved.

AB - In the last few years, it has been recognized that the unbalanced regulation of survival and apoptosis of bronchial inflammatory cells is a key component in the development of asthma. Baculoviral IAP repeat containing 5 (BIRC5) (also known as survivin) is an important anti-apoptotic protein that has been implicated in many cancer types, and recent studies provide evidence for its role in controlling inflammatory disorders as well. Our aim was to investigate at both genetic and transcriptional levels if BIRC5 has an impact on asthma development. We found that induced sputum samples of patients with bronchial asthma contained elevated levels of BIRC5 mRNA compared with healthy subjects and its level was in correlation with sputum eosinophil percentages. Furthermore, in a case-control study examining single nucleotide polymorphisms (SNPs) in the BIRC5 regulatory regions, the minor alleles of rs8073903 and rs8073069 were found to be significantly associated with asthma and especially non-allergic asthma phenotypes, which associations were more prominent among women. Two marker haplotype analyses further strengthen the impact of these two polymorphisms on both asthma and non-allergic asthma. In the female cohort, rs1508147 was also significantly associated with increased risk of non-allergic asthma. Additionally, with linear regression analysis, we showed that rs9904341 was significantly correlated with both absolute and relative serum eosinophil levels. In conclusion, our results suggest that possibly by inhibition of the eosinophil apoptosis, BIRC5 might be an important regulator of the asthmatic processes and we provide some evidence that its effect might be affected by SNPs located in the gene regulatory regions. © The Japanese Society for Immunology. 2012. All rights reserved.

KW - Apoptosis

KW - Expression

KW - mRNA

KW - Non-allergic asthma

KW - SNP

KW - Survivin

KW - biological marker

KW - messenger RNA

KW - survivin

KW - adult

KW - allele

KW - apoptosis

KW - article

KW - asthma

KW - Birc5 gene

KW - bronchus

KW - cell survival

KW - cohort analysis

KW - controlled study

KW - eosinophil

KW - female

KW - gene

KW - gene location

KW - genetic transcription

KW - genetic variability

KW - haplotype

KW - human

KW - inflammatory cell

KW - major clinical study

KW - male

KW - pathogenesis

KW - phenotype

KW - priority journal

KW - single nucleotide polymorphism

KW - sputum analysis

KW - Adult

KW - Alleles

KW - Asthma

KW - Case-Control Studies

KW - Female

KW - Haplotypes

KW - Humans

KW - Inhibitor of Apoptosis Proteins

KW - Linear Models

KW - Male

KW - Middle Aged

KW - Phenotype

KW - Polymorphism, Single Nucleotide

KW - RNA, Messenger

KW - Young Adult

U2 - 10.1093/intimm/dxs007

DO - 10.1093/intimm/dxs007

M3 - Article

VL - 24

SP - 293

EP - 301

JO - International immunology

JF - International immunology

SN - 0953-8178

IS - 5

ER -