Abstract
Chronic obstructive pulmonary disease (COPD) is a multifactorial chronic inflammatory disease of the respiratory system. A key phenomenon of COPD pathogenesis is inflammation. The goal of the present study was to investigate the association of COPD with alleles and genotypes of the genes that encode chemokines and chemokine receptors (CCL11, CX3CR1, CCR5, CCL5, CXCL12, CCL2, and CCL17), adhesion molecules (PECAM1 and ICAM1), and serum amyloid A1 (SAA1). It was found that COPD was associated with the C allele and the TC genotype of SAA1 (rs1136743C>T) (P = 0.0001, OR = 1.58 and P = 0.00001, OR = 2.15, respectively); this association was confirmed in the subgroups differentiated by smoking status. Markers of COPD risk were also the CG genotype of PECAM1 (rs281865545G>C) (P = 0.028, OR = 1.36) and the GG genotype of ICAM1 (rs5498A>G), which were significantly associated with the disease in smokers (P = 0.005, OR = 1.66). The AA genotype of CCL2 (rs1024611A>G) was associated with the disease in nonsmokers (P = 0.037, OR = 1.82). The GG genotype of PECAM1 (rs281865545G>C) and the AA genotype of CX3CR1 (rs3732378A>G) were associated with higher vital capacity (P = 0.014 and P = 0.04, respectively). Subjects with the GG genotype of ICAM1 (rs5498A>G) exhibited lower forced expiration volume in 1 s and lower forced vital capacity (P = 0.025 and P = 0.029, respectively).
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REFERENCES
From the Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD), 2017. http://goldcopd.org.
Barnes, P.J., Cellular and molecular mechanisms of asthma and COPD, Clin. Sci. (London), 2017, vol. 131, no. 13, pp. 1541—1558. https://doi.org/10.1042/CS20160487
Busch, R., Cho, M.H., and Silverman, E.K., Progress in disease progression genetics: dissecting the genetic origins of lung function decline in COPD, Thorax, 2017, vol. 72, no. 5, pp. 389—390. https://doi.org/10.1136/thoraxjnl-2016-209666
Calero, C., Arellano, E., Lopez-Villalobos, J.L., et al., Differential expression of C-reactive protein and serum amyloid A in different cell types in the lung tissue of chronic obstructive pulmonary disease patients, BMC Pulm. Med., 2014, vol. 14, p. 95. https://doi.org/10.1186/1471-2466-14-95
Sun, L. and Ye, R.D., Serum amyloid A1: structure, function and gene polymorphism, Gene, 2016, vol. 583, no. 1, pp. 48—57. https://doi.org/10.1016/j.gene.2016.02.044
De Buck, M., Gouwy, M., Wang, J.M., et al., Structure and expression of different serum amyloid A (SAA) variants and their concentration-dependent functions during host insults, Curr. Med. Chem., 2016, vol. 23, no. 17, pp. 1725—1755. https://doi.org/10.2174/0929867323666160418114600
Buraczynska, M., Zaluska, W., Baranowicz-Gaszczyk, I., et al., The intercellular adhesion molecule-1 (ICAM-1) gene polymorphism K469E in end-stage renal disease patients with cardiovascular disease, Hum. Immunol., 2012, vol. 73, no. 8, pp. 824—828. https://doi.org/10.1016/j.humimm.2012.05.007
Zhou, X., Zhu, L., Lizarraga, R., and Chen, Y., Human airway epithelial cells direct significant rhinovirus replication in monocytic cells by enhancing ICAM1 expression, Am. J. Respir. Cell Mol. Biol., 2017, vol. 57, no. 2, pp. 216—225. https://doi.org/10.1165/rcmb.2016-0271OC
Holder, A.L., Wolf, S., Walshe, C., et al., Expression of endothelial intercellular adhesion molecule-1 is determined by genotype: effects on efficiency of leukocyte adhesion to human endothelial cells, Hum. Immunol., 2008, vol. 69, no. 2, pp. 71—78. https://doi.org/10.1016/j.humimm.2007.12.004
Privratsky, J.R. and Newman, P.J., Pecam-1: regulator of endothelial junctional integrity, Cell Tissue Res., 2014, vol. 355, pp. 607—619. https://doi.org/10.1007/s00441-013-1779-3
Hackett, T.L., Holloway, R., Holgate, S.T., and Warner, J.A., Dynamics of pro-inflammatory and anti-inflammatory cytokine release during acute inflammation in chronic obstructive pulmonary disease: an ex vivo study, Respir. Res., 2008, vol. 29, no. 9, p. 47. https://doi.org/10.1186/1465-9921-9-47
Sokol, C.L. and Luster, A.D., The chemokine system in innate immunity, Cold Spring Harbor Perspect. Biol., 2015, vol. 7, no. 5, p. ii: a016303. https://doi.org/10.1101/cshperspect.a016303
Yarilin, A.A., Immunologiya: uchebnik (Immunology: Manual), Moscow: GEOTAR-Media, 2010.
International statistical classification of diseases and related health problems, tenth revision (ICD-10). http://www.who.int/classifications/icd/en/.
Open database of single nucleotide polymorphisms (SNPs) and multiple small-scale variations that include insertions/deletions, microsatellites, and non-polymorphic variants, Bethesda (MD): The National Center for Biotechnology Information Advances Science and Health by Providing Access to Biomedical and Genomic Information (US). http://www.ncbi.nlm. nih.gov/projects/SNP/.
Purcell, S., Neale, B., Todd-Brown, K., et al., PLINK: a toolset for whole-genome association and population-based linkage analysis, Am. J. Hum. Genet., 2007, vol. 81, pp. 559—575. https://doi.org/10.1086/519795
STATISTICA for Windows v. 6.0 (Computer Program Manual), Tulsa: StatSoft, 1996. http://www.statistica.com.
López-Campos, J.L., Calero, C., Rojano, B., et al., C-reactive protein and serum amyloid a overexpression in lung tissues of chronic obstructive pulmonary disease patients: a case-control study, Int. J. Med. Sci., 2013, vol. 10, no. 8, pp. 938—947. https://doi.org/10.7150/ijms.6152
Urieli-Shoval, S., Cohen, P., Eisenberg, S., and Matzner, Y., Widespread expression of serum amyloid A in histologically normal human tissues: predominant localization to the epithelium, J. Histochem. Cytochem.: Off. J. Histochem. Soc., 1998, vol. 46, pp. 1377—1384.
Pham, M.H., Bonello, G.B., Castiblanco, J., et al., The rs1024611 regulatory region polymorphism is associated with CCL2 allelic expression imbalance, PLoS One, 2012, vol. 7. e49498. https://doi.org/10.1371/journal.pone.0049498
Bai, J., Song, H., Cai, C., et al., The association of monocyte chemotactic protein-1 and CC chemokine receptor 2 gene variants with chronic obstructive pulmonary disease, DNA Cell Biol., 2012, vol. 31, no. 6, pp. 1058—1063. https://doi.org/10.1089/dna.2011.1520
Liu, S.F., Wang, C.C., and Fang, W.F., MCP1-2518 polymorphism and chronic obstructive pulmonary disease in Taiwanese men, Exp. Lung Res., 2010, vol. 36, no. 5, pp. 277—283. https://doi.org/10.3109/01902140903575989
Chaouat, A., Savale, L., Chouaid, C., et al., Role for interleukin-6 in COPD-related pulmonary hypertension, Chest, 2009, vol. 136, no. 3, pp. 678—687. https://doi.org/10.1378/chest.08-2420
McComb, J.G., Ranganathan, M., and Liu, X.H., CX3CL1 up-regulation is associated with recruitment of CX3CR1+ mononuclear phagocytes and T lymphocytes in the lungs during cigarette smoke-induced emphysema, Am. J. Pathol., 2008, vol. 173, no. 4, pp. 949—961. https://doi.org/10.2353/ajpath.2008.071034
ACKNOWLEDGMENTS
This study was supported in part by the Russian Foundation for Basic Research (project no. 18-015-00050). The DNA material was provided by the Collection of Human Biological Materials (Institute of Biochemistry and Genetics), supported by the Bioresource Collection Program of the Russian Federal Agency for Scientific Organizations (agreement no. 007-030164/2). Experiments were performed using the equipment of the “Biomika” Collective Use Center and the “Kodink” Group of the Institute of Biochemistry and Genetics.
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Statement of compliance with standards of research involving humans as subjects. The study was approved by the Ethics Committee of the Institute of Biochemistry and Genetics. All participants gave their informed consent to the use of their biological materials in the proposed experiments.
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Translated by D. Timchenko
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Korytina, G.F., Akhmadishina, L.Z., Kochetova, O.V. et al. The Role of Serum Amyloid A1, Adhesion Molecules, Chemokines, and Chemokine Receptors Genes in Chronic Obstructive Pulmonary Disease. Russ J Genet 55, 105–113 (2019). https://doi.org/10.1134/S1022795418120050
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DOI: https://doi.org/10.1134/S1022795418120050