The Role of Serum Amyloid A1, Adhesion Molecules, Chemokines, and Chemokine Receptors Genes in Chronic Obstructive Pulmonary Disease
- Autores: Korytina G.1, Akhmadishina L.1, Kochetova O.1, Aznabaeva Y.2, Zagidullin S.2, Victorova T.1,2
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Afiliações:
- Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences
- Bashkortostan State Medical University
- Edição: Volume 55, Nº 1 (2019)
- Páginas: 105-113
- Seção: Human Genetics
- URL: https://journals.rcsi.science/1022-7954/article/view/189204
- DOI: https://doi.org/10.1134/S1022795418120050
- ID: 189204
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Resumo
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).
Sobre autores
G. Korytina
Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences
Autor responsável pela correspondência
Email: guly_kory@mail.ru
Rússia, Ufa, 450054
L. Akhmadishina
Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences
Email: guly_kory@mail.ru
Rússia, Ufa, 450054
O. Kochetova
Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences
Email: guly_kory@mail.ru
Rússia, Ufa, 450054
Yu. Aznabaeva
Bashkortostan State Medical University
Email: guly_kory@mail.ru
Rússia, Ufa, 450000
Sh. Zagidullin
Bashkortostan State Medical University
Email: guly_kory@mail.ru
Rússia, Ufa, 450000
T. Victorova
Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences; Bashkortostan State Medical University
Email: guly_kory@mail.ru
Rússia, Ufa, 450054; Ufa, 450000