PMID- 33748274
OWN - NLM
STAT- MEDLINE
DCOM- 20210525
LR  - 20210525
IS  - 2314-6141 (Electronic)
IS  - 2314-6133 (Print)
VI  - 2021
DP  - 2021
TI  - Correlation between TNF-alpha -308 and +489 Gene Polymorphism and Acute Exacerbation 
      of Chronic Obstructive Pulmonary Diseases.
PG  - 6661281
LID - 10.1155/2021/6661281 [doi]
LID - 6661281
AB  - Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is becoming 
      a common respiratory disease, leading to increased morbidity and mortality 
      worldwide. Tumor necrosis factor-alpha (TNF-alpha) is a powerful proinflammatory 
      cytokine involved in the pathogenesis of AECOPD. Therefore, we proposed a close 
      correlation between the TNF-alpha polymorphism [-308G/A (rs1800629), +489G/A 
      (rs1800610)] and the disease progress of patients with AECOPD. Comparison of the 
      TNF-alpha genotypes between the 198 AECOPD diagnosed patients groups and 195 healthy 
      peoples suggested their significant differences of the three genotypes (AA, GA, 
      GG) distribution for TNF-alpha -308 (P < 0.05), but no differences of that for TNF-alpha 
      +489. We found that patients with TNF-alpha -308 GA/AA genotypes showed smaller 
      adjacent arterial diameter, thicker bronchial wall, higher bronchial artery 
      ratio, higher bronchial wall grading, and higher frequency of acute exacerbations 
      than those with TNF-alpha -308 GG genotype. Patients with TNF-alpha +489 GA/AA genotypes 
      showed the same AECOPD properties as patients with TNF-alpha -308 except for the high 
      frequency of acute exacerbations. Further experiment showed that the TNF-alpha -308 
      and+489 gene polymorphisms could affect the expression level of TNF-alpha in 
      macrophages, suggesting the involvement of the macrophage population in disease 
      regulation of AECOPD patients with TNF-alpha -308G/A and+489G/A genotype 
      heterogeneity. In conclusion, the TNF-alpha -308 G/A genotype was related to AECOPD 
      susceptibility and progress, while the TNF-alpha +489G/A genotype was related to 
      AECOPD progress, but not AECOPD susceptibility.
CI  - Copyright (c) 2021 Suyun Yu et al.
FAU - Yu, Suyun
AU  - Yu S
AUID- ORCID: 0000-0003-4351-4899
AD  - Department of Respiratory, Minhang Hospital, Fudan University, Shanghai 201199, 
      China.
FAU - Xue, Min
AU  - Xue M
AUID- ORCID: 0000-0002-5763-6339
AD  - Department of Respiratory, Minhang Hospital, Fudan University, Shanghai 201199, 
      China.
FAU - Yan, Zhijun
AU  - Yan Z
AUID- ORCID: 0000-0001-8945-5463
AD  - Department of Respiratory, Minhang Hospital, Fudan University, Shanghai 201199, 
      China.
FAU - Song, Bin
AU  - Song B
AUID- ORCID: 0000-0001-8493-2523
AD  - Department of Radiology, Minhang Hospital, Fudan University, Shanghai 201199, 
      China.
FAU - Hong, Haiping
AU  - Hong H
AUID- ORCID: 0000-0003-4678-566X
AD  - Shanghai Songjiang District Fangta Hospital of Traditional Chinese Medicine, 
      Shanghai 201699, China.
FAU - Gao, Xiwen
AU  - Gao X
AUID- ORCID: 0000-0003-1437-4866
AD  - Department of Respiratory, Minhang Hospital, Fudan University, Shanghai 201199, 
      China.
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
DEP - 20210301
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Female
MH  - *Gene Expression Regulation
MH  - *Genotype
MH  - Humans
MH  - Macrophages/metabolism/pathology
MH  - Male
MH  - *Polymorphism, Genetic
MH  - *Pulmonary Disease, Chronic Obstructive/genetics/metabolism/pathology
MH  - *Tumor Necrosis Factor-alpha/biosynthesis/genetics
PMC - PMC7943264
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2021/03/23 06:00
MHDA- 2021/05/26 06:00
PMCR- 2021/03/01
CRDT- 2021/03/22 08:23
PHST- 2020/12/24 00:00 [received]
PHST- 2021/02/05 00:00 [revised]
PHST- 2021/02/22 00:00 [accepted]
PHST- 2021/03/22 08:23 [entrez]
PHST- 2021/03/23 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
PHST- 2021/03/01 00:00 [pmc-release]
AID - 10.1155/2021/6661281 [doi]
PST - epublish
SO  - Biomed Res Int. 2021 Mar 1;2021:6661281. doi: 10.1155/2021/6661281. eCollection 
      2021.