PMID- 20819500
OWN - NLM
STAT- MEDLINE
DCOM- 20101231
LR  - 20141120
IS  - 2542-5641 (Electronic)
IS  - 0366-6999 (Linking)
VI  - 123
IP  - 12
DP  - 2010 Jun
TI  - Quantitative differentiation of dendritic cells in lung tissues of smokers with 
      and without chronic obstructive pulmonary disease.
PG  - 1500-4
AB  - BACKGROUND: Chronic obstructive pulmonary disease (COPD) is thought to be an 
      inflammatory immune response disease. In most cases, the disease is caused by 
      cigarette smoke, but it has been demonstrated that only 10% to 20% of smokers 
      will definitely suffer from COPD. Dendritic cells (DCs) are considered to be the 
      promoter of immune responses. However, the underlying mechanisms involved are 
      still unrevealed. In this study, we aimed to investigate the quantitative 
      differentiation of pulmonary DC in smokers with or without COPD to explore the 
      possible role of DCs in smokers suffering COPD. METHODS: Peripheral lung 
      specimens from non-smokers without airflow obstruction (control group, n = 7), 
      smokers without airflow obstruction (smoker group, n = 7) and patients with COPD 
      (COPD group, n = 7) were investigated to detect the quantity of S-100 and CD1a 
      positive cells by immunohistochemical or immunofluorescent assay. RESULTS: In 
      smokers with COPD, the number of S-100(+) DCs was higher than in the controls and 
      smokers without COPD (P < 0.01 and P < 0.05) and there was a higher number of 
      S-100(+) DCs in smokers with COPD than in smokers without COPD, but without a 
      significant difference (P > 0.05). An inverse correlation was found between the 
      number of DCs and forced expiratory volume in the first second (FEV(1))% pred (r 
      = -0.75, P < 0.05), which was also found between the number of DCs and 
      FEV(1)/forced vital capacity (FVC) (r = -0.72, P < 0.05). The mean number of 
      CD1a(+) DCs, increased from non-smokers to non-COPD smokers to COPD patients, 
      with significant differences between each group (P < 0.01). CONCLUSIONS: The 
      quantity of DCs significantly increased in smokers with COPD compared with 
      non-smokers or smokers without COPD. The results suggest that DCs may play an 
      important role in the pathogenesis of smoking-induced COPD, and the upregulation 
      of DCs may be a potential maker to identify the smokers who have more liability 
      to suffer from COPD.
FAU - Su, Yan-wei
AU  - Su YW
AD  - Department of Respiratory Medicine, Tongji Hospital affiliated to Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, 
      China.
FAU - Xu, Yong-jian
AU  - Xu YJ
FAU - Liu, Xian-sheng
AU  - Liu XS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (Antigens, CD1)
RN  - 0 (CD1a antigen)
RN  - 0 (S100 Proteins)
SB  - IM
MH  - Aged
MH  - Antigens, CD1/metabolism
MH  - Cell Differentiation/*physiology
MH  - Dendritic Cells/*cytology
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Immunohistochemistry
MH  - In Vitro Techniques
MH  - Lung/*metabolism/*pathology
MH  - Male
MH  - Microscopy, Confocal
MH  - Middle Aged
MH  - Pulmonary Disease, Chronic Obstructive/metabolism/pathology
MH  - S100 Proteins/metabolism
MH  - Smoking/*adverse effects
EDAT- 2010/09/08 06:00
MHDA- 2011/01/01 06:00
CRDT- 2010/09/08 06:00
PHST- 2010/09/08 06:00 [entrez]
PHST- 2010/09/08 06:00 [pubmed]
PHST- 2011/01/01 06:00 [medline]
PST - ppublish
SO  - Chin Med J (Engl). 2010 Jun;123(12):1500-4.