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Cigarette smoke extract modulates respiratory defence mechanisms through effects on T-cells and airway epithelial cells.

Glader, Pernilla LU ; Moller, Sebastian; Welch, Johanna LU ; Wieslander, Elisabet LU ; Löfdahl, Claes-Göran LU and von Wachenfeldt, Karin (2006) In Respiratory Medicine 100(5). p.818-827
Abstract
Chronic obstructive pulmonary disease (CCPD) is a disease primarily caused by cigarette smoking, which in turn has been shown to affect the susceptibility to and progression of airway infections. The question addressed in this study was how components from cigarette smoke could affect the defence mechanisms of T-cells and epithelial cells, and thereby contribute to the development of the COPD pathology. T-cells and monocytes were isolated from buffycoats from healthy donors and T-cell responses studied in response to cigarette smoke extract (CSE). Activation level (CD25 expression), proliferation (BrdU incorporation) and intracellular expression of the cytotoxic markers granzyme-b and TIA-1 were determined using flowcytometry. Normal human... (More)
Chronic obstructive pulmonary disease (CCPD) is a disease primarily caused by cigarette smoking, which in turn has been shown to affect the susceptibility to and progression of airway infections. The question addressed in this study was how components from cigarette smoke could affect the defence mechanisms of T-cells and epithelial cells, and thereby contribute to the development of the COPD pathology. T-cells and monocytes were isolated from buffycoats from healthy donors and T-cell responses studied in response to cigarette smoke extract (CSE). Activation level (CD25 expression), proliferation (BrdU incorporation) and intracellular expression of the cytotoxic markers granzyme-b and TIA-1 were determined using flowcytometry. Normal human bronchial epithelial cells were obtained from Cambrex and differentiated in air-liquid interface cultures. After exposure to CSE barrier function (trans-epithelial electric resistance, TEER), MUC5AC and interleukin-8 production were measured. T-cell activation, proliferation and expression of the cytotoxic proteins granzyme-b and TIA-1 were significantly reduced in response to 0.5-1% of CSE. The epithelial cells were more resistant to CSE and responded at doses 20 times higher than T-cells. The expression of interteukin-8 and MUC5AC was significantly increased after exposure to 15% and 30% CSE and TEER was largely unaffected at 30% CSE but clearly reduced at 40% CSE. This study shows that mechanisms, in both T-cells and airway epithelial cells, involved in the defence against infectious agents are modulated by CSE. (c) 2005 Elsevier Ltd. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
COPD, epithelial cells, cigarette smoke extract, T-cells, cytotoxicity
in
Respiratory Medicine
volume
100
issue
5
pages
818 - 827
publisher
Elsevier
external identifiers
  • wos:000237093500007
  • scopus:33645859914
ISSN
1532-3064
DOI
10.1016/j.rmed.2005.09.008
language
English
LU publication?
yes
id
88789ec7-1b57-4f37-9a33-d632dfc8e1ef (old id 144470)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16242311&dopt=Abstract
date added to LUP
2007-07-11 09:58:04
date last changed
2019-07-02 02:54:33
@article{88789ec7-1b57-4f37-9a33-d632dfc8e1ef,
  abstract     = {Chronic obstructive pulmonary disease (CCPD) is a disease primarily caused by cigarette smoking, which in turn has been shown to affect the susceptibility to and progression of airway infections. The question addressed in this study was how components from cigarette smoke could affect the defence mechanisms of T-cells and epithelial cells, and thereby contribute to the development of the COPD pathology. T-cells and monocytes were isolated from buffycoats from healthy donors and T-cell responses studied in response to cigarette smoke extract (CSE). Activation level (CD25 expression), proliferation (BrdU incorporation) and intracellular expression of the cytotoxic markers granzyme-b and TIA-1 were determined using flowcytometry. Normal human bronchial epithelial cells were obtained from Cambrex and differentiated in air-liquid interface cultures. After exposure to CSE barrier function (trans-epithelial electric resistance, TEER), MUC5AC and interleukin-8 production were measured. T-cell activation, proliferation and expression of the cytotoxic proteins granzyme-b and TIA-1 were significantly reduced in response to 0.5-1% of CSE. The epithelial cells were more resistant to CSE and responded at doses 20 times higher than T-cells. The expression of interteukin-8 and MUC5AC was significantly increased after exposure to 15% and 30% CSE and TEER was largely unaffected at 30% CSE but clearly reduced at 40% CSE. This study shows that mechanisms, in both T-cells and airway epithelial cells, involved in the defence against infectious agents are modulated by CSE. (c) 2005 Elsevier Ltd. All rights reserved.},
  author       = {Glader, Pernilla and Moller, Sebastian and Welch, Johanna and Wieslander, Elisabet and Löfdahl, Claes-Göran and von Wachenfeldt, Karin},
  issn         = {1532-3064},
  keyword      = {COPD,epithelial cells,cigarette smoke extract,T-cells,cytotoxicity},
  language     = {eng},
  number       = {5},
  pages        = {818--827},
  publisher    = {Elsevier},
  series       = {Respiratory Medicine},
  title        = {Cigarette smoke extract modulates respiratory defence mechanisms through effects on T-cells and airway epithelial cells.},
  url          = {http://dx.doi.org/10.1016/j.rmed.2005.09.008},
  volume       = {100},
  year         = {2006},
}