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Circulating monocytes from healthy individuals and COPD patients.

Aldonyte, Ruta LU ; Jansson, Lennart LU ; Piitulainen, Eeva LU and Janciauskiene, Sabina LU (2003) In Respiratory Research 4(1). p.11-11
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction associated with inflammation in which monocytes/macrophages are the predominant inflammatory cells. The only known genetic factor related to COPD is inherited PiZZ deficiency of alpha1-antitrypsin (AAT), an inhibitor of serine proteases. Methods: We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency. Results: After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD... (More)
Background: Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction associated with inflammation in which monocytes/macrophages are the predominant inflammatory cells. The only known genetic factor related to COPD is inherited PiZZ deficiency of alpha1-antitrypsin (AAT), an inhibitor of serine proteases. Methods: We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency. Results: After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD patient monocytes than from controls. LPS-stimulated release of IL-6 and MCP-1 was greater from COPD patient's monocytes relative to controls, while activation of control cells resulted in enhanced secretion of ICAM-1 and MMP-9 compared to COPD patients. Independent of disease status, monocytes from PiZZ AAT carriers released less TNFalpha (by 2.3-fold, p < 0.03). Conclusions: The basal and LPS-stimulated secretion of specific pro-inflammatory molecules from circulating monocytes differs between healthy and COPD subjects. These findings may be valuable for further studies on the mechanisms involved in recruitment and activation of inflammatory cells in COPD. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Respiratory Research
volume
4
issue
1
pages
11 - 11
publisher
BioMed Central
external identifiers
  • wos:000187113500001
  • pmid:14624669
  • scopus:10644267224
ISSN
1465-9921
DOI
10.1186/1465-9921-4-11
language
English
LU publication?
yes
id
465c67cd-88cc-4b09-8cdc-5f4ba09c21ea (old id 118830)
date added to LUP
2007-07-09 16:40:14
date last changed
2018-02-18 03:45:24
@article{465c67cd-88cc-4b09-8cdc-5f4ba09c21ea,
  abstract     = {Background: Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction associated with inflammation in which monocytes/macrophages are the predominant inflammatory cells. The only known genetic factor related to COPD is inherited PiZZ deficiency of alpha1-antitrypsin (AAT), an inhibitor of serine proteases. Methods: We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency. Results: After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p &lt; 0.02 greater, whereas IL-8 was 1.8-fold (p &lt; 0.01) lower from COPD patient monocytes than from controls. LPS-stimulated release of IL-6 and MCP-1 was greater from COPD patient's monocytes relative to controls, while activation of control cells resulted in enhanced secretion of ICAM-1 and MMP-9 compared to COPD patients. Independent of disease status, monocytes from PiZZ AAT carriers released less TNFalpha (by 2.3-fold, p &lt; 0.03). Conclusions: The basal and LPS-stimulated secretion of specific pro-inflammatory molecules from circulating monocytes differs between healthy and COPD subjects. These findings may be valuable for further studies on the mechanisms involved in recruitment and activation of inflammatory cells in COPD.},
  author       = {Aldonyte, Ruta and Jansson, Lennart and Piitulainen, Eeva and Janciauskiene, Sabina},
  issn         = {1465-9921},
  language     = {eng},
  number       = {1},
  pages        = {11--11},
  publisher    = {BioMed Central},
  series       = {Respiratory Research},
  title        = {Circulating monocytes from healthy individuals and COPD patients.},
  url          = {http://dx.doi.org/10.1186/1465-9921-4-11},
  volume       = {4},
  year         = {2003},
}