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Copyright ©ERS Journals Ltd 2003
Imbalanced secretion of IL-1ß and IL-1RA in Chlamydia pneumoniae-infected mononuclear cells from COPD patients
1 Institute of Medical Microbiology and Hygiene and 2 Depts of #Medicine III and 3 Rheumatology, University of Lübeck
CORRESPONDENCE: J. Rupp, Institute of Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. Fax: 49 4515002808. E-mail: jan.rupp@hygiene.ukl.mu-luebeck.de
Keywords: anti-inflammation, Chlamydia pneumoniae, chronic obstructive pulmonary disease
Received: January 21, 2003
Accepted March 13, 2003
Balanced secretion of pro- and anti-inflammatory cytokines is essential in limiting pulmonary inflammation in respiratory infections. It was hypothesised that, in acute infection with Chlamydia pneumoniae, mononuclear cells from chronic obstructive pulmonary disease (COPD) patients lack the opportunity to compensate for the inflammatory immune response by secreting adequate amounts of anti-inflammatory cytokines.
Alveolar macrophages (AMs) and peripheral blood mononuclear cells (PBMCs) from eight COPD patients and eight healthy controls were infected with C. pneumoniae in order to determine interleukin (IL)-1ß, IL-1 receptor antagonist (IL-1RA) and IL-8 expression and messenger ribonucleic acid levels.
Secretion of IL-1ß was significantly enhanced in AMs (six-fold) and PBMCs (four-fold) from COPD patients after infection with C. pneumoniae. Compared to the control group, release of its anti-inflammatory counterpart IL-1RA was diminished inCOPD patients, resulting in a significantly higher IL-1ß/IL-1RA ratio in C.pneumoniae-infected AMs and PBMCs from COPD patients.
Mononuclear cells from chronic obstructive pulmonary disease patients have less capacity for balancing the pro-inflammatory immune response caused by Chlamydia pneumoniae infection than those from healthy controls. These findings suggest that, during acute exacerbation with intracellular pathogens, chronic obstructive pulmonary disease patients are predisposed to inflammatory changes in the lungs.
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