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Thorax 2001;56:121-125 ( February )

Leucocyte response and anti-inflammatory cytokines in community acquired pneumonia

U K Kollinga, F Hansena, J Brauna, L Rinkb, H A Katusa, K Dalhoffa

a Department of Medicine II, Medizinische Universität Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany, b Institute of Immunology and Transfusion Medicine

Correspondence to: Dr K Dalhoff Klaus.Dalhoff{at}medinf.mu-luebeck.de

Accepted for publication 14 November 2000

BACKGROUND---In the host defence of the lung neutrophils (PMN) play a central role. Apart from antimicrobial properties, recent data indicate that PMN also exert anti-inflammatory effects by stimulation and release of cytokine antagonists such as interleukin-1 receptor antagonist (IL-1ra).
METHODS---Cytokine release from lipopolysaccharide stimulated whole blood was studied in 18 patients with community acquired pneumonia (CAP) and severe co-morbidities at admission and after 24 hours. Release of IL-1ra, interleukin-1beta (IL-1beta ), tumour necrosis factor alpha  (TNFalpha ), soluble TNF receptor type I (sTNF-RI), and IL-8 was determined by ELISA.
RESULTS---The mean (SD) leucocyte level at admission was 12.5 (4.1)/nl. There was a significant correlation between the release of anti-inflammatory cytokines such as IL-1ra and sTNF-RI and the leucocyte count at admission and after 24 hours. Additional in vitro experiments showed that co-incubation of peripheral blood mononuclear cells with autologous PMN led to a marked dose dependent increase in IL-1ra and sTNF-RI release.
CONCLUSION---These results indicate that PMN may be responsible for the increase in anti-inflammatory cytokines in CAP. Strategies to increase neutrophil counts may exert beneficial effects, not only by augmenting the antimicrobial activity but also by modulating the inflammatory cytokine response.


Keywords: community acquired pneumonia; neutrophils; anti-inflammatory cytokines


© 2001 by Thorax



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