title: Leucocyte response and anti-inflammatory cytokines in community acquired pneumonia.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Medicine II, Medizinische Universität Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany.
authors.forename: U K
authors.initials: UK
authors.lastname: Kolling
authors.forename: F
authors.initials: F
authors.lastname: Hansen
authors.forename: J
authors.initials: J
authors.lastname: Braun
authors.forename: L
authors.initials: L
authors.lastname: Rink
authors.forename: H A
authors.initials: HA
authors.lastname: Katus
authors.forename: K
authors.initials: K
authors.lastname: Dalhoff
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002478:Cells, Cultured; D017714:Community-Acquired Infections / Q000276:immunology*; D016207:Cytokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000276:immunology; D016209:Interleukin-8 / Q000276:immunology; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D011014:Pneumonia / Q000276:immunology*; D018124:Receptors, Tumor Necrosis Factor / Q000276:immunology; D012795:Sialoglycoproteins / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D016207:Cytokines; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D016209:Interleukin-8; D008070:Lipopolysaccharides; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D000068800:Etanercept