Systemic cytokine levels in community-acquired pneumonia and their association with disease severity
Antunes, G., Evans, S.A., Lordan, J.L. and Frew, A.J. (2002) Systemic cytokine levels in community-acquired pneumonia and their association with disease severity. European Respiratory Journal, 20, (4), 990-995. (doi:10.1183/09031936.02.00295102).
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Pro-inflammatory and anti-inflammatory cytokines are important mediators in the host response to infection. In contrast to the pro-inflammatory cytokines little is known about anti-inflammatory cytokines in community-acquired pneumonia (CAP) and their relation to disease severity.
Circulating levels of three pro-inflammatory cytokines (interleukin (IL)-1ß, IL-6 and tumour necrosis factor (TNF)-) and two anti-inflammatory cytokines (IL-10, IL-1 receptor antagonist (IL-1ra)) were measured using an enzyme immunoassay on admission, day 3 and day 5 in 24 patients with CAP. The modified British Thoracic Society (BTS) prognostic rule and Acute Physiology and Chronic Health Evaluation (APACHE) II score were used to assess disease severity.
IL-6, TNF-, IL-10 and IL-1ra concentrations were detected in most patients on admission and decreased significantly on day 3 and day 5 in all survivors. A significant difference between the BTS high-risk and low-risk groups was only found for IL-6 (median (range) 477 pg·mL–1 (7.6–1402 pg·mL–1) versus 81.6 pg·mL–1 (0–943 pg·mL–1); p<0.05). IL-6 also correlated with the APACHE II scores on admission.
Concentrations of anti-inflammatory cytokines were elevated on admission in community-acquired pneumonia but they did not correlate with disease severity scores.
|Keywords:||community-acquired, pneumonia, cytokines, disease severity score|
|Subjects:||R Medicine > RB Pathology
R Medicine > RM Therapeutics. Pharmacology
Q Science > QP Physiology
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
|Date Deposited:||25 Apr 2006|
|Last Modified:||06 Aug 2015 02:27|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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