Literature DB >> 9893770

Inhalation of swine-house dust increases the concentrations of interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-1ra) in peripheral blood.

Z Wang1, A Manninen, P Malmberg, K Larsson.   

Abstract

Inhalation of dust in swine confinement buildings causes airway inflammation and systemic symptoms. The proinflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) increase in bronchoalveolar and nasal lavage fluid, and in serum. The aim of this investigation was to study changes in the IL-1 family of cytokines in peripheral blood in 36 healthy volunteers exposed to swine house dust for 3 h. Interleukin (IL-1 beta) was measured in platelet poor plasma and in a mononuclear cell fraction (PBMC) and interleukin-1 receptor antagonist (IL-Ira), IL-6 and TNF-alpha were measured in serum 4 and 7 h after the start of 3 h exposure. Lung function and a methacholine bronchial provocation test were performed before and 7 h after the start of exposure. The leukocyte count in whole blood and the mononuclear cell count in PBMC were examined before, and 4 and 7 h after the start of exposure. The concentration of airborne inhalable dust and endotoxin were measured using personal samples. The concentration of inhalable dust was 23 (20-30) mg m-3 (median 25th-75th percentile) endotoxin was 1.1 (0.8-1.4) micrograms m-3 and respirable dust (n = 8) was 1.0 (0.7-1.2) mg m-3. IL-1 beta increased from < 0.125 to 0.9 (0.5-1.3) ng l-1 in plasma and from 1.6 to 2.7 (1.1-4.4) ng l-1 in PBMC (P < 0.01). IL-1 ra, IL-6 and TNF-alpha increased 2-, 12- and 2-fold in serum after exposure, respectively. Changes in IL-1 ra correlated with changes in FEV1, bronchial responsiveness, oral temperature (P < 0.01) and blood white cell count (P < 0.05). IL-1 beta correlated significantly with temperature (P < 0.05). These results indicate that IL-1 beta and IL-1 ra increase in peripheral blood following inhalation of swine house dust and may participate in and modulate the inflammatory response together with IL-6 and TNF-alpha.

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Year:  1998        PMID: 9893770     DOI: 10.1016/s0954-6111(98)90349-3

Source DB:  PubMed          Journal:  Respir Med        ISSN: 0954-6111            Impact factor:   3.415


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