Circulating levels of interleukin-18 in asbestos-exposed workers

• Published in: Toxicology and industrial health Vol. 21; no. 3-4; pp. 125 - 129
• Main Authors: Gangemi, Sebastiano, Rapisarda, Venerando, Minciullo, Paola Lucia, Di Pasquale, Giuseppe, Lombardo, Giuseppe, Valentino, Matteo, Fenga, Concettina
• Format: Journal Article
• Language: English
• Published: Thousand Oaks, CA SAGE Publications 01.05.2005; Sage Publications Ltd
• Subjects: Asbestos; Chemokines; Computed tomography; Cytokines; Gene expression; Immunocompetence; Medicine; Neutrophils; Occupational exposure; Pathogenesis; Questionnaires; Respiratory function; Signal transduction; Tomography; Toxicology; Tumor necrosis factor-TNF; proinflammatory cytokine; asbestos exposure; interleukin-18; pulmonary fibrosis
• ISSN: 0748-2337; 1477-0393
• DOI: 10.1191/0748233705th221oa

Occupational exposure to asbestos has been associated with the development of pulmonary diseases through a persistent inflammatory response initiated by reactive oxygen species and the subsequent release of proinflammatory mediators such as interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-a. Recently, IL-18, a pleiotropic proinflammatory cytokine and potent inducer of gene expression and synthesis of INF-g, TNF-a and IL-1 in immunocompetent cells, has been described. IL-18 serum concentrations were measured in 20 asbestos-exposed workers and in a group of 20 healthy donors. The workers underwent physical examination, pulmonary function tests and high-resolution computed tomography (HRCT). IL-18 levels were assayed in peripheral blood using the immunoenzymatic method with a commercial kit. The pulmonary function tests revealed a restrictive ventilatory deficit in nine (45%) cases and an obstructive ventilatory deficit in five (25%). The remaining six (30%) workers exhibited normal spirometric values. HRCT findings were: bilateral pleural plaques in 8 (40%) workers and bilateral parenchymal fibrosis in 12 (60%), with mean scores of 2.559 / 1.89. The exposed workers displayed significantly higher IL-18 concentrations than controls and those with parenchymal fibrosis displayed significantly higher values than workers with pleural plaques (P=0.001). In subjects with parenchymal fibrosis, HRCT scores significantly correlated with serum levels of IL-18 (P=0.001). Although the mechanisms leading to IL-18 release in asbestosis are unknown, the present preliminary results underscore the potential role of this cytokine in the pathogenesis of pulmonary toxicity.