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)-alpha. Recently, IL-18, a pleiotropic proinflammatory cytokine and potent inducer of gene expression and synthesis of INF-gamma, TNF-alpha 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 2.55 +/- 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.

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)-alpha. Recently, IL- 18, a pleiotropic proinflammatory cytokine and potent inducer of gene expression and synthesis of INF-gamma, TNF-alpha 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 2.55 +/- 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.

Circulating levels of interleukin-18 in asbestos-exposed workers

RAPISARDA, VENERANDO;
2005

Abstract

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)-alpha. Recently, IL-18, a pleiotropic proinflammatory cytokine and potent inducer of gene expression and synthesis of INF-gamma, TNF-alpha 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 2.55 +/- 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.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/20.500.11769/240956
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 7
  • ???jsp.display-item.citation.isi??? 6
social impact