Details

Autor(en) / Beteiligte

• Lasithiotaki, Ismini
• Giannarakis, Ioannis
• Tsitoura, Eliza
• Samara, Katerina D
• Margaritopoulos, George A
• Choulaki, Christiana
• Vasarmidi, Eirini
• Tzanakis, Nikolaos
• Voloudaki, Argyro
• Sidiropoulos, Prodromos
• Siafakas, Nikolaos M
• Antoniou, Katerina M

Titel

NLRP3 inflammasome expression in idiopathic pulmonary fibrosis and rheumatoid lung

Ist Teil von

• The European respiratory journal, 2016-03, Vol.47 (3), p.910-918

Ort / Verlag

England

Erscheinungsjahr

2016

Quelle

MEDLINE

Beschreibungen/Notizen

• In this study we investigated the implication of NLRP3 inflammasomes in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and rheumatoid arthritis-usual interstitial pneumonia (RA-UIP).NLRP3 inflammasome activation at baseline and following stimulation with lipopolysaccharide/ATP was evaluated by measuring interleukin (IL)-1β and IL-18 levels released in the bronchoalveolar lavage fluid (BALF) fluid and by cultures of BALF cells. IL-1β and IL-18 levels were significantly elevated in the BALF and BALF macrophage cultures from RA-UIP patients, consistent with pre-existing inflammasome activation in these patients. In contrast, in IPF, BALF levels of IL-1β were significantly less elevated relative to RA-UIP and IL-18 was lower than controls. Furthermore, upon inflammasome stimulation, IPF BALF macrophage cultures failed to upregulate IL-1β and partly IL-18 secretion, in contrast to controls, which showed robust IL-1β and IL-18 upregulation. Interestingly, RA-UIP BALF cell cultures treated with lipopolysaccharide/ATP showed a potent stimulation of IL-18 secretion but not IL-1β, the latter being already elevated in the unstimulated cultures, while examination of the intracellular IL-1β levels in RA-UIP BALF cells upon NLRP3 inflammasome stimulation showed a significant upregulation of IL-1β suggesting the NLRP3 pathway could be further activated.Taken together, our results suggest distinct inflammasome activation profiles between autoimmune and idiopathic lung fibrosis.