RT Journal Article
SR Electronic
T1 NLRP3 inflammasome expression in idiopathic pulmonary fibrosis and rheumatoid lung
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 910
OP 918
DO 10.1183/13993003.00564-2015
VO 47
IS 3
A1 Ismini Lasithiotaki
A1 Ioannis Giannarakis
A1 Eliza Tsitoura
A1 Katerina D. Samara
A1 George A. Margaritopoulos
A1 Christiana Choulaki
A1 Eirini Vasarmidi
A1 Nikolaos Tzanakis
A1 Argyro Voloudaki
A1 Prodromos Sidiropoulos
A1 Nikolaos M. Siafakas
A1 Katerina M. Antoniou
YR 2016
UL http://erj.ersjournals.com/content/47/3/910.abstract
AB 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.Distinct NLRP3 inflammasome activation profiles between autoimmune and IPF lung macrophages compared with controls http://ow.ly/UKYlp