Journal
EUROPEAN RESPIRATORY JOURNAL
Volume 47, Issue 3, Pages 910-918Publisher
EUROPEAN RESPIRATORY SOC JOURNALS LTD
DOI: 10.1183/13993003.00564-2015
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Funding
- Hellenic Thoracic Society grant
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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)-1 beta and IL-18 levels released in the bronchoalveolar lavage fluid (BALF) fluid and by cultures of BALF cells. IL-1 beta 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-1 beta 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-1 beta and partly IL-18 secretion, in contrast to controls, which showed robust IL-1 beta 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-1 beta, the latter being already elevated in the unstimulated cultures, while examination of the intracellular IL-1 beta levels in RA-UIP BALF cells upon NLRP3 inflammasome stimulation showed a significant upregulation of IL-1 beta suggesting the NLRP3 pathway could be further activated. Taken together, our results suggest distinct inflammasome activation profiles between autoimmune and idiopathic lung fibrosis.
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