The year 2020 is characterized by the COVID-19 pandemic that has resulted in more than half a million deaths in recent months. The high mortality is associated with acute severe respiratory failure that results in ICU admission and intubation. While facing this fatal disease, research and clinical observations need to be carried out in order to evaluate the long-term effects of the COVID-19 acute respiratory distress syndrome (ARDS). Potent clinical and laboratory biomarkers should be studied to be able to predict the subgroup of patients that are going to deteriorate or develop lung fibrosis. The opportunity of personalized medicine is a good way to consider for these patients. Contents 1. Introduction 2. Post-ARDS lung fibrosis 3. Possible biomarkers of disease progression 4. Is there a role for antifibrotic therapy? 5. Conclusion

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. @ERSpublications Distinct NLRP3 inflammasome activation profiles between autoimmune and IPF lung macrophages compared with controls

The two novel drugs approved for IPF, pirfenidone and nintedanib, open a new scenario in which treated patients with fibrosis will live longer, and possibly have a lower incidence of lung cancer. However, prospective studies are urgently needed to definitively clarify the role of lung cancer treatment in the management of IPF patients. Furthermore, common epigenetic alterations may represent a promising target for therapeutic approaches in the near future.

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