Complicated Rheumatoid Nodules in Lung

A 65-year-old nonsmoker lady carrying a diagnosis of seropositive erosive rheumatoid arthritis for nine years presented with acute shortness of breath, following a spontaneous pneumothorax while on combination therapy with methotrexate, leflunomide, and tocilizumab. Imaging studies revealed multiple cavitory lung nodules, and a transbronchial lung biopsy favoured a diagnosis of rheumatoid lung nodules. Her initial pathological samples were negative for any infectious cause. A follow-up computerized tomography scan (CT scan) confirmed enlargement of lung nodules with a positive antibody test for aspergillosis which needed antifungal therapy, and currently, her arthritis is managed well with rituximab therapy, sulfasalazine, and hydroxychloroquine.

NLRP3 inflammasome expression in idiopathic pulmonary fibrosis and rheumatoid lung

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.