Increased NFAT and NFkB signalling contribute to the hyperinflammatory phenotype in response to Aspergillus fumigatus in cystic fibrosis.

The article discusses the role of NFAT and NFkB signaling in contributing to the hyperinflammatory response to Aspergillus fumigatus in individuals with cystic fibrosis. It highlights the impact of CFTR deficiency on alveolar macrophage death, persistent inflammation, and impaired fungal control in murine models of pulmonary aspergillosis. The study suggests that CFTR deficiency promotes increased activation of inflammatory pathways, leading to a hyperinflammatory phenotype in cystic fibrosis during Aspergillus infection. [Extracted from the article]