PMC:7565665 / 36390-38536 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7565665","sourcedb":"PMC","sourceid":"7565665","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7565665","text":"4.5. Autophagy Defects in Cystic Fibrosis\nCystic fibrosis is a chronic obstructive lung disease which is marked by recurrent infections, chronic inflammatory-oxidative stress, and mucus overproduction that contributes to severe airway obstruction. Initial seminal studies by Luciani A et al. established the link between defective CFTR and the presence of aggresome bodies, lung inflammation, and ROS-mediated autophagy inhibition [53]. We and others have not only validated that defective CFTR-mediated ROS-TG2 pathway drives the crosslinking of Beclin-1, which results in the accumulation of misfolded ΔF508-CFTR into p62+HDAC6+ aggresome bodies leading to autophagy dysfunction, but we have also demonstrated the key central role of autophagy in regulating CF pathogenesis and exacerbations [42,58,149,150]. These studies describe the specific role of defective autophagy in CF-related chronic infections and resulting inflammatory-oxidative stress. In addition, CF macrophages demonstrate impaired phagocytic activity and thus CF patients are more prone to bacterial infections, such as P. aeruginosa and Burkholderia cenocepacia (B. cenocepacia) [45,51,58,106,151,152,153]. A recent study investigated the precise mechanism of weak autophagic activity in CF macrophages. Using the technique of reduced representation bisulfite sequencing (RRBS) to determine the DNA methylation profile, the authors found that the promoter regions of Atg12 in CF macrophages are significantly more methylated as compared to the control WT cells, thereby elucidating a novel mechanism for reduced autophagy activity in CF immune cells [154].\nIn a separate study, an increased expression of the microRNA (Mir)c1/Mir17-92 cluster was identified as a potential negative regulator of autophagy in CF macrophages when compared to normal control cells [105]. Furthermore, the in vivo downregulation of Mir17 and Mir20a, partially restored autophagy gene expression and improved the clearance of B. cenocepacia [105]. These studies highlight the importance of autophagy as a key protective mechanism in CF exacerbation, and lung disease pathogenesis and 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