Endoplasmic reticulum stress in chronic obstructive lung diseases.

Area of Science:

• Cellular biology
• Respiratory medicine
• Immunology

Background:

• Chronic airway inflammation is a hallmark of diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD).
• The airway environment in these conditions alters airway epithelia, enhancing their innate defense mechanisms.
• Luminal inflammatory stimuli trigger adaptive changes in human airway epithelia, including endoplasmic reticulum (ER) expansion and increased Ca(2+) stores.

Purpose of the Study:

• To review the connection between airway epithelial inflammation and the activation of the unfolded protein response (UPR).
• To discuss the potential relevance of UPR activation in the context of CF and COPD.
• To explore UPR-targeting as a therapeutic strategy for obstructive airway diseases.

Main Methods:

• Literature review of studies investigating airway inflammation, ER stress, and UPR.
• Analysis of the role of UPR pathways in epithelial adaptation to inflammatory stimuli.
• Examination of UPR activation by triggers like cigarette smoke.

Main Results:

• Epithelial adaptation to inflammation involves ER expansion and Ca(2+) store changes, mediating hyperinflammatory responses.
• Activation of the unfolded protein response (UPR) by ER stress is implicated in these inflammatory processes.
• Cigarette smoke, a key factor in COPD, is known to activate the UPR.

Conclusions:

• UPR activation plays a functional role in airway inflammation.
• Targeting UPR pathways presents a promising therapeutic avenue for obstructive airway diseases like CF and COPD.
• Understanding UPR's role in airway epithelia is crucial for developing new treatments.