Autophagy Mechanisms in Allergic Airway Inflammation

Autophagy, the cellular process that degrades and recycles cytoplasmic components, has emerged as a central regulator of allergic airway inflammation. In asthma and related disorders, controlled autophagic flux contributes to immune homeostasis by clearing damaged organelles and dampening excessive inflammatory signalling. Conversely, dysregulated autophagy can amplify type 2 immune responses, promote eosinophil survival and exacerbate airway remodelling. Key molecular sensors such as the mammalian target of rapamycin (mTOR) integrate metabolic cues with autophagic initiation, while specialised forms of selective autophagy—mitophagy—ensure mitochondrial quality control under allergic stress. In epithelial cells, autophagy supports barrier repair and progenitor‐cell proliferation, whereas in immune cells it modulates inflammasome activation and cytokine production. The dual role of autophagy in resolving environmental insults and in perpetuating chronic airway remodelling underscores its global significance and highlights potential therapeutic avenues targeting autophagic pathways.

Research from Nature Portfolio

Recent studies have elucidated a pivotal requirement for mTOR pathway activation in the onset and progression of allergic airway inflammation. Clinical samples from asthmatic patients exhibit elevated phosphorylation of mTOR effectors alongside imbalances in Th17/Treg and Th1/Th2 cell subsets. In an ovalbumin‐induced mouse model, inhibition of mTOR with pathway‐specific compounds not only reduced eosinophilic infiltration and airway hyper-responsiveness but also restored cytokine homeostasis. These experiments confirm that mTOR signalling controls autophagic flux in airway tissues and that its pharmacological modulation can attenuate hallmark features of asthma. This work establishes a mechanistic link between autophagy regulation and adaptive immunity in allergic inflammation and validates mTOR as a promising target for precision therapies.

Autophagy Mechanisms in Allergic Airway Inflammation publication trend

The graph below shows the total number of articles in autophagy mechanisms in allergic airway inflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Autophagy: A cellular housekeeping process that degrades and recycles cytoplasmic components via lysosomal pathways.

Mitophagy: A selective form of autophagy targeting damaged mitochondria to maintain mitochondrial integrity.

mTOR (mammalian target of rapamycin): A central kinase that inhibits autophagy initiation in response to nutrient abundance and growth signals.

Inflammasome: A multiprotein complex that activates inflammatory caspases and promotes secretion of interleukin-1β.

Type 2 immune response: An adaptive immune pathway characterised by eosinophils, IL-4, IL-5 and IL-13 production, commonly associated with allergic asthma.

References

1. DEK deficiency suppresses mitophagy to protect against house dust mite-induced asthma. Frontiers in Immunology (2024).
2. Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence. Frontiers in Immunology (2019).
3. Activation of the mTOR signaling pathway is required for asthma onset. Scientific Reports (2017).
4. Airway epithelial regeneration requires autophagy and glucose metabolism. Cell Death & Disease (2019).