Exosomes for the Respiratory System

Core functional proteins: IL-10, IL-1Ra, sTNFR, TGF-β3, HSP70, SOD, KGF, lactoferrin, IDO

Targets: Airway ciliated epithelium, submucosal macrophages, airway smooth muscle, bronchial T cells

Targeting logic: Asthma, COPD and infection-driven airway inflammation secretes high CXCL12 and exposes integrin receptors on damaged epithelium; the exosome’s CXCR4 reads the inflammation gradient and anchors only to swollen, damaged airway mucosa, sparing healthy bronchial epithelium.

1. IL-1Ra and sTNFR neutralise airway TNF-α and IL-6, blocking the NF-κB cascade to quickly reduce swelling, mucus over-secretion and bronchospasm.
2. IL-10 and TGF-β3 reprogram M1 macrophages to reparative M2 and balance Th1/Th2 immunity, lowering airway hyper-reactivity, cough and wheeze.
3. HSP70 and SOD clear oxidative free radicals, easing epithelial damage from smoke, viruses and pollutants.
4. KGF repairs ciliated epithelium and restores the mucosal barrier, reducing entry of particles and pathogens.
5. Lactoferrin suppresses harmful colonisation and IDO induces regulatory T cells, preventing chronic recurrent inflammation and airway-remodelling fibrosis.

Core functional proteins: KGF, EGF, bFGF, VEGF, BMPR2, TGF-β3, fibronectin, MMP inhibitors, SOD, IL-10, ENaC regulators

Targets: Type II (AT2) & type I (AT1) alveolar cells, alveolar macrophages, alveolar capillary endothelium, interstitial fibroblasts

Targeting logic: Pneumonia, acute lung injury and fibrosis break alveolar septa and cause collapse and oedema, releasing high CXCL12; exosomes pass through the airway into the alveolar space and bind damaged AT2 stem cells and broken microvascular endothelium.

1. KGF and EGF activate AT2 stem-cell proliferation and drive AT2→AT1 differentiation via BMPR2–SMAD to rebuild the gas-exchange structure and repair the alveolar wall.
2. VEGF regenerates alveolar microvasculature and repairs the endothelial barrier, reducing exudation and oedema; ENaC speeds clearance of intra-alveolar fluid.
3. TGF-β3 + MMP inhibitors restrain over-activated fibroblasts and block abnormal collagen build-up, preventing alveolar fibrosis and stiffening.
4. Fibronectin rebuilds the alveolar matrix scaffold and repairs broken septa, preventing alveolar fusion and collapse.
5. IL-10 and SOD suppress local inflammation and oxidative stress, reducing epithelial apoptosis and maintaining stable ventilation.

Core functional proteins: TGF-β3, HGF, BMP-7, MMP inhibitors, IL-10, HSP70, SOD, decorin, FGF inhibitors, PDGF antagonists

Targets: Interstitial fibroblasts, myofibroblasts, alveolar epithelium, pulmonary vascular smooth muscle, alveolar macrophages

Targeting logic: In fibrotic lesions, fibroblasts are over-activated with abnormal collagen, continuously releasing pro-fibrotic signals (CXCL12, TGF-β1); exosomes home via CXCR4 to the lesion and target activated fibroblasts, sparing normal parenchyma.

1. TGF-β3 and decorin competitively block the pro-fibrotic TGF-β1/Smad pathway, inhibiting fibroblast-to-myofibroblast conversion and cutting abnormal collagen at the source.
2. HGF and BMP-7 regenerate alveolar epithelium, repair damaged walls and reverse epithelial–mesenchymal transition (EMT), reducing lesion formation.
3. MMP inhibitors rebalance metalloproteinases and their inhibitors, degrading deposited abnormal collagen and easing stiffness.
4. PDGF antagonists inhibit pulmonary vascular smooth-muscle proliferation, reducing vascular remodelling and improving circulation.
5. IL-10, HSP70 and SOD suppress chronic inflammation and oxidative stress, lowering fibrosis drivers and slowing functional decline.