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Damaged AECs release pro-inflammatory and pro-fibrotic mediators, including interleukin (IL) -1 and tumor necrosis factor (TNF) -, which promote fibroblast recruitment, inflammatory cell activation (e.g., neutrophils, Th17, gdT cells), and myofibroblast differentiation, ultimately leading to ECM accumulation and fibrotic tissue remodeling [20, 29, 33, 34]
Chronic conditions involving persistent inflammation, incomplete tissue healing, or adaptive dysfunction respond well to the sustained gentle support that micro-dosing provides
The study supports further clinical adoption of this combination therapy and suggests that it could enhance long-term patient outcomes in CHB management
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