Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model

Area of Science:

• Immunology
• Pulmonology
• Pathophysiology

Background:

• Chronic obstructive pulmonary disease (COPD) pathogenesis is linked to immune response dysregulation.
• An imbalance between pro-inflammatory and anti-inflammatory immune cells, specifically Th17 and Treg cells, is implicated in COPD.

Purpose of the Study:

• To investigate the temporal dynamics of immune responses in a cigarette smoke (CS)-induced COPD mouse model.
• To analyze the balance between T-helper 17 (Th17) and regulatory T (Treg) cell responses during COPD progression.

Main Methods:

• C57BL/6 mice were exposed to CS or filtered air for 1, 3, or 6 months.
• Functional (respiratory mechanics) and structural (alveolar analysis) assessments were performed.
• Immune cell markers (NF-κB, TNF-α, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, TGF-β) and gene expression were quantified.

Main Results:

• CS exposure led to increased pro-inflammatory markers (IL-17, IL-6, TNF-α) and decreased anti-inflammatory markers (FOXP3, IL-10, TGF-β).
• These immune alterations correlated with alveolar enlargement and impaired lung function.
• The observed changes were evident as early as one month of CS exposure.

Conclusions:

• COPD progression involves a shift in the immune microenvironment, favoring pro-inflammatory cytokines.
• This leads to a Th17/Treg imbalance, contributing to the development and exacerbation of COPD.