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An immunometabolic pathomechanism for chronic obstructive pulmonary disease
Sara Bruzzaniti1, Marialuisa Bocchino2, Marianna Santopaolo1
1Laboratorio di Immunologia, Istituto per l'Endocrinologia e l'Oncologia Sperimentale "G. Salvatore," Consiglio Nazionale delle Ricerche, 80131 Naples, Italy.
Summary
Leptin overproduction in chronic obstructive pulmonary disease (COPD) impairs regulatory T (Treg) cell function and generation. This leads to increased inflammation and reduced lung function, highlighting an autoimmune-like mechanism in COPD progression.
Area of Science:
- Immunology
- Metabolic pathways
- Respiratory medicine
Background:
- Chronic obstructive pulmonary disease (COPD) involves inflammation and abnormal immune responses, with T helper 1 (Th1) and T helper 17 (Th17) cells accumulating in the lungs.
- Regulatory T (Treg) cells are crucial for controlling autoimmune responses, and their function is regulated by the adipocytokine leptin.
Purpose of the Study:
- To investigate the link between systemic leptin overproduction, reduced glycolysis in T cells, and decreased Treg cell frequency in COPD patients.
- To explore the impact of leptin on the generation of inducible Treg (iTreg) cells from conventional T (Tconv) cells.
Main Methods:
- Analysis of systemic leptin levels, T cell glycolysis engagement, and peripheral Treg cell frequency in COPD subjects across different stages.
- Molecular investigation of leptin's effect on forkhead-boxP3 (FoxP3) expression and its splicing variants in T cells.
Main Results:
- Leptin overproduction, reduced T cell glycolysis, and lower Treg cell frequency were observed in COPD.
- Leptin was found to inhibit FoxP3 and FoxP3-E2 expression, correlating inversely with inflammation and lung function decline.
- Impaired generation of iTreg cells from Tconv cells was noted in COPD patients.
Conclusions:
- The immunometabolic mechanism in COPD progression involves leptin overproduction, decreased FoxP3 splicing forms, and impaired Treg cell function.
- These findings offer insights into the autoimmune-like characteristics of COPD and the mechanisms driving lung damage.
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