β2-microglobulin as a biomarker of pulmonary fibrosis development in COPD patients

Expression of beta 2-microglobulin (beta 2M) is involved in fibrosis progression in kidney, liver, and heart. In this case controlled retrospective study, we investigated the role of beta 2M in the development of pulmonary fibrosis in patients with chronic obstructive pulmonary disease (COPD). Analysis of 450 COPD patients revealed that patients with decreased pulmonary diffusing capacity (DLCO) had increased beta 2M serum levels. Compared to patients with lower beta 2M serum levels, patients with increased beta 2M levels exhibited increased alveolar wall/septal thickening and lung tissue beta 2M expression. In addition, patients with increased beta 2M levels had increased lung expression of TGF-beta 1, Smad4, and a-SMA. Animal experiments showed that increased beta 2M expression resulted in epithelial-mesenchymal transition (EMT), alveolar wall/septal thickening, and pulmonary fibrosis in a rat COPD model. Together, these results indicate that beta 2M serum levels may serve as a new indicator for assessment of pulmonary diffusion function and pulmonary fibrosis severity in clinical practice and may provide a potential target for treatment of pulmonary fibrosis in the future.

Automated summary

The expression of beta 2-microglobulin (β2M) is implicated in the progression of fibrosis in various organs. A retrospective study on COPD patients found that increased levels of β2M in serum were associated with pulmonary fibrosis development, including thickening of the alveolar wall/septum. This research suggests that β2M serum levels may serve as a potential indicator for evaluating lung function and severity of fibrosis in clinical settings and may offer a promising target for future treatment of pulmonary fibrosis.