Abstract
BMP and activin membrane-bound inhibitor (BAMBI) is postulated to inhibit or modulate transforming growth factor β (TGF-β) signaling. Furthermore, strong upregulation of BAMBI expression following in vitro infection of chronic obstructive pulmonary disease (COPD) lung tissue has been demonstrated. In this study, we investigated whether TGF-β/BAMBI pathway is associated with COPD. Blood samples were obtained from 27 healthy controls (HC), 24 healthy smokers (HS) and 29 COPD patients. Elevated Th17/Treg ratios, and increased levels of BAMBI protein and mRNA (in plasma and CD4+ T cells respectively), were observed in COPD compared with HC and HS. BAMBI expression was first observed on human CD4+ T cells, with a typical membrane-bound pattern. The enhanced plasma BAMBI levels in COPD positively correlated with the increased plasma TGF-β1 levels and Th17/Treg ratio. Together, an impaired TGF-β/BAMBI pathway may promote the inflammation leading to Th17/Treg imbalance, which is a new mechanism in smokers who develop COPD.
Highlights
Expression can be upregulated by TGF-βin a feedback loop[28], making the prediction of the function or mode of this pseudo-receptor difficult
Th17/Treg imbalance was observed in peripheral blood samples from Chronic obstructive pulmonary disease (COPD) patients
No significant differences in circulating Th17 frequencies were observed between HC and HS subjects, a trend toward higher levels was detected in peripheral blood from HS subjects compared with that from HC subjects
Summary
Expression can be upregulated by TGF-βin a feedback loop[28], making the prediction of the function or mode of this pseudo-receptor difficult. Little is known regarding their role in human immunity and their capacity to influence the Th17-Treg axis and immune balance in COPD. In light of our initial findings both in vivo and in vitro[14,15,31,32], the present study was initiated to further understand the contribution of immune imbalance to COPD. Given its counteractive influence on TGF-βsignaling, we hypothesized that BAMBI may play an important regulatory role in the internal environment of COPD. By assessing peripheral blood samples from donors with or without airway obstruction, we confirmed an immune imbalance of peripheral Th17/Tregs and TGF-βsignaling in COPD. Our data further suggest that BAMBI is expressed in both peripheral CD4+ T cells and plasma and that upregulated BAMBI could be linked to the Th17/ Treg balance through the TGF-β/BAMBI pathway in smokers who develop COPD
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