我们前期研究表明，大潮气量机械通气激活肺泡巨噬细胞分泌含大量活性分子的微囊泡，微囊泡作为载体传递活性分子且放大其生物学效应。有报道, 调节性B淋巴细胞（Breg）通过免疫调控作用，显著改善炎症反应。在VILI中，激活Breg细胞促进M2型巨噬细胞募集，分泌大量TGF-β促进中性粒细胞凋亡，减弱VILI炎症反应？机制如何？未见报道。因此，我们提出假说：炎症发生后，启动B细胞免疫调节作用，活化Breg介导M2型巨噬细胞募集，分泌大量TGF-β，增强中性粒细胞凋亡，减轻VILI炎症反应，促进组织修复作用。为验证假说，建立VILI动物及细胞模型，探讨Breg细胞激活、M1/M2型肺泡巨噬细胞极化及M2型肺泡巨噬细胞募集作用机制；分析TGF-β减轻炎症反应分子机制；采用细胞膜涂层纳米技术致微囊泡包裹TGF-β，探讨内外源性Breg细胞在VILI中的保护作用及分子机制，为VILI防治提供新靶点与思路。

Our previous studies showed that mechanical ventilation with high tidal volume activates alveolar macrophages to release microvesicles packaging massive active molecules, and proved that microvesicles would regarded as carriers to transfer active molecules and amplify their biological effects. Recent studies showed that regulatory B lymphocytes (Breg) would significantly attenuate inflammatory responses through regulation of immune system. Whether Breg interacted with alveolar macrophages to release transforming growth factor (TGF)-β that promotes necrosis in neutrophils, resulting in attenuation of inflammation in VILI? Its mechanism have not yet been fully elucidated. Hence, we hypothesized that immune regulation of B lymphocytes is activated while inflammation occurred, and activated Breg promotes the recruitment of M2 alveolar macrophages to release massive TGF-β, which promotes necrosis in neutrophils resulting in attenuation of inflammation and tissue repair in VILI. To verify this hypothesis, animal and cellular VILI model were established to explore the mechanism of Breg promoting the differentiation of M1/M2 alveolar macrophages and recruitment of M2 alveolar macrophages; study the molecular mechanism of TGF-β attenuating pulmonary inflammation. Then, TGF-β were packaged in macrophage derived microvesicle-coated nanoparticles via cell membrane coating nanotechnology to study the protective effect and molecular mechanism of endogenous and exogenous Breg in VILI, This study will provide a new target and idea for the prevention and target treatment of VILI.