Abstract：
The inflammatory response caused by early lung injury is one of the important causes of the development of idiopathic pulmonary fibrosis (IPF), which is accompanied by the activation of inflammatory cells such as macrophages and neutrophils, as well as the release of inflammatory factors including TNF-α, IL-1β, and IL-6. Early inflammation caused by activated pulmonary interstitial macrophages (IMs) in response to IL-33 stimulation is known to play a vital role in the pathological process of IPF. This protocol describes the adoptive transfer of IMs stimulated by IL-33 into the lungs of mice to study IPF development. It involves the isolation and culture of primary IMs from host mouse lungs, followed by the adoptive transfer of stimulated IMs into the alveoli of bleomycin (BLM)-induced IPF recipient mice (which have been previously depleted of alveolar macrophages by treatment with clodronate liposomes), and the pathological evaluation of those mice. The representative results show that the adoptive transfer of IL-33-stimulated macrophages aggravates pulmonary fibrosis in mice, suggesting that the establishment of the macrophage adoptive transfer experiment is a good technical means to study IPF pathology.
摘要：
早期肺毁伤惹起的炎症反响是特发性肺纤维化(IPF)成长的重要缘由之一，伴随着巨噬细胞和中性粒细胞等炎症细胞的活化，以及炎症因子包括TNF-α的释放，IL-1β,IL-6IL-33刺激引起的肺间质巨噬细胞（IM）活化引起的早期炎症在IPF的病理过程中起着至关重要的作用。该方案描述了由IL-33刺激的IM过继转移到小鼠的肺中以研究IPF发育。它涉及从宿主小鼠肺中分离和培养原代IM，然后将受刺激的IM过继性转移到博来霉素（BLM）诱导的IPF受体小鼠的肺泡中（以前已经通过用氯膦酸盐脂质体治疗耗尽了肺泡巨噬细胞），和这些小鼠的病理学评估。代表性结果表明，IL-33刺激的巨噬细胞过继转移加重了小鼠肺纤维化，提示巨噬细胞过继转移实验的建立是研究IPF病理的良好技术手段。
