Department of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
J Pathol. 2011 Feb;223(3):417-24. doi: 10.1002/path.2814. Epub 2010 Nov 18.
Pulmonary macrophages exist in two different anatomical compartments in the lower respiratory tract: alveolar macrophages in the alveoli and interstitial macrophages in the interstitium. Depending on the micro-environmental stimulation, macrophages follow different activation pathways. According to their inflammatory response pattern, activated macrophages have been characterized as pro-inflammatory (M1), wound-healing (M2a) and regulatory (M2b). Since acute pancreatitis occurs in parallel with acute lung injury, the profile of the different macrophage subpopulations could be relevant in the progression of the disease. The activation of lung alveolar and interstitial macrophages was assessed in an experimental model of severe acute pancreatitis induced in rats by intraductal infusion of 3.5% sodium taurocholate. Alveolar and interstitial macrophages were obtained and the expression of markers of different activations was evaluated. Activation of nuclear factors PPARγ and NF-κB, which are involved in the acquisition of different phenoytpes, was also measured. Alveolar macrophages acquired an early M1 phenotype characterized by the expression of inflammatory cytokines and NF-κB activation. In contrast, interstitial macrophages followed the inhibitory M2b pathway. In these macrophages, PPARγ became activated and the anti-inflammatory cytokine IL-10 was expressed. These results suggest that alveolar and interstitial macrophages play different roles in acute lung injury associated with acute pancreatitis. Alveolar macrophages promote an early inflammatory response, whereas interstitial macrophages help resolve inflammation.
肺泡中的肺泡巨噬细胞和间质中的间质巨噬细胞。根据微环境的刺激，巨噬细胞遵循不同的激活途径。根据其炎症反应模式，已将激活的巨噬细胞特征化为促炎（M1）、伤口愈合（M2a）和调节（M2b）。由于急性胰腺炎与急性肺损伤同时发生，不同巨噬细胞亚群的特征可能与疾病的进展有关。在通过胆管内输注 3.5%牛磺胆酸钠诱导的大鼠严重急性胰腺炎实验模型中评估了肺肺泡和间质巨噬细胞的激活。获得肺泡和间质巨噬细胞，并评估不同激活标志物的表达。还测量了参与获得不同表型的核因子 PPARγ和 NF-κB 的激活。肺泡巨噬细胞获得了早期的 M1 表型，其特征是表达炎症细胞因子和 NF-κB 激活。相比之下，间质巨噬细胞遵循抑制性 M2b 途径。在这些巨噬细胞中，PPARγ被激活并表达抗炎细胞因子 IL-10。这些结果表明，肺泡和间质巨噬细胞在与急性胰腺炎相关的急性肺损伤中发挥不同的作用。肺泡巨噬细胞促进早期炎症反应，而间质巨噬细胞有助于缓解炎症。
