Macrophages play a central role in dictating the tissue response to infection and orchestrating subsequent repair of the damage. In this context, macrophages residing in the lungs continuously sense and discriminate among a wide range of insults to initiate the immune responses important to host-defense. Inflammatory tissue injury also leads to activation of proteases, and thereby the coagulation pathway, to optimize injury and repair post-infection. However, long-lasting inflammatory triggers from macrophages can impair the lung's ability to recover from severe injury, leading to increased lung vascular permeability and neutrophilic injury, hallmarks of Acute Lung Injury (ALI). In this review, we discuss the roles of toll-like receptor 4 (TLR4) and protease activating receptor 2 (PAR2) expressed on the macrophage cell-surface in regulating lung vascular inflammatory signaling.

巨噬细胞在决定组织对感染的反应以及协调对损伤的后续修复中起着核心作用。在这种情况下，驻留在肺中的巨噬细胞不断地感知并区分各种侮辱，以启动对宿主防御至关重要的免疫反应。炎性组织损伤还导致蛋白酶的活化，从而导致凝血途径的活化，以优化损伤并修复感染后。然而，巨噬细胞的长期炎症触发会损害肺部从严重损伤中恢复的能力，从而导致肺血管通透性和中性粒细胞损伤的增加，这是急性肺损伤（ALI）的标志。在这篇评论中