When ACE2 function is reduced in the lung as a result of endotoxin, free DABK increases, which in turn activates the B1 receptor and also interferes with adaptive immunity by activating macrophages and other immune system cells, thereby increasing the secretion of IL-6, IL-10 and other inflammatory factors, thereby exacerbating the PAH process (140). Here, IL6 is linked to pulmonary arterial hypertension.