From the article:
To profile the inflammatory attack that produces aortic dissection, Brasier’s group injected the hormone angiotensin into both ordinary lab mice and those genetically modified to “knock out” IL-6 or a cellular receptor for another molecule also involved, known as MCP-1. The human samples, used to substantiate a link between the mouse findings and human disease, came from volunteers undergoing surgical aortic dissection repair without a family history of the disease.
“Angiotensin is a blood-pressure regulating hormone – people who have what we call essential high blood pressure have increased production of angiotensin, and it’s the target for anti-hypertension therapies,” Brasier said. “What we’ve found in earlier studies is that it has an inflammatory role as well, causing cells in blood vessel walls to produce IL-6 as well as MCP-1. And this study showed us that MCP-1 helps recruit monocytes [a type of white blood cell] to the vessel where IL-6 activates them.”
Playing host to a large number of cells meant for immune defense is bad news for an aorta already strained by an aneurysm, since activated white blood cells produce proteins that destabilize the structure of the vessel. At the same time, signals produced by the activated white blood cells encourage the blood vessel to generate more IL-6.