Researchers at the University of Texas Medical Branch at Galveston (UTMB) have released information about the catastrophic rupture of the aorta known as an aortic dissection. It turns out that some 16,000 U.S. individuals die of this abnormality each year. An Aortic dissection (disruption) occurs when a large blood vessel separates and as it does it can become larger and bleed into the surrounding area.
Researchers at UTMB at Galveston have found that there is a blood pressure-regulating molecule known as angiotensin II responsible for this. This molecule communicates with IL6, which is a chemical phone call from the immune system. IL stands for “interleukin,” and number 6 is one of some 30 or more chemical messengers known to date. The communication between angiotensin II and IL6 is believed to play a major role in producing aortic dissection. This study was to determine how IL6 generated the inflammation that leads to aortic dissection.
UTMB is looking at Th17 lymphocytes that are responsible for this overall effect. Under normal conditions, these cells provide a protective function. They produce a chemical messenger known as IL17 that stimulates an immune response in a positive way. The researchers report in their mouse models that locally produced IL6 supports Th17 formation and accumulation in the vascular wall. Th17 is a newly discovered interleukin (chemical messenger) involved with genetic expression and researchers understand that Th17 lymphocytes bring about an error signal causing aortic dysfunction.
Details of the UTMB Study On Aortic Dissection
UTMB researchers conducted an experiment to compare the effects of angiotensin II on normal mice and mice deficient in Th17 white blood cells either genetically or by blocking its action to test their hypothesis. Results of the experiment demonstrate that interfering with Th17 lymphocytes significantly lower aortic dissections, suggesting that Th17 cells (lymphocytes, white blood cells) are the master coordinator of cellular inflammation in the aortic wall.
Since the studies were conducted in mice, researchers examined tissue samples from human patients with a genetic mutation that predisposed them to an aortic dissection. Tissue samples were obtained from University of Texas Health Science Center at Houston that demonstrated signs of Th17 cell accumulation.
The take home message is that the immune system under normal conditions protects us against invaders, like bacteria and viruses, but under abnormal conditions the immune system can turn this around and create a disease state. And, in this case, produce chronic inflammation that destroys the aorta.
The following video from the NYU Langone Medical Center provides an overview of Aortic Dissection and Aortic Aneurysm: