AUGUSTA, Ga.– Dr. Clinton Webb is chairman of the Department of Physiology at the Medical College of Georgia at Augusta University. He and Dr. Dr. Michael P. Madaio, nephrologist and Chairman of the Department of Medicine at MCG, join Jennie to talk about inflammation, which is the body’s natural response to injury.
Dr. Webb says the mounting debris from dying cells gets the attention of our immune system, causing inflammation and blood vessel constriction that contributes to worsening hypertension.
He’s studying all of this through a $9,000,000+ grant.
Here’s more from MCG at Augusta University:
(Feb. 9, 2017) – It’s been known for decades that a bacterial infection can raise your blood pressure short term, but now scientists are putting together the pieces of how our own dying cells can fuel chronically high, destructive pressure.
Quite literally billions of our cells die daily and their remains are mostly taken up by garbage-eating immune cells like macrophages. But scientists have increasing evidence that when cell carnage increases because of high blood pressure, the mounting debris also gets the attention of our immune system, causing inflammation and blood vessel constriction that contributes to worsening hypertension.
“It’s a circle,” said Dr. R. Clinton Webb, chairman of the Department of Physiology at the Medical College of Georgia at Augusta University, in which inflammation is a constant and, which isn’t addressed in today’s treatment regimens.
“The more blood pressure goes up, the more injury you have,” said Webb, and he and his colleagues want to understand the signaling pathways that are driving this inflammation that further drives blood pressure.
Webb, a vascular expert, is principal investigator on a $9.4 million Program Project Grant from the National Heart, Lung and Blood Institute, that will further parse how contents regularly split from a surplus of dying cells contribute to this unhealthy and seemingly vicious circle.
While the chicken or the egg question isn’t answered, it’s clear that higher blood pressure – from causes like obesity to genetics to salt sensitivity – increases cell death. Once outside the dying cell, typical contents like DNA as well as HMGB1, which helps stabilize the DNA, are categorized as damage associated molecular patterns, or DAMPs.
The scientists call DAMPs “alarm signals” because they look like bacterial or viral invaders to the immune system. That sets in motion likely well-intended inflammation to fight the invader but blood-vessel constriction and narrowing, kidney and other organ damage, and more cell death also follow.
The new grant is enabling Webb and his team to look at what happens when the increased cell carnage inside blood vessel walls increases the release of DNA from cell powerhouses called mitochondria – DNA which actually is distinctly different from our own.
Hypertension affects about one third of the adult population in the United States, according to the Centers for Disease Control and Prevention, and Webb thinks DAMPs are both the result of and initiators of hypertension in many.
“There is no doubt there are more dead cells in the hypertensive blood vessel,” Webb said.
All this internal debris has to go somewhere and some finds its way into nearby cells. There it can activate immune receptors that instead of just consuming it, mount a fight that further damages the form and function of blood vessels and organs, Webb said.
The long-term goal of Webb and his colleagues: identifying targets that could block some of the unintended results without putting people at risk for additional disease by generally suppressing their natural immune response.
Webb noted that a burned tongue from a hot cup of morning coffee that is mostly better by that afternoon illustrates normal cell death and typically rapid recovery. It’s when diseases such as hypertension start killing off an excessive number of cells throughout the body, that normal compensatory mechanisms become overwhelmed. Age makes us less able to cope with increased debris from dying cells.