Not long ago, inflammation had a clear role: It was a sidekick to the body's healers, briefly setting in as immune cells rebuilt tissue damaged by trauma or infection. Today, that's an afterthought. Inflammation has hit the big time. Over the past decade, it has become widely accepted that inflammation is a driving force behind chronic diseases that will kill nearly all of us. Cancer. Diabetes and obesity. Alzheimer's disease. Atherosclerosis. Here, inflammation wears a grim mask, shedding its redeeming features and making sick people sicker.A growing body of evidence suggests that C-reactive protein (CRP), a molecular marker for inflammation, may be as crucial as cholesterol in assessing risk of heart attack. Macrophages, the white blood cells that are a hallmark of inflammation, appear around fatty plaques that build up in the arteries in atherosclerosis, infiltrate fat tissue in obesity, surround cancer cells to stimulate circulation and coax them along, help to kill neurons in neurodegenerative diseases such as Alzheimer's and Parkinson's, and promote two components of type 2 diabetes: insulin resistance and the death of pancreatic beta cells that produce insulin. Anti-inflammatory drugs (that suppresses action of proinflammatory cytokines released by immune cells) have been shown in several cases to retard disease progression.
Friday, December 24, 2010
The dark side of inflammation
Couzin-Frankel does an interesting piece in the News section of the Dec. 17 issue of Science, consonant with my opinion that inflammatory processes are one of the main issues in aging. The abstract: