胃溃疡和胃癌的发病机理
长了点医学知识
Sent to you by arnold via Google Reader:
Diagram 1: The immune system responds to the invasion
H. pylori use a specialised system to inject a
toxin called Cag A into epithelial cells. The cells
signal to the white blood cells of the immune system to
produce destructive oxygen compounds. H. pylori is
protected from these compounds by enzymes that break
them down and render them inactive. H. pylori strains that
do not make Cag A are less virulent than H. pylori that do.
Infection with Cag A strains also increases the risk of
developing cancer. This, and other genetic differences in
H. pylori strains, could explain why most people infected
with H. pylori do not develop ulcers or cancers.
The programmed cell death of epithelial cells -- also called
apoptosis -- that results from infection with H. pylori is
thought to be the main reason for the development
of cancer.
Diagram 2: H. pylori invades epithelial cells
H. pylori are able to attach to the epithelial cells
of the stomach and duodenum which stops them from
being washed out of the stomach. Once attached, the
bacteria start to cause damage to the cells by secreting
degradative enzymes, toxins and initiating a
self-destructive immune response.
Diagram 3: The protective mucus layer of the stomach
H. pylori make an enzyme called urease, which
degrades urea to produce bicarbonate and ammonia. The
ammonia neutralises the acid in the area, increasing the
pH in the mucus to about seven. But the ammonia is also
toxic to the cells lining the stomach and, along with other
toxins made by the bacteria, causes the cells to become
inflamed or to die. Inflammation is caused by the body's
immune system trying to defend itself against invasion
by the bacteria.
Things you can do from here:
- on People's Republic of Desire
- Subscribe to People's Republic of Desire using Google Reader
- Get started using Google Reader to easily keep up with all your favorite sites
0 Comments:
发表评论
<< Home