Chlamydia Pneumonia, heart disease, macrophage involvement

[Guest guest]

Here's an excerpt from an interesting article from the

ImmunoSciences lab on C. Pneumonia and heart disease (among other

ailments). Also talks about how macrophages actually become co-

culprits. C. pneumonia is capable of invading the macrophages (as

are other organisms) resulting in the macrophages doing more harm

than good.

More and more I'm convinced that there's a good chance that many of

my problems may have begun with C. Pneumonia as a child (repeated

bronchitis and pneumonia), and I'd like to get tested for it. Does

anyone know the best tests to get? My doc's suggesting

ImmunoSciences, but I want to be certain I get the best possible

test to see if this may be an underlying issue that's allowing all

these other pathogens to take hold as well. It could explain a lot

of my heart problems, as well as the sinus and jaw disease.

Anyone tested for this and how were you tested?

thanks,

penny

http://www.immuno-sci-lab.com/html/chlamydia_pneumoniae.html

Scientists have long known that atherosclerosis is an inflammatory

disease which affects vessels throughout the body in particular

those supporting the heart and the brain. So far no one has shown

conclusively that C. pneumoniae causes the damage that leads to

heart attack but there are good reasons to believe that it plays an

important role in the inflammatory response.

One of the functions of the immune system is to remove fat,

cholesterol and other irritants from the vessel walls.

As it is shown by its designation, Chlamydia pneumoniae has been

established as an important human respiratory pathogen causing both

endemic and epidemic disease, including pneumonia, bronchitis,

pharyngitis and sinusitis.9,10 Up to 10% of community-acquired

pneumonia cases in adults and up to 50% of pneumonia cases during

epidemics are caused by this organism emphasizing the role of the

respiratory system in this cross-infection. Although association of

this organism with coronary heart disease, erythema nodosum and

asthma has been demonstrated it is not clear how this organism is

transferred from respiratory system to the circulation.9,10

It seems that macrophages which have helped to clear C. pneumoniae

from the respiratory system under certain conditions become active

carriers of the microbe. And when an infected macrophage travels

down on a vessel wall, it may infect the cells lining the arterial

surface. Under these conditions, the artery would attract more

immune cells, which will deliver more bacteria to the site and cause

more serious inflammation. This hypothesis with preliminary

evidence supporting it nicely is depicted in Figure 1.

Researchers at s Hopkins and Louisiana State University have

shown in test-tube experiments (in-vitro) that C. pneumoniae can

indeed survive within macrophages and arterial cells.28-31

In these studies the ability of C. pneumoniae to infect cells that

make up atherosclerotic lesions, including endothelial cells, smooth

muscle cells, and cholesterol-loaded smooth muscle cells was

examined. It was shown that C. pneumoniae can infect rabbit,

bovine, and human smooth muscle cells, and cholesterol-loaded smooth

muscle cells were more susceptible to C. pneumoniae infection.28-31

At the same time C. trachomatis inefficiently infected smooth muscle

cells, demonstrating that this is not a characteristic of all

members of the genus Chlamydia.31

It was concluded that C. pneumoniae has the capacity to infect one

of the most important types of cells (smooth muscle) found within

atherosclerotic lesions.

Recent animal studies reinforce evidence found in test-tubes during

1997 where different groups from Canada, USA and Finland have shown

that C. pneumoniae invades arterial tissues.28-31

In these studies researchers infected a dozen rabbits through the

nose and within seven weeks of contracting the organism, the

majority of them developed arterial plaques. This plaque formation

occurred despite the fact that rabbits do not normally get

atherosclerosis, even when they are fed high-fat diets.

Even with this extensive information about the role of C. pneumoniae

in heart disease, there will still be plenty of questions.

1.What is the mechanism of action?

2.Why are some people more susceptible than others?

3.Do fat and cholesterol make us sick by themselves, or only in

combination

with C. pneumoniae?

4.Could antibodies quickly rid the body of infection?

5.Would clearing the infection stop the disease process?