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The complement system #1

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The complement system can be activated by a bacteria, a yeast, an

allergic reaction, or it can be activated by an autoimmune condition.

IMO, the most likely suspect for complement activation in CFS is

allergic reactions to chemicals and tiny particals of food that get

into the blodd stream via increased gut permeabilty.

The next few messages will contain abstracts, such as the one below,

about how the complement system might be involved in the symptoms of

CFS.

Dave

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Am J Pathol 2000 Jun;156(6):2103-10

Complement activation promotes muscle inflammation during modified

muscle use.

Frenette J, Cai B, Tidball JG

Departments of Physiological Science and Pathology and Laboratory

Medicine, University of California, Los Angeles 90095-1527, USA.

Modified muscle use can result in muscle inflammation that is

triggered by unidentified events. In the present investigation, we

tested whether the activation of the complement system is a component

of muscle inflammation that results from changes in muscle loading.

Modified rat hindlimb muscle loading was achieved by removing weight-

bearing from the hindlimbs for 10 days followed by reloading through

normal ambulation. Experimental animals were injected with the

recombinant, soluble complement receptor sCR1 to inhibit complement

activation. Assays for complement C4 or factor B in sera showed that

sCR1 produced large reductions in the capacity for activation of the

complement system through both the classical and alternative

pathways. Analysis of complement C4 concentration in serum in

untreated animals showed that the classical pathway was activated

during the first 2 hours of reloading. Analysis of factor B

concentration in untreated animals showed activation of the

alternative pathway at 6 hours of reloading. Administration of sCR1

significantly attenuated the invasion of neutrophils (-49%) and ED1

(+) macrophages (-52%) that occurred in nontreated animals after 6

hours of reloading. The presence of sCR1 also reduced significantly

the degree of edema by 22% as compared to untreated animals.

Together, these data show that increased muscle loading activated the

complement system which then briefly contributes to the early

recruitment of inflammatory cells during modified muscle loading.

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