C-reactive protein can be viewed as a basic marker of activity of the inflammatory response, which modulates the
development and the progression of atherosclerosis including its life-threatening complications. At the same time,
C-reactive protein represents an active partaker or mediator of this same inflammatory reaction. However, at the very
beginning of atherosclerotic disease, C-reactive protein exerts a clear-cut antiatherogenic activity. The two aspects of
CRP’s function, i.e. both the pro-inflammatory and the anti-inflammatory one, respectively, stem from CRP’s extent
of co-operation with the complement system. From the evolutional point of view, the anti-inflammatory activity of
CRP is the primary one, in that it sets stage for the host to remove foreign particles and to accelerate wound healing.
The influence of well-known atherogenic risk factors converts the originally beneficial influence of CRP into proinflammatory
and pro-atherogenic effects. This review article presents new conclusions from the „Mainz hypothesis“.
It shows that the primary protective action of CRP resides in its regulatory influence on the extent of activation of the
complement system after the latter has been triggered by enzymatically remodeled low-density lipoproteins. In further
course of atherosclerotic disease, C-reactive protein exhibits a full-blown proinflammatory activity. It can result
in the progression of the primary morphologic lesions up to the development of sudden vascular events.
atherosclerosis, C-reactive protein, the complement system, enzymatic remodelation, low-density