Inflammation in atherosclerosis and other conditions: a response to danger

In the last few years atherosclerosis has been recognized as an inflammatory process. Assessment of low-grade inflammation with indexes like C-reactive protein (CRP) is considered indicative and potentially predictive for this disease. On the other hand, in a large number of clinical studies, a grade of microinflammation has been found to be associated with numerous other processes that may be directly, indirectly or not related to atherosclerosis. The most interesting finding these studies have yielded is that innate immunity is activated in various, previously unexpected, conditions. This phenomenon is better explained by the application of a recently proposed immune activation mechanism, namely, the 'danger model'. It seems that many conditions related to metabolic or homeostatic stress or to pro-atherosclerotic and pre-diabetic dysfunctions, established atherosclerosis or diabetes, but also other early tissue injury -- like renal, pulmonary or connective tissue -- and several exogenous stimuli, constitute 'danger signals' that induce inflammation which interacts with and complicates the above-mentioned processes. On this basis the complex relationships between CVD risk factors, atherosclerotic process, other tissue injury and inflammation is examined. The practical application of this hypothesis, namely the new clinical use of CRP as a sensitive -- although not specific for atherosclerosis -- index of low-grade inflammatory activity as well as to the atherosclerosis treatment are also discussed.