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Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/47735

**1. Introduction** 

C- reactive protein (CRP) was so named because it was first discovered as a substance in the serum of patients with acute inflammation that reacted with the C- (capsular) polysaccharide of pneumococcus [1].

Discovered by *Tillett* and *Francis* in 1930[2], it was initially thought that CRP might be a pathogenic secretion as it was elevated in people with a variety of illnesses including cancer [3], however, the discovery of hepatic synthesis demonstrated that it is a native protein [4][5][6][7].

CRP is phylogenetically a highly conserved plasma protein, with homolog in vertebrates and many invertebrates that participates in the systemic response to inflammation. Its plasma concentration increases during inflammatory states, a character that has long been employed for clinical purposes. CRP is a pattern recognition molecule, binding to specific molecular configurations that are typically exposed during cell death or found on the surfaces of pathogens. Its rapid increase in synthesis within hours after tissue injury or infection suggests that it contributes to host defense and that it is part of the innate immune response [8].
