The C-Reactive Protein Response in Βeta-Hemolytic Streptococcal Infections

Abstract

C-reactive protein (CRP) was introduced into medical practice in the 1990s as a rapid orientation test [1]. Some factors that may influence CRP levels are age, sex, weight, cholesterol level, blood pressure, smoking status [1]. The native CRP is composed of 5 identical subunits bound by non-covalent bonds, placed around a central pore, in the characteristic form of “lectin fold”, as a betafolded sheet [2]. It irreversibly dissociates in inflammation into 5 monomers, the monomeric CRP. The native CRP activates the classical complement pathway and it induces apoptosis and phagocytosis. The monomeric CRP plays an important role in chemotaxis and in directing leukocytes to the inflammatory area, delaying apoptosis. The human CRP gene can be found at 1q23.2 on the long arm of chromosome 1, and, to date, there have been no allelic variations or genetic deficiencies discovered for this gene although some polymorphisms have been identified [1]. CRP synthesis starts in response to pro-inflammatory cytokines, particularly IL6, IL1 and TNF alpha [3].