Description

SAA proteins comprise a family of small (12-14 kDa. 104-112 amino acid residues), differentially expressed proteins that are highly conserved among vertebrates. SAA proteins are involved in the acute phase responses, these are the immediately early host respones to inflammation. SAAs have been implicated several disease states including rheumatoid arthritis, atherosclerosis, A amyloidosis and coronary artery disease.

Liver is the major site of SAA synthesis, although extrahepatic expression also has been reported. In humans, four SAA genes and three protein products have been identified: human SAA1 and SAA2 are designated the acute phase SAA (A-SAA) isoforms, while SAA4 is constitutively expressed and SAA3 is a pseudogene.

SAA is released into bloodstream where it immediately binds the HDL particles. There are a number of important homeostatic functions associated with the circulating SAA-HDL complex-es, these functions are categorized as immune modulation, lipid transport and anti-inflammatory. It is an acute phase marker responds rapidly, similar to CRP, levels of SAA increase within hours after inflammatory stimulus, and the magnitude of increase may be greater than CRP. It has been suggested that SAA levels correlate better with disease activity in early inflammatory joint disease than do ESR and CRP.