Human SAA(Serum Amyloid A) ELISA Kit (E-EL-H2183)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human SAA. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Human SAA and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human SAA, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Human SAA. You can calculate the concentration of Human SAA in the samples by comparing the OD of the samples to the standard curve.

Serum amyloid A (SAA) is a family of small apolipoproteins encoded by multiple genes and synthesized mainly by the liver, circulating in plasma largely bound to high-density lipoprotein. SAA1 and SAA2 encode the acute-phase forms (A-SAA), whereas SAA4 encodes a constitutively expressed form (C-SAA); during inflammation, hepatic production and plasma concentration of the acute-phase members rise sharply, ranking SAA among the major acute-phase proteins alongside C-reactive protein. During the acute-phase response SAA can rise within 24 hours of an inflammatory stimulus, remain elevated for about two to three days and return to normal within roughly seven to ten days. Beyond cholesterol transport and recycling of lipid from damaged tissue, SAA acts as a cytokine-like mediator that engages receptors such as FPR2, TLR2 and SR-BI to mobilize macrophages, neutrophils, lymphocytes and endothelial cells in inflammation, chemotaxis and tissue repair, and persistent elevation during chronic or recurrent inflammation can drive deposition of SAA-derived amyloid fibrils, causing secondary AA amyloidosis. Measurement of SAA is a sensitive marker of the acute-phase response and of ongoing inflammation. Because it rises earlier and more markedly than many acute-phase proteins, it is used to monitor disease activity in rheumatoid arthritis, inflammatory bowel disease, familial Mediterranean fever, viral and bacterial infection and COVID-19, to detect residual inflammation during therapy and to study amyloidogenic complications.