RACTIVITY : Human
SENSITIVITY : <1.1 ng/mL
ASSAY RANGE : 5 ng/mL-16 μg/mL
REAGENTS PROVIDED : SAA MICROTITER PLATE
SAA CONJUGATE
SAA STANDARD
CALIBRATOR DILUENT I
SAA QUALITY CONTROL SAMPLE I
SAA QUALITY CONTROL SAMPLE II
WASH BUFFER (20X)
SUBSTRATE A
SUBSTRATE B
STOP SOLUTION
INTENDED USE
This Human SAA ELISA Kit is to be used
for the in vitro quantitative determination of human serum amyloid A (SAA)
concentrations in serum, plasma, and other biological fluids. This kit is
intended FOR LABORTORY RESEARCH USE ONLY and is not for use in diagnostic or
therapeutic procedures.
INTRODUCTION
Serum Amyloid A (SAA) is an acute-phase
protein. During acute events, the rise
in SAAlevels is
the most rapid and intense increase of all acute phase proteins. Cytokines such as IL-1, IL-6, and TNF are
considered mediators of SAAprotein
synthesis. They stimulate hepatocytes in
the liver to produce and release SAAinto the bloodstream. When elevated above normal levels SAAis
almost exclusively bound to High Density Lipoproteins (HDL), causing SAAto
behave like an apolipoprotein - a protein moiety occurring in plasma lipoprotiens. SAAcirculates at
trace levels (1-7 µg/mL) during normal conditions; however 4-6 hours after
inflammatory stimulus, SAAlevels can
increase by as much as 1000 fold to remarkably elevated levels (500-1000
µg/mL), thus making SAAa
sensitive marker. 1,2
Structural analysis revealed this 104
amino acid (a.a.)
polypeptide in its native state has a molecular mass of 12-14 kDa. Serum amyloid A is the serum precursor of
amyloid A (AA) protein (8.5 kDa), which is formed when the first 76
amino acids of amyloid A protein are cleaved.
The human SAAprotein is
polymorphic being made up of a family of several related proteins (SAA1 to
SAA4). SAA genes are located on
chromosome 11p.1 SAA1 and SAA2 are
similar genes, which differ by 7 amino acids or more, and encode acute-phase
SAAs. SAA3 appears to be a pseudogene
and is substantially different from the others.
SAA4 does not vary significantly during the acute phase response and is
an isoform that is present on HDL during homeostasis.3,4 Each of the acute phase proteins have a
unique function in modulating host immune responses but the role of SAA remains
unclear. It is known that HDL inhibits
SAA's function. This suggests that SAA
needs to be released from HDL complexes in order to become active.5 It was reported that SAA may have an
important pro-inflammatory and immunostimulating role
by recruiting neutrophils, monocytes, and T-lymphocytes into inflammatory
lesions.5,6 As a result of SAA's
association with HDL, a role in cholesterol metabolism has been proposed. SAA, after dissociation from HDL, may play a
role in cholesterol transport at local tissues sites during inflammation by
binding cholesterol.2,7
High levels of SAAcan be
seen in patients with acute and chronic inflammation. Secondary amyloidosis may
develop as a result prolonged or repeated inflammatory conditions in which SAAlevels
remain elevated. This progressive, fatal
condition is characterized by a gradual loss of organ function, in which
fibrils are deposited in peripheral tissues and major organs. The fibrils are caused by the incomplete
degradation of SAAin
which the AA fragment (8.5 kDa) from the original SAAprotein has
been enzymatically cleaved. Measuring SAAlevels in
these patients may be a useful indicator of degree of inflammation and response
to therapy. Inflammatory disorders such
as rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, familial mediterranean
fever, progressive sclerosis as well as chronic infections such as tuberculosis
and osteomyelitis are predisposed to developing amyloidosis.8,9 Measuring SAA levels is also significant in
determining pulmonary inflammation in patients with cystic fibrosis,10
diagnosing and predicting renal allograft rejection,11 determining
anti-microbial therapy response in urinary tract infections,12 opportunistic
infections in AIDS,13 inflammation in acute viral infections,14 biocompatiblility of
hemodialysis,15 tissue damage in post-acute myocardial infarction, 17 and the
outcome in severe unstable angina.16 Also, a differential diagnosis of
inflammatory disease may be employed by measuring SAA levels. Acute viral infections may be distinguished
from bacterial infections by determining SAA levels.14-17 It may be useful to
confirm diagnosis of acute viral diseases if SAA is assayed at the same time as
C-reactive protein, which is a useful inflammatory marker for bacterial
infections and does not rise during viral disease.16
This SAA ELISA is a 2.5-hour solid phase
immunoassay readily applicable to measure SAA in serum, plasma, and other
biological fluids in the range of 0 to 16mg/mL.
It showed no cross reactivity with other cytokines tested. This SAA ELISA is expected to be effectively
used for further investigations into the relationship between SAA and the
various conditions mentioned.
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