Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum amyloid A (SAA) and C-reactive protein (CRP) are acute phase plasma proteins which increases 100- to 1000-fold after inflammatory stimuli. In this study pregnant rabbits were given lipopolysaccharide (LPS) or subjected to laparotomy with fetal injections of LPS at different stages of gestation. Newborn rabbits were given LPS or saline. SAA and CRP mRNA were studied using Northern blot analyses and scanning densitometry. In vitro transcribed RNAs were used as standards for quantitative mRNA analyses. A gradual increase in LPS-induced SAA and CRP mRNA levels was observed during development, but only SAA mRNA induction was seen at gestational day 19. Fetal SAA and CRP mRNA induction was not seen after maternal LPS stimulation. The constitutive level of SAA and CRP mRNA was significantly lower in fetal rabbits than in adults. The control level of SAA mRNA in one-day-old rabbits was higher than the normal adult level, while the neonatal CRP mRNA level was lower. SAA2 seemed to be the major acute phase reactant in both fetal, neonatal and adult rabbits, while relatively more SAA3 was found during early developmental stages. The study demonstrated that CRP and three SAA genes are differentially regulated during development.
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PMID:Developmental regulation of expression of rabbit C-reactive protein and serum amyloid A genes. 865 73

The constellation of changes known as the acute phase response (APR) is a cytokine-driven process initiated by tissue inflammation. The proinflammatory cytokines, TNF, IL-1 and IL-6, are considered to be the primary mediators of the APR. IL-6 and IL-1beta gene-deleted mice (Fattori et al., J. Exp. Med. 1994. 180: 1243-1250; Kopf et al., Nature 1994. 368: 339-342; Fantuzzi et al., J. Immunol. 1996. 157: 291-296, respectively), exhibit impaired APR to turpentine injection but only a slight reduction in plasma acute phase protein levels in response to lipopolysaccharide (LPS). This infers an important role for TNF in the LPS-induced APR, however, in the present study, normal APR to both turpentine and LPS were observed in TNF/LTalpha-deficient mice. A striking absence of elevated major acute phase proteins, SAP and SAA, was observed in mice deficient in TNF/LTalpha and IL-6, suggesting that TNF-alpha or LTalpha do indeed exert important nonredundant synergism in the IL-1/IL-6 primary response. The regulation of other parameters typically altered in an APR, body weight, blood glucose and haptoglobin, was normal in LPS-dosed TNF/LTalpha-deficient and wild-type mice. The observed transcriptional response for SAA and SAP in these TNF/LTalpha/IL-6-deficient mice, in lieu of elevated plasma levels, suggests that SAA and SAP expression is possibly posttranscriptionally regulated.
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PMID:The combined inactivation of tumor necrosis factor and interleukin-6 prevents induction of the major acute phase proteins by endotoxin. 986 49

Serum amyloid A (A-SAA) has previously been reported to be an acute-phase protein in salmonids. Hepatocytes represent a major source of A-SAA in salmonids, but nothing is known about hepatocyte SAA synthesis in fish. In the present work, the expression of A-SAA transcripts in primary cultures of Atlantic salmon hepatocytes in response to macrophage derived cytokines, human recombinant cytokines and bacterial lipopolysaccharide (LPS) was studied by Northern blot analysis. The macrophage supernatants were prepared by stimulating Atlantic salmon head kidney macrophages with LPS, yeast glucan or a leukocyte derived macrophage activating factor (MAF). The supernatants from glucan- or MAF-stimulated macrophages had no effect on A-SAA expression of the hepatocytes, while supernatants from LPS-stimulated macrophages gave about a 2-fold increase in expression. The combination of either glucan and MAF, or LPS and MAF were more effective and these supernatants gave a 3.4- and 5.2-fold increase in A-SAA expression, respectively. The hepatocytes were also treated with the human recombinant cytokines TNFalpha, IL-1beta and IL-6, alone or in combination. The A-SAA response to each of them alone was modest, but TNFalpha and IL-6 or IL-1beta and IL-6 in combination gave a higher response than each cytokine alone. These data suggest that the expression of A-SAA by hepatocytes from Atlantic salmon is induced by cytokine-like molecules. Interestingly, hepatocytes treated directly with LPS gave a more than 10-fold increase in SAA mRNA expression, but it is not known if this is a direct effect of LPS on the hepatocytes or if it is mediated by other contaminating cell types.
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PMID:Serum amyloid A transcription in Atlantic salmon (Salmo salar L.) hepatocytes is enhanced by stimulation with macrophage factors, recombinant human IL-1 beta, IL-6 and TNF alpha or bacterial lipopolysaccharide. 1083 90

Serum amyloid A (SAA) proteins are acute-phase apolipoproteins that are associated with high-density lipoprotein (HDL) particles: SAA proteins are precursors to secondary amyloid fibril proteins and under certain conditions of chronic or recurrent inflammation these proteins are deposited as amyloid fibrils. Of two isotypes found in mouse, SAA1.1 and SAA2.1, only SAA1.1 is deposited into amyloid. The CE/J mouse is unique, in that the only isoform identified is a hybrid between SAA1.1 and SAA2.1 and the mouse does not show amyloid deposition. In the rat, a deletion in the SAA1/SAA2 gene is associated with the absence of protein in the plasma and subsequently no amyloid deposition is detected. We have generated adenoviral vectors to study the expression of SAA proteins on HDL metabolism and amyloid formation. Injection of SAA viruses into rats resulted in expression of the mouse SAA proteins in the plasma with specific association of the SAA with HDL particles. The induction of SAA proteins was comparable to that seen in mice presented with the inflammatory agent, bacterial lipopolysaccharide (LPS). Adenoviral induced SAA levels were maintained for up to several weeks without a significant decrease in SAA expression. Injection of rats with the mouse SAA1.1 adenoviral vector, followed by amyloid enhancing factor (AEF) and silver nitrate resulted in the deposition of amyloid fibrils in the spleen. After 2 weeks, amyloid could be detected in other tissues, including the heart, liver, kidneys and lungs. When animals were injected with null or the SAA2.2 virus no amyloid was detected. These studies demonstrate that the inability of the rat to develop AA amyloid is due to the lack of synthesizing an amyloidogenic SAA protein. Furthermore, the expression of the adenoviral SAA protein from the liver and incorporation onto HDL particles further supports the hypothesis that AA amyloid is derived from circulating SAA protein. The ease of use of the adenoviral vectors and the rat provide an excellent model to study the function of SAA proteins.
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PMID:Amyloid formation in the rat: adenoviral expression of mouse serum amyloid A proteins. 1084 3

In most mammalian species, serum amyloid A isoform 3 (SAA3) appears to be the predominant SAA isoform expressed extrahepatically. However, human SAA3 gene expression has not been detected previously and, therefore, this gene was referred to as a pseudogene. We report for the first time the transcriptional expression of human SAA3. Human SAA3 gene expression was detected by RT-PCR after stimulation of mammary gland epithelial cells with either prolactin (PRL) or lipopolysaccharide (LPS). The full-length 655bp cDNA sequence for this mammary-associated serum amyloid A3 (M-SAA3) was obtained using 5' and 3' rapid amplification of cDNA ends (RACE). The human M-SAA3 transcript would conceptually translate into a 42 residue mature protein, which is smaller than other mammalian SAA3 isoforms that are typically 104-113 amino acids in length. This study defines the cDNA sequence for human SAA3 and also demonstrates the upregulation of M-SAA3 expression in response to the lactational hormone PRL or to an acute phase stimulant such as LPS.
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PMID:Induction of human mammary-associated serum amyloid A3 expression by prolactin or lipopolysaccharide. 1258 16

Mastitis is one of the most costly diseases of agriculturally important animals and is a common problem for lactating cows. Current methods used to detect clinical and especially subclinical mastitis are either inadequate or problematic. Pathogens such as the gram-positive bacterium Staphylococcus aureus or the gram-negative bacterium Escherichia coli typically cause mastitis. E. coli induces clinical mastitis, whereas, S. aureus causes a subclinical, chronic infection of the mammary gland. In this study we report the differential expression and secretion of mammary-derived serum amyloid A3 (SAA3) by bovine mammary epithelial cells following stimulation with the S. aureus cell wall component, lipotechoic acid (LTA). Two-dimensional immunoblot analyses confirmed that bovine SAA3 is the predominant SAA isoform produced by LTA stimulated mammary epithelial cells. Our previous study showed that bovine SAA3 is also differentially expressed in response to the gram-negative bacterial endotoxin lipopolysaccharide. Collectively, these data indicate that the local production of SAA3 by mammary epithelial cells in response to either gram-positive or gram-negative bacterial components may provide a sensitive indicator for early detection and treatment of mastitis in vivo, minimizing chronic cases of infection, the spread of mastitis to other animals, and economic losses.
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PMID:Staphylococcus aureus lipotechoic acid induces differential expression of bovine serum amyloid A3 (SAA3) by mammary epithelial cells: Implications for early diagnosis of mastitis. 1613 67

Acute serum amyloid A (A-SAA) has been considered a major acute-phase reactant and an effector of innate immunity in all vertebrates. The work presented here shows that the expression of A-SAA is strongly induced in a wide variety of immune-relevant tissues in rainbow trout, either naturally infected with Flavobacterium psychrophilum or challenged with lipopolysaccharide (LPS) or CpG oligonucleotides (CpG ODN). Nevertheless, A-SAA was undetectable by Western blot either in the plasma or in high-density lipoprotein (HDL) of infected or challenged fish, using either an anti-mouse SAA1 IgG or an anti-trout A-SAA peptide serum, which recognise both the intact recombinant trout A-SAA and fragments derived from it. However, the anti-peptide serum was the immunoreactive in all primary defence barriers and in mononuclear cells of head kidney, spleen and liver. These findings reveal that, unlike mammalian SAA, trout A-SAA does not increase significantly in the plasma of diseased fish, suggesting it is more likely to be involved in local defence.
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PMID:Serum amyloid A: a typical acute-phase reactant in rainbow trout? 1844 Jun 34

A minimally invasive liver biopsy technique was tested for its applicability to study the hepatic acute phase response (APR) in dairy cows with Escherichia coli lipopolysaccharide (LPS)-induced mastitis. The hepatic mRNA expression profiles of the inflammatory cytokines, tumor necrosis factor alpha (TNF-alpha), IL-1beta, IL-6, and IL-10, and the acute phase proteins serum amyloid A isoform 3 (SAA3), haptoglobin (Hp), and alpha(1)-acid glycoprotein (AGP) were determined by real-time reverse transcription-PCR. Fourteen primiparous cows in mid lactation were challenged with 200 microg of LPS (n = 8) or NaCl solution (n = 6) in 1 front quarter. Six repeated liver biopsies were collected at -22, 3, 6, 9, 12, and 48 h relative to LPS challenge in 4 LPS-infused cows and 3 NaCl-infused cows. The remaining cows had 3 liver biopsies taken at -22, 9, and 48 h. Production data and clinical signs were recorded and white blood cell counts and somatic cell counts (SCC) were analyzed to investigate the effect of repeated liver biopsies and verify the LPS model. Plasma concentrations of TNF-alpha, SAA3, Hp, and AGP were determined for comparison with the liver expression data. Repeated liver biopsies had no effects on the production data, clinical signs, or APR of dairy cows. Compared with the NaCl-infused cows the LPS-infused cows responded to the LPS treatment by increased body temperature (38.6 +/- 0.1 vs. 39.4 +/- 0.1 degrees C), short-term leukopenia followed by leukocytosis (6.44 +/- 0.4 vs. 5.69 +/- 0.3 x 10(6) cells/mL), an increased SCC (log(10) 2.1 +/- 0.1 vs. log(10) 2.8 +/- 0.1 x 10(3) cells/mL), heart rate (76 +/- 1 vs. 93 +/- 1 beats/min), and respiratory rate (32 +/- 2 vs. 36 +/- 1 breaths/min) in the acute phase of the disease. The LPS treatment upregulated the hepatic expression of TNF-alpha (103 +/- 24 vs. 255 +/- 18 units), IL-1beta (37 +/- 23 vs. 296 +/- 18 units), IL-6 (8 +/- 17 vs. 122 +/- 12 units), and IL-10 (130 +/- 66 vs. 541 +/- 50 units), and SAA3 (64 +/- 36 vs. 128 +/- 28 units) and Hp (9 +/- 82 vs. 762 +/- 65 units) reaching maximum levels at 3 to 6 h and 9 to 12 h postinfusion, respectively. Plasma concentrations of TNF-alpha (nondetectable vs. 1.9 +/- 0.3 ng/mL), SAA (19.8 +/- 19.4 vs. 149.7 +/- 15.5 microg/mL) and Hp (71.4 +/- 143.7 vs. 1,013.8 +/- 111.5 microg/mL) were elevated in the LPS-infused cows at 4 to 12 h, 8 to 120 h, and 24 to 120 h postinfusion, respectively. The hepatic expression of AGP and the AGP plasma concentration remained unaltered in LPS-induced cows. In conclusion, a minimally invasive liver biopsy technique can be used for studying the hepatic APR in diseased cattle. Lipopolysaccharide-induced mastitis resulted in a time-dependent production of inflammatory cytokines and SAA and Hp in the liver of dairy cows.
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PMID:Cytokine and acute phase protein gene expression in repeated liver biopsies of dairy cows with a lipopolysaccharide-induced mastitis. 1923 85

Preterm labor (PTL) is frequently associated with inflammation. We hypothesized that biomarkers during pregnancy can identify pregnancies most at risk for development of PTL. An inflammation-induced mouse model of PTL was used. Surface-enhanced laser desorption/ionization time-of-flight mass spectrometry was used to analyze and compare the plasma protein (PP) profile between CD-1 mice injected intrauterine with either lipopolysaccharide (LPS) or PBS on d 14.5 of gestation. The median differences of normalized PP peaks between the two groups were determined using the Mann-Whitney U test and the false discovery rate. In a second series of experiments, both groups of mice were injected with a lower dose of LPS. A total of 1665 peaks were detected. Thirty peaks were highly differentially expressed (p < 0.0001) between the groups. Two 11 kDa protein peaks were identified by MALDI-TOF/TOF-MS and confirmed to be mouse serum amyloid A (SAA) 1 and 2. Plasma SAA2 levels were increased in LPS-treated animals compared with controls and in LPS-treated animals that delivered preterm vs. those that delivered at term. SAA2 has the potential to be a plasma biomarker that can identify pregnancies at risk for development of PTL.
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PMID:Plasma biomarkers in a mouse model of preterm labor. 1928 48

Atherosclerosis is linked to inflammation. HDL protects against atherosclerotic cardiovascular disease, mainly by mediating cholesterol efflux and reverse cholesterol transport (RCT). The present study aimed to test the impact of acute inflammation as well as selected acute phase proteins on RCT with a macrophage-to-feces in vivo RCT assay using intraperitoneal administration of [(3)H]cholesterol-labeled macrophage foam cells. In patients with acute sepsis, cholesterol efflux toward plasma and HDL were significantly decreased (P < 0.001). In mice, acute inflammation (75 microg/mouse lipopolysaccharide) decreased [(3)H]cholesterol appearance in plasma (P < 0.05) and tracer excretion into feces both within bile acids (-84%) and neutral sterols (-79%, each P < 0.001). In the absence of systemic inflammation, overexpression of serum amyloid A (SAA, adenovirus) reduced overall RCT (P < 0.05), whereas secretory phospholipase A(2) (sPLA(2), transgenic mice) had no effect. Myeloperoxidase injection reduced tracer appearance in plasma (P < 0.05) as well as RCT (-36%, P < 0.05). Hepatic expression of bile acid synthesis genes (P < 0.01) and transporters mediating biliary sterol excretion (P < 0.01) was decreased by inflammation. In conclusion, our data demonstrate that acute inflammation impairs cholesterol efflux in patients and macrophage-to-feces RCT in vivo in mice. Myeloperoxidase and SAA contribute to a certain extent to reduced RCT during inflammation but not sPLA(2). However, reduced bile acid formation and decreased biliary sterol excretion might represent major contributing factors to decreased RCT in inflammation.
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PMID:Myeloperoxidase and serum amyloid A contribute to impaired in vivo reverse cholesterol transport during the acute phase response but not group IIA secretory phospholipase A(2). 2007 95


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