Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the interrelations between the changes of acute phase proteins and those of serum lipoproteins in acute infections we measured the concentrations of different lipoproteins, serum amyloid-A protein and C-reactive protein and activities of lipoprotein lipase and hepatic lipase during acute and convalescence phase and after complete recovery in 64 patients with infectious diseases (30 with viral infection and 34 with bacterial infection). The maximal decrements of both low density lipoprotein and high density lipoprotein cholesterol correlated significantly with the acute phase levels of C-reactive protein and serum amyloid-A protein. The acute phase concentration of very low density lipoprotein triglyceride correlated inversely to C-reactive protein level (r = -0.31, P less than 0.05) but not to serum amyloid-A protein level. Regression analysis showed that the concentration of C-reactive protein was a significant predictor of very low density lipoprotein triglyceride level in the acute phase of infection but not during convalescence. These results and the previous findings that C-reactive protein binds to low and very low density lipoproteins and that serum amyloid-A protein is associated with high density lipoprotein give credence to the view that C-reactive protein and serum amyloid-A protein interfere with the metabolism of serum lipoproteins during acute phase of infection.
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PMID:Lipoproteins and acute phase response during acute infection. Interrelationships between C-reactive protein and serum amyloid-A protein and lipoproteins. 212 35

To study the effects of acute infections on serum lipids and lipoproteins we measured the concentration and composition of different lipoproteins, apoproteins A-I, A-II, and B, and the activities of plasma postheparin lipolytic enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL) during acute and convalescence phase and after complete recovery in 72 infectious patients (33 with viral infection and 39 with bacterial infection). The mass concentrations of both low density lipoprotein (LDL) (P less than .001) and high density lipoprotein (HDL)2 (P less than .002) were reduced during acute infections due to the lowering of their cholesterol, phospholipid, and protein contents. The reduction of LDL cholesterol was maximal at the acute stage of infection (change -15%, P less than .001) while the reduction of HDL2 cholesterol was maximal during the convalescence (change -35%, P less than .001). During acute infections LDL became triglyceride-enriched (11.8 v 8.6%, P less than .0001) but cholesterol-poor (36.6 v 39.3%, P less than .0001). The ratio of HDL cholesterol/LDL cholesterol was significantly reduced during the convalescence (0.42 +/- 0.15 v 0.53 +/- 0.19, P less than .0001). The concentrations of apo A-I and apo A-II were decreased during acute infections (changes -22%, P less than .001, and -16%, P less than .001, respectively). The very low density lipoprotein (VLDL) was 18% higher during the convalescence period than after the recovery due to the elevations of VLDL triglycerides, cholesterol, and phospholipids. The activity of LPL was reduced both in the acute and convalescence phase, whereas that of HL was reduced only in the acute phase of infections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum lipoprotein pattern induced by acute infections. 341 23

Abnormalities in serum lipids, including hypertriglyceridemia, are common during infectious disorders. However, the lipoprotein pattern during infections, particularly in children, has been investigated to only a limited extent. We have monitored alterations in serum lipoproteins in eight children with a severe bacterial infection (meningitis) by a quantitating method measuring cholesterol and triglycerides in each major class. The levels of triglycerides in serum and in low-density lipoproteins were markedly elevated during the infection, whereas the amount of cholesterol in high-density lipoproteins was decreased. The cholesterol to triglyceride ratio was decreased in low-, as well as in high-density lipoproteins. These lipoprotein abnormalities may, at least in part, be explained by a depressed lipolytic activity of lipoprotein lipase, the key enzyme for removal of triglycerides in man. Serum triglycerides and the levels of cholesterol in high-density lipoproteins, as well as the ratio between these parameters, may be used as indicators of inflammatory activity.
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PMID:Lipoprotein alterations in children with bacterial meningitis. 837 22

Inflammation resulting from bacterial infection of the respiratory mucosal surface during pneumonia and cystic fibrosis contributes to pathology. A major consequence of the inflammatory response is recruitment of polymorphonuclear cells (PMNs) to the infected site. To reach the airway, PMNs must travel through several cellular and extracellular barriers, via the actions of multiple cytokines, chemokines, and adhesion molecules. Using a model of polarized lung epithelial cells (A549 or Calu-3) grown on Transwell filters and human PMNs, we have shown that Pseudomonas aeruginosa induces PMN migration across lung epithelial barriers. The process is mediated by epithelial production of the eicosanoid hepoxilin A(3) (HXA(3)) in response to P. aeruginosa infection. HXA(3) is a PMN chemoattractant metabolized from arachidonic acid (AA). Given that release of AA is believed to be the rate-limiting step in generating eicosanoids, we investigated whether P. aeruginosa infection of lung epithelial cells resulted in an increase in free AA. P. aeruginosa infection of A549 or Calu-3 monolayers resulted in a significant increase in [(3)H]AA released from prelabeled lung epithelial cells. This was partially inhibited by PLA(2) inhibitors ONO-RS-082 and ACA as well as an inhibitor of diacylglycerol lipase. Both PLA(2) inhibitors dramatically reduced P. aeruginosa-induced PMN transmigration, whereas the diacylglycerol lipase inhibitor had no effect. In addition, we observed that P. aeruginosa infection caused an increase in the phosphorylation of cytosolic PLA(2) (cPLA(2)), suggesting a mechanism whereby P. aeruginosa activates cPLA(2) generating free AA that may be converted to HXA(3), which is required for mediating PMN transmigration.
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PMID:Involvement of phospholipase A2 in Pseudomonas aeruginosa-mediated PMN transepithelial migration. 1627 74

Antimicrobial peptides (AMPs) are effective against a wide range of microbes, but still no research results have reported their use in duck disease therapy. Riemerella anatipestifer (RA) is a Gram-negative bacterium which infects ducks and causes very significant economic losses. The minimum inhibitory concentrations (MICs) of epinecidin-1 for the tested RA strains ranged 6.25-50microg/ml, those of the SALF55-76 cyclic peptide ranged 12.5-25microg/ml, those of the SALF55-76 linear peptide ranged 6.25-25microg/ml, those of hepcidin TH1-5 ranged 25-400microg/ml, and those of hepcidin TH2-3 ranged 100-400microg/ml. The antimicrobial activities of these peptides were confirmed by transmission electron microscopy which showed that RA disruption of the outer membrane brought about cell death. In addition, pretreatment, co-treatment, and post-treatment with peptides were all effective in promoting a significant decrease in duck mortality and decreasing the number of infectious bacteria. A quantitative RT-PCR was performed to survey levels of gene expressions of Mn superoxide dismutase in the brain, lipoprotein lipase in the liver, and H5 histone in the spleen induced in response to bacterial infection and an injection of the AMPs in experiments with the duck, Cairina moschata. Our results indicated that the rescue of ducks by the peptides and the behavior of the peptides, which was like an enhancer in immunology, may involve regulation of the expressions of these genes. Collectively, these peptides reduced the mortality in ducks during bacterial challenge, suggesting that AMPs have the potential to serve as therapeutic drugs for use against bacterial infectious diseases in ducks.
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PMID:Antimicrobial peptides of an anti-lipopolysaccharide factor, epinecidin-1, and hepcidin reduce the lethality of Riemerella anatipestifer sepsis in ducks. 2013 98