cholera/triglyceride

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A Putative Acetylation System in Vibrio cholerae Modulates Virulence in Arthropod Hosts.

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Acetylation is a broadly conserved mechanism of covalently modifying the proteome to precisely control protein activity. In bacteria, central metabolic enzymes and regulatory proteins, including those involved in virulence, can be targeted for acetylation. In this study, we directly link a putative

Herman Award Lecture, 1995: infection-induced malnutrition--from cholera to cytokines.

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Infection-induced malnutrition, the most common form of cytokine-induced malnutrition, results from the actions of proinflammatory cytokines, ie, tumor necrosis factor (TNF) and interleukins 1,6, and 8 (IL-1, IL-6, and IL-8). During acute generalized infections, these cytokines initiate the

Triglyceride-rich lipoprotein lipolysis increases aggregation of endothelial cell membrane microdomains and produces reactive oxygen species.

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Triglyceride-rich lipoprotein (TGRL) lipolysis may provide a proinflammatory stimulus to endothelium. Detergent-resistant plasma membrane microdomains (lipid rafts) have a number of functions in endothelial cell inflammation. The mechanisms of TGRL lipolysis-induced endothelial cell injury were

Malabsorption of long-chain fatty acid in cholera toxin-induced secretory diarrhea.

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The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly

Isoproterenol, TNFalpha, and insulin downregulate adipose triglyceride lipase in 3T3-L1 adipocytes.

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Recently, adipose triglyceride lipase (ATGL, also called desnutrin and calcium-independent phospholipase A2 [iPLA(2)] zeta) was isolated as a novel adipose-expressed triglyceride lipase which is downregulated in obesity and may contribute to obesity-associated metabolic disorders such as

Anti-diabetic effects of CTB-APSL fusion protein in type 2 diabetic mice.

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To determine whether cholera toxin B subunit and active peptide from shark liver (CTB-APSL) fusion protein plays a role in treatment of type 2 diabetic mice, the CTB-APSL gene was cloned and expressed in silkworm (Bombyx mori) baculovirus expression vector system (BEVS), then the fusion protein was

Effect of cyclic AMP on lipid accumulation and metabolism in human atherosclerotic aortic cells.

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The effects of dibutyryl cyclic AMP (db cAMP), cholera toxin, and methylisobutylxanthine on the content and metabolism of lipids in smooth muscle cells cultured from normal and atherosclerotic intima of human aorta have been studied. Db cAMP (0.1 mM) decreased the levels of triglycerides and

Agents that increase cellular cyclic AMP inhibit proliferative activity and decrease lipid content in cells cultured from atherosclerotic human aorta.

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Cholera toxin, methylisobutylxanthine and prostacyclin (PGI2) analogues as well as dibutyryl cyclic AMP inhibit by 2-7-fold 3H-thymidine uptake into intimal cells isolated from atherosclerotic human aorta in primary culture. These agents also decrease cholesteryl ester and triglyceride levels and do

[Decrease in the lipid content of human atherosclerotic aorta cells as affected by compounds increasing the intracellular level of cyclic AMP].

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A study was made of the effect of cholera toxin, an adenylate cyclase activator, and methylisobutylxanthine, an inhibitor of cAMP phosphodiesterase, on the content of main class lipids in intimal cells isolated from unaffected and atherosclerotic areas of the human aorta in primary culture. Both the

Primary culture of human aortic intima cells as a model for testing antiatherosclerotic drugs. Effects of cyclic AMP, prostaglandins, calcium antagonists, antioxidants, and lipid-lowering agents.

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Smooth muscle cells isolated from atherosclerotic lesions of human aorta retain in primary culture their intrinsic in vivo characteristics: namely, enhanced proliferative activity and high lipid levels. We have tested the effect of different compounds on [3H]thymidine uptake and on the levels of

On the role of cyclic nucleotides in the pathogenesis of human atherosclerosis.

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The content of cAMP and cGMP was measured in the intima and media of unaffected and atherosclerotic areas of human aorta in a short-term organ and cell cultures. In an organ culture the cAMP content in fatty streaks and atherosclerotic plaques is significantly (2 to 7-fold) lower than in unaffected

Targeting the signaling pathway of acylation stimulating protein.

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Acylation stimulating protein (ASP; C3adesArg) stimulates triglyceride synthesis (TGS) and glucose transport in preadipocytes/adipocytes through C5L2, a G-protein-coupled receptor. Here, ASP signaling is compared with insulin in 3T3-L1 cells. ASP stimulation is not Galpha(s) or Galpha(i) mediated

Oral immunization with a novel lipid-based adjuvant protects against genital Chlamydia infection.

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Oral immunization is attractive as a delivery route because it is needle-free and useful for rapid mass vaccination programs to target pandemics or bioterrorism. This potential has not been realized for human vaccination, due to the requirement of large antigen doses and toxic (to humans) adjuvants

Lipid synthesis in isolated intestinal cells.

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Since the small intestine contributes significantly to serum cholesterol and very low density lipoprotein levels, acute regulation of lipid synthesis was investigated in isolated rat intestinal cells incubated in Krebs-Ringer bicarbonate buffer with 5 mM glucose and [14c]acetate or 3H2O.

[Point mutation of the Virbrio cholerae O139 cef (CHO cell elongating factor) gene alters the substrate specificity of its product].

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Sequencing of the cef (CHO cell elongating factor) of Vibrio cholerae serogroup O139 revealed one nucleotide substitution (C for T in position 2015) in comparison with classical V. cholerae O1 and two substitutions (AC for GT in positions 2014-2015) in comparison with V. cholerae O1 E1 Tor. A

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