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C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes

BACKGROUND: Chlamydia trachomatis is a prevalent sexually transmitted disease and the leading cause of infectious blindness in developing nations. It was not known if C. trachomatis-infection influenced metabolism of lipoprotein-derived phospholipids. Nor was it known if C. trachomatis-infection alt...

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Autores principales: Hatch, Grant M, McClarty, Grant
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC362871/
https://www.ncbi.nlm.nih.gov/pubmed/15018642
http://dx.doi.org/10.1186/1471-2180-4-8
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author Hatch, Grant M
McClarty, Grant
author_facet Hatch, Grant M
McClarty, Grant
author_sort Hatch, Grant M
collection PubMed
description BACKGROUND: Chlamydia trachomatis is a prevalent sexually transmitted disease and the leading cause of infectious blindness in developing nations. It was not known if C. trachomatis-infection influenced metabolism of lipoprotein-derived phospholipids. Nor was it known if C. trachomatis-infection altered phosphatidylcholine (PC) secretion from hepatocytes. In the current study, low density lipoprotein (LDL)-derived [methyl-(3)H]PC metabolism was examined in L929 cells infected with C. trachomatis to determine if PC derived from LDL could serve as a potential source of PC trafficked to C. trachomatis. In addition, release of endogenously synthesized [methyl-(3)H]PC into the medium was examined in rat liver hepatocytes infected with C. trachomatis to determine if infection altered PC secretion. RESULTS: L929 cells 20 h post infection exhibited a 39% (p < 0.05) reduction in radioactivity in PC but total radioactivity incorporation was unaltered compared to controls. Lysophosphatidyl [methyl-(3)H]choline (LPC) and aqueous [methyl-(3)H]choline metabolites were elevated 3.6-fold (p < 0.05) and 16.5-fold (p < 0.05), respectively, in C. trachomatis-infected cells and this was due to a 51% increase (p < 0.05) in calcium-dependent phospholipase A(2 )activity. Hepatocytes 22 h post infection then incubated for 16 h with [methyl-(3)H]choline showed elevated [methyl-(3)H]PC biosynthesis but [methyl-(3)H]PC secreted into the medium was unaltered compared to controls. In contrast, both cellular and medium lyso [methyl-(3)H]PC were elevated in C. trachomatis-infected cells. CONCLUSION: This study is the first to show that metabolism of LDL-derived PC is accelerated in C. trachomatis infection and to support the notion that LDL-delivered PC may potentially serve as a source of PC trafficked to Chlamydia. In addition, C. trachomatis-infection does not inhibit PC secretion from hepatocytes indicating that the pool of newly synthesized PC destined for lipoprotein secretion may differ from the pool of PC used for C. trachomatis membrane biosynthesis.
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spelling pubmed-3628712004-03-11 C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes Hatch, Grant M McClarty, Grant BMC Microbiol Research Article BACKGROUND: Chlamydia trachomatis is a prevalent sexually transmitted disease and the leading cause of infectious blindness in developing nations. It was not known if C. trachomatis-infection influenced metabolism of lipoprotein-derived phospholipids. Nor was it known if C. trachomatis-infection altered phosphatidylcholine (PC) secretion from hepatocytes. In the current study, low density lipoprotein (LDL)-derived [methyl-(3)H]PC metabolism was examined in L929 cells infected with C. trachomatis to determine if PC derived from LDL could serve as a potential source of PC trafficked to C. trachomatis. In addition, release of endogenously synthesized [methyl-(3)H]PC into the medium was examined in rat liver hepatocytes infected with C. trachomatis to determine if infection altered PC secretion. RESULTS: L929 cells 20 h post infection exhibited a 39% (p < 0.05) reduction in radioactivity in PC but total radioactivity incorporation was unaltered compared to controls. Lysophosphatidyl [methyl-(3)H]choline (LPC) and aqueous [methyl-(3)H]choline metabolites were elevated 3.6-fold (p < 0.05) and 16.5-fold (p < 0.05), respectively, in C. trachomatis-infected cells and this was due to a 51% increase (p < 0.05) in calcium-dependent phospholipase A(2 )activity. Hepatocytes 22 h post infection then incubated for 16 h with [methyl-(3)H]choline showed elevated [methyl-(3)H]PC biosynthesis but [methyl-(3)H]PC secreted into the medium was unaltered compared to controls. In contrast, both cellular and medium lyso [methyl-(3)H]PC were elevated in C. trachomatis-infected cells. CONCLUSION: This study is the first to show that metabolism of LDL-derived PC is accelerated in C. trachomatis infection and to support the notion that LDL-delivered PC may potentially serve as a source of PC trafficked to Chlamydia. In addition, C. trachomatis-infection does not inhibit PC secretion from hepatocytes indicating that the pool of newly synthesized PC destined for lipoprotein secretion may differ from the pool of PC used for C. trachomatis membrane biosynthesis. BioMed Central 2004-02-17 /pmc/articles/PMC362871/ /pubmed/15018642 http://dx.doi.org/10.1186/1471-2180-4-8 Text en Copyright © 2004 Hatch and McClarty; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
spellingShingle Research Article
Hatch, Grant M
McClarty, Grant
C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title_full C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title_fullStr C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title_full_unstemmed C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title_short C. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
title_sort c. trachomatis-infection accelerates metabolism of phosphatidylcholine derived from low density lipoprotein but does not affect phosphatidylcholine secretion from hepatocytes
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC362871/
https://www.ncbi.nlm.nih.gov/pubmed/15018642
http://dx.doi.org/10.1186/1471-2180-4-8
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