Biosynthesis of phosphatidylcholine in bacteria

Sohlenkamp, Christian; López‐Lara, Isabel M.; Geiger, Otto

doi:10.1016/s0163-7827(02)00050-4

Cited by 275 publications

(297 citation statements)

References 188 publications

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“…Thus, it is plausible that the carriage of toxin-producing C. difficile may potentially induce gut microbiota deficient in phosphatidylcholine-containing bacteria. This idea was confirmed by examining the composition of bacterial groups known to contain phosphatidylcholine (Sohlenkamp et al, 2003) and by showing statistically significant differences (P-value o0.05) between their average taxon abundance in patients with toxin + C. difficile (∼0.11% of the total 16S rRNA sequences) and in patients with toxin − C. difficile (∼1.46%) or in non-colonised controls (∼7.56%). N-acetylputrescine, along with other acetyl polyamines, results from the breakdown of amino acids and their further metabolism (Chae et al, 2012).…”

Section: Overall Impact Of Cdad In Gut Microbial Metabolismmentioning

confidence: 77%

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Clostridium difficile heterogeneously impacts intestinal community architecture but drives stable metabolome responses

et al. 2015

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Clostridium difficile-associated diarrhoea (CDAD) is caused by C. difficile toxins A and B and represents a serious emerging health problem. Yet, its progression and functional consequences are unclear. We hypothesised that C. difficile can drive major measurable metabolic changes in the gut microbiota and that a relationship with the production or absence of toxins may be established. We tested this hypothesis by performing metabolic profiling on the gut microbiota of patients with C. difficile that produced (n = 6) or did not produce (n = 4) toxins and on non-colonised control patients (n = 6), all of whom were experiencing diarrhoea. We report a statistically significant separation (P-value o0.05) among the three groups, regardless of patient characteristics, duration of the disease, antibiotic therapy and medical history. This classification is associated with differences in the production of distinct molecules with presumptive global importance in the gut environment, disease progression and inflammation. Moreover, although severe impaired metabolite production and biological deficits were associated with the carriage of C. difficile that did not produce toxins, only previously unrecognised selective features, namely, choline-and acetylputrescine-deficient gut environments, characterised the carriage of toxin-producing C. difficile. Additional results showed that the changes induced by C. difficile become marked at the highest level of the functional hierarchy, namely the metabolic activity exemplified by the gut microbial metabolome regardless of heterogeneities that commonly appear below the functional level (gut bacterial composition). We discuss possible explanations for this effect and suggest that the changes imposed by CDAD are much more defined and predictable than previously thought.

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Section: Overall Impact Of Cdad In Gut Microbial Metabolismmentioning

confidence: 77%

“…Phosphatidylcholine is a membrane-forming phospholipid that is present in approximately 10% of all bacteria (Sohlenkamp et al, 2003). Thus, it is plausible that the carriage of toxin-producing C. difficile may potentially induce gut microbiota deficient in phosphatidylcholine-containing bacteria.…”

Section: Overall Impact Of Cdad In Gut Microbial Metabolismmentioning

confidence: 99%

Clostridium difficile heterogeneously impacts intestinal community architecture but drives stable metabolome responses

et al. 2015

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“…However, different classes of bacteria have developed very complex sets of chemically diverse lipid components to complement this basic inventory. The lipids of mycobacteria are a leading example but other clinically important pathogenic bacteria such as Helicobacter pylori are likely be investigated with enhanced scrutiny in this respect [34].…”

Section: Pathogenic Bacteria (Mycobacteria Salmonella)mentioning

confidence: 99%

Lipidomics of host–pathogen interactions

Wenk

2006

FEBS Letters

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The cell biology of intracellular pathogens (viruses, bacteria, eukaryotic parasites) has provided us with molecular information of host-pathogen interactions. As a result it is becoming increasingly evident that lipids play important roles at various stages of host-pathogen interactions. They act in first line recognition and host cell signaling during pathogen docking, invasion and intracellular trafficking. Lipid metabolism is a housekeeping function in energy homeostasis and biomembrane synthesis during pathogen replication and persistence. Lipids of enormous chemical diversity play roles as immunomodulatory factors. Thus, novel biochemical analytics in combination with cell and molecular biology are a promising recipe for dissecting the roles of lipids in host-pathogen interactions.

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“…It has been estimated that only 10% of bacteria contain PC as a membrane phospholipid; in these prokaryotes, PC is synthesized through methylation of PE or via a novel enzymatic activity, PC synthase, which condenses choline directly with CDP-DAG to form PC in one step (9). Even though the Kennedy pathway is not functional in bacteria, some of its enzymatic components are present and used for the phosphocholine modification of cell surface components.…”

Section: Introductionmentioning

confidence: 99%

“…Even though the Kennedy pathway is not functional in bacteria, some of its enzymatic components are present and used for the phosphocholine modification of cell surface components. For example, phosphocholine is likely activated to CDP-choline and then transferred to cell surface polysaccharides such as lipopolysaccharide (LPS) and (lipo)teichoic acids (9).…”

Section: Introductionmentioning

confidence: 99%

The Kennedy pathway—De novo synthesis of phosphatidylethanolamine and phosphatidylcholine

2010

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SummaryThe glycerophospholipids phosphatidylcholine (PC) and phosphatidylethanolamine (PE) account for greater than 50% of the total phospholipid species in eukaryotic membranes and thus play major roles in the structure and function of those membranes. In most eukaryotic cells, PC and PE are synthesized by an aminoalcoholphosphotransferase reaction, which uses sn-1,2-diradylglycerol and either CDP-choline or CDP-ethanolamine, respectively. This is the last step in a biosynthetic pathway known as the Kennedy pathway, so named after Eugene Kennedy who elucidated it over 50 years ago. This review will cover various aspects of the Kennedy pathway including: each of the biosynthetic steps, the functions and roles of the phospholipid products PC and PE, and how the Kennedy pathway has the potential of being a chemotherapeutic target against cancer and various infectious diseases. IUBMBIUBMB Life, 62(6): [414][415][416][417][418][419][420][421][422][423][424][425][426][427][428] 2010

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Biosynthesis of phosphatidylcholine in bacteria

Cited by 275 publications

References 188 publications

Clostridium difficile heterogeneously impacts intestinal community architecture but drives stable metabolome responses

Clostridium difficile heterogeneously impacts intestinal community architecture but drives stable metabolome responses

Lipidomics of host–pathogen interactions

The Kennedy pathway—De novo synthesis of phosphatidylethanolamine and phosphatidylcholine

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