Chemistry and Biology of the Enterobacterial Common Antigen (ECA)

Mayer, Hubert; Schmidt, G.

doi:10.1007/978-3-642-67322-1_3

Cited by 79 publications

(72 citation statements)

References 289 publications

(91 reference statements)

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“…In contrast, the virulence of some bacterial pathogens appears to be enhanced by the O acetylation of cell surface polysaccharides (1,2,9). ECA PG is a component of all gram-negative enteric bacteria (23,29,31,44), and the available evidence strongly supports the conclusion that this is also the case for ECA CYC . Moreover, the O-acetyl groups of ECA CYC , and presumably ECA PG as well, also appear to constitute prominent immunogenic epitopes.…”

Section: Discussionmentioning

confidence: 89%

“…The phosphoglyceride-linked form of enterobacterial common antigen (ECA) (ECA PG ) is a glycolipid located on the cell surface of all gram-negative enteric bacteria (23,29,31,44,45). The carbohydrate portion of ECA PG consists of a linear polysaccharide comprised of the amino sugars N-acetyl-D-glucosamine (GlcNAc), N-acetyl-D-mannosaminuronic acid (ManNAcA), and 4-acetamido-4,6-dideoxy-D-galactose (Fuc4NAc).…”

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confidence: 99%

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O Acetylation of the Enterobacterial Common Antigen Polysaccharide Is Catalyzed by the Product of the yiaH Gene of Escherichia coli K-12

et al. 2006

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The carbohydrate component of the enterobacterial common antigen (ECA) of Escherichia coli K-12 occurs primarily as a water-soluble cyclic polysaccharide located in the periplasm (ECACYC) and as a phosphoglyceride-linked linear polysaccharide located on the cell surface (ECAPG). The polysaccharides of both forms are comprised of the amino sugars N-acetyl-d-glucosamine (GlcNAc), N-acetyl-d-mannosaminuronic acid (ManNAcA), and 4-acetamido-4,6-dideoxy-d-galactose (Fuc4NAc). These amino sugars are linked to one another to form trisaccharide repeat units with the structure →3-α-d-Fuc4NAc-(1→4)-β-d-ManNAcA-(1→4)-α-d-GlcNAc-(1→. The hydroxyl group in the 6 position of the GlcNAc residues of both ECACYC and ECAPG are nonstoichiometrically esterified with acetyl groups. Random transposon insertion mutagenesis of E. coli K-12 resulted in the generation of a mutant defective in the incorporation of O-acetyl groups into both ECACYC and ECAPG. This defect was found to be due to an insertion of the transposon into the yiaH locus, a putative gene of unknown function located at 80.26 min on the E. coli chromosomal map. Bioinformatic analyses of the predicted yiaH gene product indicate that it is an integral inner membrane protein that is a member of an acyltransferase family of enzymes found in a wide variety of organisms. The results of biochemical and genetic experiments presented here strongly support the conclusion that yiaH encodes the O-acetyltransferase responsible for the incorporation of O-acetyl groups into both ECACYC and ECAPG. Accordingly, we propose that this gene be designated wecH.

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Section: Discussionmentioning

confidence: 89%

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confidence: 99%

O Acetylation of the Enterobacterial Common Antigen Polysaccharide Is Catalyzed by the Product of the yiaH Gene of Escherichia coli K-12

et al. 2006

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“…Enterobacterial common antigen (ECA) is a cell surface glycolipid that is present in all gram-negative enteric bacteria thus far examined (19,23,25,38). The carbohydrate portion of the polymer contains the amino sugars N-acetyl-D-glucosamine (GlcNAc), N-acetyl-D-mannosaminuronic acid (ManNAcA), and 4-acetamido-4,6-dideoxy-D-galactose (Fuc4NAc).…”

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confidence: 99%

Assembly of Cyclic Enterobacterial Common Antigen in Escherichia coli K-12

2005

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We describe here the purification and quantification of a water-soluble cyclic form of enterobacterial common antigen (ECA CYC ) from Escherichia coli K-12 as well as information regarding its subcellular location and the genetic loci involved in its assembly. Structural characterization of purified ECA CYC molecules obtained from E. coli K-12 revealed that they uniformly contained four trisaccharide repeat units, and they were substituted with from zero to four O-acetyl groups. Cells from overnight cultures contained approximately 2 g ECA CYC per milligram (dry weight), and cell fractionation studies revealed that these molecules were localized exclusively in the periplasm. The synthesis and assembly of ECA CYC were found to require the wzxE and wzyE genes of the wec gene cluster. These genes encode proteins involved in the transmembrane translocation of undecaprenylpyrophosphate-linked ECA trisaccharide repeat units and the polymerization of trisaccharide repeat units, respectively. Surprisingly, synthesis of ECA CYC was dependent on the wzzE gene, which is required for the modulation of the polysaccharide chain lengths of phosphoglyceride-linked ECA (ECA PG ). The presence of ECA CYC in extracts of several other gram-negative enteric organisms was also demonstrated; however, it was not detected in cell extracts of Pseudomonas aeruginosa. These data suggest that in addition to ECA PG , ECA CYC may be synthesized in many, if not all, members of the Enterobacteriaceae.

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“…Fecal and howel extracts have been used m the initial stud ies, hut the crudeness of these preparations and the variability and inconsistency of results make the reported results difficult to evaluate (38). The pn:sence of immunity to enterobacterial common antigen has already been mentioned, but this 1s not specific for IBD (39). The isolation of purified and well characterized intestinal antigens has added more scientific credibility co the investigation of autoimmune phenomena in IBO.…”

Section: Evidence For Mycobacterial Involvement In Crohn's Diseasementioning

confidence: 99%

Overview of Inflammatory Bowel Disease Pathogenesis

Fiocchi¹

1990

Canadian Journal of Gastroenterology

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Inflammatory bowel disease (IBD) represents a difficult and challenging condition for patients, clinicians and basic investigators alike. Its etiology and pathogenesis are still unclear in spite of extensive investigations that have yielded a wealth of clinical. epidemiological, biochemical, bacteriological and immunological data on Crohn 's disease and ulcerative colitis. Although the precise mechanism(s) responsible for the intestinal inflammatory process remain to be defined, enough information has been assembled to hypothesize which components are likely to be important for this probably multifactorial disease. A consistent association between class I or II histocompatibility antigens and either Crohn's disease or ulcerative colitis has yet to be found. Nevertheless, ample epidemiological studies leave no doubt about the high frequency of familial clustering, and it must be determined whether this phenomenon translates a true genetic predisposition or a common environmental exposure, or both. Immune events occurring in the gastrointestinal tract are unquestionably linked to the pathogenesis of IBD, but it is unknown which are primary or secondary in nature. While most immune abnormalities detected in patients with established disease are likely to represent secondary events, these are no less important, as they probably contribute to the perpetuation of gut inflammation and tissue damage. This does not exclude that IBD is due to a primary defect of intestinal immunity, but this may no longer be detectable at the time of clinical manifestations. The answer to the question of wh1ch of the various intestinal immune abnormalities is central to pathogenesis must wait for additional research. Whether immune responses to the luminal flora, antigen processing mechanisms, antibody production, immunoregulation, cytotoxic activity, cytokine and mediator release are defective or disregulated is under intense investigation. It is likely that several of these events are involved, but they may interact in a complex and unpredictable fashion. lt is almost certain that there are various initiating and secondary events, and different immune mechanisms share relatively few common pathways for damaging the intestine, eg, cytokines, arachidonic acid metabolites, and oxidants. Perseverance in the study of these substances is finally yielding promising new approaches to the manipulation of immune and inflammatory responses chat cause bowel destruction. Future drugs may consist of combinations of highly specific inhibitors, antagonists or receptor blockers, that may selectively block one or several steps of the inflammatory cascade which is chronically active in the intestine of affected individuals. Therefore, we may soon face a situation not too dissimilar from what we have recently witnessed for peptic ulcer disease. The specific cause of IBD may still be beyond our comprehension, but a better understanding of its pathogenesis al lows us to put highly effective therapies within reach.

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Chemistry and Biology of the Enterobacterial Common Antigen (ECA)

Cited by 79 publications

References 289 publications

O Acetylation of the Enterobacterial Common Antigen Polysaccharide Is Catalyzed by the Product of the yiaH Gene of Escherichia coli K-12

O Acetylation of the Enterobacterial Common Antigen Polysaccharide Is Catalyzed by the Product of the yiaH Gene of Escherichia coli K-12

Assembly of Cyclic Enterobacterial Common Antigen in Escherichia coli K-12

Overview of Inflammatory Bowel Disease Pathogenesis

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