Cloning, nucleotide sequence, and expression of a gene encoding an adhesin subunit protein of Helicobacter pylori

Evans, Dolores G.; Karjalainen, T.; Evans, Doyle J.; Graham, David Y.; Lee, Chao‐Hung

doi:10.1128/jb.175.3.674-683.1993

Cited by 200 publications

(146 citation statements)

References 48 publications

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“…H. pylori possesses several putative colonization factors, including flagella motility (Marshall & Warren, 1984), various adhesins (Evans et al, 1993;Falk et al, 1993;O'Toole et al, 1995), vacA (Salama et al, 2001) and urease (Marshall & Warren, 1984;Tsuda et al, 1994), some of which have been shown to be necessary for gastric colonization. Isogenic flaA 2 , flaB 2 and flaA flaB 2 mutant strains do not show full motility, and are unable to form effective colonies in the stomachs of germ-free piglets (Eaton et al, 1996).…”

Section: Implications Of Experimental Datamentioning

confidence: 99%

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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Helicobacter pylori is associated with gastric disorders in humans and some experimental animals, and possesses the luxS/type 2 autoinducer (AI-2) system. The effects of a specific luxS mutation on the characteristics of H. pylori were examined. On 0?3 % agar medium, motility of H. pylori HPKY08 (luxS : : cat) was significantly lower than that of wild-type H. pylori TK1402. The luxS-complemented strain HPKY21 exhibited motility comparable to that of H. pylori TK1402. It was shown that the luxS/AI-2 system plays an important role in H. pylori motility. The luxS mutant exhibited a reduced infection rate relative to the wild-type parent strain TK1402 in a Mongolian gerbil model. At 3 months after oral inoculation, lower numbers of H. pylori were detected by semi-quantitative real-time reverse transcription PCR (qRT-PCR) in luxS " mutant-infected gerbils than in TK1402-infected gerbils. Gastric inflammation and increased antibody titre for H. pylori were observed in TK1402-infected gerbils only. INTRODUCTIONQuorum sensing (QS) is a cell-to-cell communication system that regulates bacterial phenotypes, including the expression of virulence factor genes. The signalling molecules are known as autoinducers (AIs), and when these molecules reach a critical threshold concentration within a bacterial population, a signal transduction cascade is triggered, and this forms the basis for alterations in gene expression (Fuqua et al., 1994). Many Gram-negative bacteria utilize N-acylhomoserine lactone molecules, AI-1, as signals, while Gram-positive bacteria actively export peptides as signalling molecules. There is a second signalling system involved in a wide range of bacterial species (Schauder et al., 2001), and this system is utilized by both Gram-positive and Gram-negative bacteria. The signalling molecule known as type 2 autoinducer (AI-2) is a furanosyl borate diester (Chen et al., 2002), and the enzyme responsible for its synthesis is encoded by the luxS gene (Surette & Bassler, 1999). The genomes of many bacterial species, notably Escherichia coli, Salmonella enterica serovar Typhimurium, Shigella flexneri, Proteus mirabilis, Vibrio cholerae, Vibrio vulnificus, Campylobacter jejuni, Porphyromonas gingivalis, Bacillus subtilis, Streptococcus pyogenes, Streptococcus mutans, Clostridium perfringens and Clostridium difficile, include luxS homologues. In several of these, luxS-related AI-2 signals are involved in bacterial characteristics such as biofilm formation (Balestrino et al., 2005;Blehert et al., 2003;Fong et al., 2001;Wen & Burne 2004), flagella and motility (Jeon et al., 2003;Schneider et al., 2002;Stroeher et al., 2003), type III secretion systems (Sperandio et al., 1999), toxin production (Ohtani et al., 2002) and virulence (Lyon et al., 2001; Parsonnet et al., 1991;Stroeher et al., 2003).Helicobacter pylori has been identified as the aetiological agent of chronic active gastritis, peptic ulcer disease (Blaser, 1992;Graham, 1989), gastric adenocarcinoma (Parsonnet et al., 1991) and mucosal-associated lymphoid t...

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Section: Implications Of Experimental Datamentioning

confidence: 99%

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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“…A. Moore, B. Beckthold, S. Wong, A. Kureishi and L. E. Bryan, unpublished work (GenBank accession no. 29481) ; [45]q. Thus motifs A to C identified upstream of the H. pylori aroQ gene may also be potential promotors.…”

Section: Gene Signalsmentioning

confidence: 99%

Cloning, sequencing, expression, purification and preliminary characterization of a type II dehydroquinase from Helicobacter pylori

Bottomley

Clayton²,

Chalk³

et al. 1996

Biochemical Journal

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A heat-stable dehydroquinase was purified to near homogeneity from a plate-grown suspension of the Gram-negative stomach pathogen Helicobacter pylori, and shown from both its subunit and native molecular masses to be a member of the type II family of dehydroquinases. This was confirmed by N-terminal amino acid sequence data. The gene encoding this activity was isolated following initial identification, by random sequencing of the H. pylori genome, of a 96 bp fragment, the translated sequence of which showed strong identity to a C-terminal region of other type II enzymes. Southern blot analysis of a cosmid library identified several potential clones, one of which complemented an Escherichia coliaroD point mutant strain deficient in host dehydroquinase. The gene encoding the H. pylori type II dehydroquinase (designated aroQ) was sequenced. The translated sequence was identical to the N-terminal sequence obtained directly from the purified protein, and showed strong identity to other members of the type II family of dehydroquinases. The enzyme was readily expressed in E. coli from a plasmid construct from which several milligrams of protein could be isolated, and the molecular mass of the protein was confirmed by electrospray MS. The aroQ gene in H. pylori may function in the central biosynthetic shikimate pathway of this bacterium, thus opening the way for the construction of attenuated strains as potential vaccines as well as offering a new target for selective enzyme inhibition.

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“…Lewis b is commonly, but not universally, expressed on the surface of gastric epithelial cells (17). HpaA has been characterized as an N-acetylneuraminyllactose-binding hemagglutinin which is critical for mouse colonization (7,16). The HorB protein is paralogous with BabA, AlpA, and AlpB.…”

mentioning

confidence: 99%

Helicobacter pylori AlpA and AlpB Bind Host Laminin and Influence Gastric Inflammation in Gerbils

et al. 2011

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Helicobacter pylori persistently colonizes humans, causing gastritis, ulcers, and gastric cancer. Adherence to the gastric epithelium has been shown to enhance inflammation, yet only a few H. pylori adhesins have been paired with targets in host tissue. The alpAB locus has been reported to encode adhesins involved in adherence to human gastric tissue. We report that abrogation of H. pylori AlpA and AlpB reduces binding of H. pylori to laminin while expression of plasmid-borne alpA or alpB confers laminin-binding ability to Escherichia coli. An H. pylori strain lacking only AlpB is also deficient in laminin binding. Thus, we conclude that both AlpA and AlpB contribute to H. pylori laminin binding. Contrary to expectations, the H. pylori SS1 mutant deficient in AlpA and AlpB causes more severe inflammation than the isogenic wild-type strain in gerbils. Identification of laminin as the target of AlpA and AlpB will facilitate future investigations of host-pathogen interactions occurring during H. pylori infection.

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Cloning, nucleotide sequence, and expression of a gene encoding an adhesin subunit protein of Helicobacter pylori

Cited by 200 publications

References 48 publications

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Cloning, sequencing, expression, purification and preliminary characterization of a type II dehydroquinase from Helicobacter pylori

Helicobacter pylori AlpA and AlpB Bind Host Laminin and Influence Gastric Inflammation in Gerbils

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