Urease-mediated destruction of bacteria is specific for Helicobacter urease and results in total cellular disruption

C Williams, W.D. Neithercut, M. Hossack, J. Hair, K.E.L. McColl

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The survival of Helicobacter mustelae, Proteus mirobilis, Escherichia coli and Campylobacter jejuni in the presence of urea and citrate at pH 6.0 was examined. H. mustelae, which has urease activity similar to H. pylori, had a markedly reduced survival, median 2.5% (0-78%) (P < 0.001) when incubated under these conditions. Only 7% of the ammonia produced by H. mustelae urease activity was recovered from the buffer, a similar percentage to that previously reported with H. pylori. None of the other organisms, all of which had lower urease activity, had impaired survival under these conditions. Electron microscopical studies demonstrated extensive structural damage to H. pylori following exposure to urea and citrate at pH 6.0. This structural damage to the organisms makes it unlikely that the low recovery of ammonia was due to retention of ammonia within the bacteria and suggests that the ammonia may have been incorporated into glutamate or other amino acids. Incorporation of ammonia into these compounds would deplete the cell of the key metabolic intermediate alpha-ketoglutarate and could thus explain the mechanism of the urease-dependent destruction of the organism.

Original languageEnglish
Pages (from-to)273-80
Number of pages8
JournalFEMS immunology and medical microbiology
Volume9
Issue number4
Publication statusPublished - Oct 1994
Externally publishedYes

Fingerprint

Helicobacter
Urease
Helicobacter mustelae
Ammonia
Pylorus
Bacteria
Citric Acid
Urea
Proteus
Campylobacter jejuni
Glutamic Acid
Buffers
Electrons
Escherichia coli
Amino Acids

Keywords

  • Ammonia
  • Citrates
  • Citric Acid
  • Helicobacter
  • Hydrogen-Ion Concentration
  • Urea
  • Urease
  • Journal Article

Cite this

Williams, C ; Neithercut, W.D. ; Hossack, M. ; Hair, J. ; McColl, K.E.L. / Urease-mediated destruction of bacteria is specific for Helicobacter urease and results in total cellular disruption. In: FEMS immunology and medical microbiology. 1994 ; Vol. 9, No. 4. pp. 273-80.
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Urease-mediated destruction of bacteria is specific for Helicobacter urease and results in total cellular disruption. / Williams, C; Neithercut, W.D.; Hossack, M.; Hair, J.; McColl, K.E.L.

In: FEMS immunology and medical microbiology, Vol. 9, No. 4, 10.1994, p. 273-80.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Urease-mediated destruction of bacteria is specific for Helicobacter urease and results in total cellular disruption

AU - Williams, C

AU - Neithercut, W.D.

AU - Hossack, M.

AU - Hair, J.

AU - McColl, K.E.L.

PY - 1994/10

Y1 - 1994/10

N2 - The survival of Helicobacter mustelae, Proteus mirobilis, Escherichia coli and Campylobacter jejuni in the presence of urea and citrate at pH 6.0 was examined. H. mustelae, which has urease activity similar to H. pylori, had a markedly reduced survival, median 2.5% (0-78%) (P < 0.001) when incubated under these conditions. Only 7% of the ammonia produced by H. mustelae urease activity was recovered from the buffer, a similar percentage to that previously reported with H. pylori. None of the other organisms, all of which had lower urease activity, had impaired survival under these conditions. Electron microscopical studies demonstrated extensive structural damage to H. pylori following exposure to urea and citrate at pH 6.0. This structural damage to the organisms makes it unlikely that the low recovery of ammonia was due to retention of ammonia within the bacteria and suggests that the ammonia may have been incorporated into glutamate or other amino acids. Incorporation of ammonia into these compounds would deplete the cell of the key metabolic intermediate alpha-ketoglutarate and could thus explain the mechanism of the urease-dependent destruction of the organism.

AB - The survival of Helicobacter mustelae, Proteus mirobilis, Escherichia coli and Campylobacter jejuni in the presence of urea and citrate at pH 6.0 was examined. H. mustelae, which has urease activity similar to H. pylori, had a markedly reduced survival, median 2.5% (0-78%) (P < 0.001) when incubated under these conditions. Only 7% of the ammonia produced by H. mustelae urease activity was recovered from the buffer, a similar percentage to that previously reported with H. pylori. None of the other organisms, all of which had lower urease activity, had impaired survival under these conditions. Electron microscopical studies demonstrated extensive structural damage to H. pylori following exposure to urea and citrate at pH 6.0. This structural damage to the organisms makes it unlikely that the low recovery of ammonia was due to retention of ammonia within the bacteria and suggests that the ammonia may have been incorporated into glutamate or other amino acids. Incorporation of ammonia into these compounds would deplete the cell of the key metabolic intermediate alpha-ketoglutarate and could thus explain the mechanism of the urease-dependent destruction of the organism.

KW - Ammonia

KW - Citrates

KW - Citric Acid

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KW - Hydrogen-Ion Concentration

KW - Urea

KW - Urease

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