Functional and structural aspects of <i>helicobacter pylori</i> acidic stress response factors

Zanotti, Giuseppe; Cendron, Laura

doi:10.1002/iub.382

Cited by 18 publications

(12 citation statements)

References 44 publications

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“…Foster & Hall, (1991& Hall, ( , 1990 Arginine (Kieboom & Abee, 2006); lysine (Park et al, 1996); ornithine (Viala et al, 2011) DnaK (Bearson et al, 2006) Alvarez-Ordonez et al (2009) and Kim et al (2005) Vibrio cholerae ATR Lysine (Merrell & Camilli, 1999) Helicobacter pylori Acid acclimation Mobley et al (1995) and Weeks et al (2000) GroEL*, GroES* (Zanotti & Cendron, 2010) Haque et al (1996) Brucella spp.…”

Section: Xar and Atrmentioning

confidence: 99%

“…2; see section 'Mechanisms of detection of low pH'). Besides the urease gene cluster, the H. pylori ArsRS regulon includes more than 100 genes, among which are the amiE and amiF genes (Pflock et al, 2006), encoding the corresponding NH 3 -producing enzymes, AmiE and AmiF, which are aliphatic amidases probably with an active role in H. pylori acid acclimation (Zanotti & Cendron, 2010).…”

Section: Helicobacter Pylorimentioning

confidence: 99%

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Coping with low pH: molecular strategies in neutralophilic bacteria

2014

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As part of their life cycle, neutralophilic bacteria are often exposed to varying environmental stresses, among which fluctuations in pH are the most frequent. In particular, acid environments can be encountered in many situations from fermented food to the gastric compartment of the animal host. Herein, we review the current knowledge of the molecular mechanisms adopted by a range of Gram-positive and Gram-negative bacteria, mostly those affecting human health, for coping with acid stress. Because organic and inorganic acids have deleterious effects on the activity of the biological macromolecules to the point of significantly reducing growth and even threatening their viability, it is not unexpected that neutralophilic bacteria have evolved a number of different protective mechanisms, which provide them with an advantage in otherwise life-threatening conditions. The overall logic of these is to protect the cell from the deleterious effects of a harmful level of protons. Among the most favoured mechanisms are the pumping out of protons, production of ammonia and proton-consuming decarboxylation reactions, as well as modifications of the lipid content in the membrane. Several examples are provided to describe mechanisms adopted to sense the external acidic pH. Particular attention is paid to Escherichia coli extreme acid resistance mechanisms, the activity of which ensure survival and may be directly linked to virulence.

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Section: Xar and Atrmentioning

confidence: 99%

Section: Helicobacter Pylorimentioning

confidence: 99%

Coping with low pH: molecular strategies in neutralophilic bacteria

2014

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“…UreE, UreF, UreG and UreH are accessory proteins involved in nickel incorporation and enzyme assembly. Together with arginase, UreI is responsible for a sustained supply of urea under acidic environmental conditions [70]. In contrast to the hypothesis of surface-localized urease, another current model assumes that the main urease activity resides in the bacterial cytoplasm [71].…”

Section: Reviewmentioning

confidence: 99%

The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis

2013

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Infections with the human pathogen Helicobacter pylori (H. pylori) can lead to severe gastric diseases ranging from chronic gastritis and ulceration to neoplastic changes in the stomach. Development and progress of H. pylori-associated disorders are determined by multifarious bacterial factors. Many of them interact directly with host cells or require specific receptors, while others enter the host cytoplasm to derail cellular functions. Several adhesins (e.g. BabA, SabA, AlpA/B, or OipA) establish close contact with the gastric epithelium as an important first step in persistent colonization. Soluble H. pylori factors (e.g. urease, VacA, or HtrA) have been suggested to alter cell survival and intercellular adhesions. Via a type IV secretion system (T4SS), H. pylori also translocates the effector cytotoxin-associated gene A (CagA) and peptidoglycan directly into the host cytoplasm, where cancer- and inflammation-associated signal transduction pathways can be deregulated. Through these manifold possibilities of interaction with host cells, H. pylori interferes with the complex signal transduction networks in its host and mediates a multi-step pathogenesis.

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“…We did find potential sigma 70 Ϫ10 regions for most of these genes, and previous studies have shown that nucleotide biosynthesisrelated genes in H. pylori generally have ϳ30-nucleotide-long 5=-untranslated regions (UTRs) (compared to much larger and variable 5=-UTRs for most other gene classes, such as protein synthesis or transcription), indicating their apparent optimization for translation (64). The single caveat in regard to the regulation of the purine nucleotide salvage pathway is the apparent upregulation of GMP reductase in the presence of acid, and numerous studies have noted this phenomena (10,64,73), although none have yet identified the regulatory mechanism responsible.…”

Section: Fig 12mentioning

confidence: 99%

Helicobacter pylori Relies Primarily on the Purine Salvage Pathway for Purine Nucleotide Biosynthesis

Liechti

Goldberg

2012

J Bacteriol

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Helicobacter pylori is a chronic colonizer of the gastric epithelium and plays a major role in the development of gastritis, peptic ulcer disease, and gastric cancer. In its coevolution with humans, the streamlining of the H. pylori genome has resulted in a significant reduction in metabolic pathways, one being purine nucleotide biosynthesis. Bioinformatic analysis has revealed that H. pylori lacks the enzymatic machinery for de novo production of IMP, the first purine nucleotide formed during GTP and ATP biosynthesis. This suggests that H. pylori must rely heavily on salvage of purines from the environment. In this study, we deleted several genes putatively involved in purine salvage and processing. The growth and survival of these mutants were analyzed in both nutrient-rich and minimal media, and the results confirmed the presence of a robust purine salvage pathway in H. pylori. Of the two phosphoribosyltransferase genes found in the H. pylori genome, only gpt appears to be essential, and an ⌬apt mutant strain was still capable of growth on adenine, suggesting that adenine processing via Apt is not essential. Deletion of the putative nucleoside phosphorylase gene deoD resulted in an inability of H. pylori to grow on purine nucleosides or the purine base adenine. Our results suggest a purine requirement for growth of H. pylori in standard media, indicating that H. pylori possesses the ability to utilize purines and nucleosides from the environment in the absence of a de novo purine nucleotide biosynthesis pathway. Helicobacter pylori is a Gram-negative, microaerophilic helixshaped bacterium that colonizes the gastric mucosa of roughly half of the world's population (19,53). Unlike numerous other pathogenic bacteria capable of existing in diverse environmental niches, H. pylori is only capable of sustained growth within its human host (19). Identified only 27 years ago (45), this bacterium was the first to have two different strains sequenced, allowing for the first genome-wide comparative bioinformatic analysis of a bacterial species (1, 16). The results of this comparative sequencing project (16) as well as subsequent sequencing projects (3) show a relatively small genome with numerous alterations in its metabolic pathways compared with those of other bacterial species. Initial conclusions were that the missing pathway enzymes simply were divergent enough to escape classification by homology screening (16); however, subsequent analysis of the genome has identified 48 potential "dead-end metabolites" (metabolites only consumed or only produced within a metabolic network), indicating missing knowledge about a particular pathway or absence of a fully functional pathway (67). One hypothesis developed to explain these abnormalities was that, having evolved alongside humans for so long, the metabolism of H. pylori was streamlined to coexist in the human niche. Apparent holes in the metabolic pathways of H. pylori suggest the loss of genes no longer required for growth in its relatively stable environment of the huma...

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Functional and structural aspects of helicobacter pylori acidic stress response factors

Cited by 18 publications

References 44 publications

Coping with low pH: molecular strategies in neutralophilic bacteria

Coping with low pH: molecular strategies in neutralophilic bacteria

The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis

Helicobacter pylori Relies Primarily on the Purine Salvage Pathway for Purine Nucleotide Biosynthesis

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