Oxidative and nitrosative stress defences of<i>Helicobacter</i>and<i>Campylobacter</i>species that counteract mammalian immunity

Flint, Annika; Stintzi, Alain; Saraiva, Lı́gia M.

doi:10.1093/femsre/fuw025

Cited by 45 publications

(55 citation statements)

References 274 publications

(367 reference statements)

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“…This protein may also serve the same function in the majority of Helicobacter species, although this has not been well studied since the model species, H. pylori , lacks NrfA and has alternative mechanisms for coping with nitrosative stress (Flint et al, 2016). In contrast to the concatenated protein-based monophyly of the heterotrophs ( Figure 3 ), phylogenetic inference of NrfA reveals at least two independent clades, the first comprising Sulfurospirillum , Wolinella and some Arcobacter , and the second Campylobacter and Helicobacter (Supplementary Figure S10).…”

Section: Resultsmentioning

confidence: 99%

Comparative Genomic Analysis of the Class Epsilonproteobacteria and Proposed Reclassification to Epsilonbacteraeota (phyl. nov.)

et al. 2017

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The Epsilonproteobacteria is the fifth validly described class of the phylum Proteobacteria, known primarily for clinical relevance and for chemolithotrophy in various terrestrial and marine environments, including deep-sea hydrothermal vents. As 16S rRNA gene repositories have expanded and protein marker analysis become more common, the phylogenetic placement of this class has become less certain. A number of recent analyses of the bacterial tree of life using both 16S rRNA and concatenated marker gene analyses have failed to recover the Epsilonproteobacteria as monophyletic with all other classes of Proteobacteria. In order to address this issue, we investigated the phylogenetic placement of this class in the bacterial domain using 16S and 23S rRNA genes, as well as 120 single-copy marker proteins. Single- and concatenated-marker trees were created using a data set of 4,170 bacterial representatives, including 98 Epsilonproteobacteria. Phylogenies were inferred under a variety of tree building methods, with sequential jackknifing of outgroup phyla to ensure robustness of phylogenetic affiliations under differing combinations of bacterial genomes. Based on the assessment of nearly 300 phylogenetic tree topologies, we conclude that the continued inclusion of Epsilonproteobacteria within the Proteobacteria is not warranted, and that this group should be reassigned to a novel phylum for which we propose the name Epsilonbacteraeota (phyl. nov.). We further recommend the reclassification of the order Desulfurellales (Deltaproteobacteria) to a novel class within this phylum and a number of subordinate changes to ensure consistency with the genome-based phylogeny. Phylogenomic analysis of 658 genomes belonging to the newly proposed Epsilonbacteraeota suggests that the ancestor of this phylum was an autotrophic, motile, thermophilic chemolithotroph that likely assimilated nitrogen from ammonium taken up from the environment or generated from environmental nitrate and nitrite by employing a variety of functional redox modules. The emergence of chemoorganoheterotrophic lifestyles in several Epsilonbacteraeota families is the result of multiple independent losses of various ancestral chemolithoautotrophic pathways. Our proposed reclassification of this group resolves an important anomaly in bacterial systematics and ensures that the taxonomy of Proteobacteria remains robust, specifically as genome-based taxonomies become more common.

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Section: Resultsmentioning

confidence: 99%

Comparative Genomic Analysis of the Class Epsilonproteobacteria and Proposed Reclassification to Epsilonbacteraeota (phyl. nov.)

et al. 2017

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“…Genes involved in Campylobacter oxidative stress resistance, as cataloged in a recent review by Flint et al (2016b), were identified in C. coli OR12 and the corresponding protein sequences compared with orthologs from C. jejuni NCTC11168. These data are presented in Supplementary Table 1.…”

Section: Resultsmentioning

confidence: 99%

“…These data are presented in Supplementary Table 1. All the functional genes cataloged by Flint et al (2016b) could be identified with the exception of those encoding the regulators of response to peroxide A and B ( rrpA and rrpB ). No significant sequence similarity to the latter two genes could be identified in the sequences of C. coli OR12 or C. coli RM1875 or C. coli 15-537360.…”

Section: Resultsmentioning

confidence: 99%

“…ROS damage DNA, proteins and lipids, limiting growth or killing the bacteria (Flint et al, 2016a). C. jejuni lacks several of the key oxidative stress response regulators identified in Escherichia coli , such as SoxRS, OxyR or Crp, and whereas E. coli possesses three separate superoxide dismutase and two catalase enzymes, C. jejuni encodes only one of each (Parkhill et al, 2000; Imlay, 2013; Flint et al, 2016b). …”

Section: Introductionmentioning

confidence: 99%

“…The DNA–binding protein from starved cells (Dps) has also been identified as a colonization factor for C. jejuni in a chick model and has been studied as a potential antigen candidate for a subunit anti- Campylobacter vaccine (Theoret et al, 2012). Other proteins involved in oxidative stress resistance of Campylobacter include cytochrome c peroxidases, quinone reductases, and DNA repair proteins (Atack and Kelly, 2009; Flint et al, 2016b). The response to oxidative stress is coordinated by a complex and overlapping network of regulators.…”

Section: Introductionmentioning

confidence: 99%

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Characterisation of Aerotolerant Forms of a Robust Chicken Colonizing Campylobacter coli

O'Kane

Connerton

2017

Front. Microbiol.

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Campylobacter contaminated poultry meat is a major source of human foodborne illness. Campylobacter coli strain OR12 is a robust colonizer of chickens that was previously shown to outcompete and displace other Campylobacter strains from the chicken’s gastrointestinal tract. This strain is capable of aerobic growth on blood agar. Serial aerobic passage increased this aerotolerance as assessed by quantitative assays for growth and survival on solid media. Aerotolerance was also associated with increased peroxide stress resistance. Aerobic passage did not alter cellular morphology or motility or hinder the microaerobic growth rate. Colonization of broiler chickens by aerotolerant C. coli OR12 was significantly lower than the wild-type strain at 3 days after challenge but not by 7 days, suggesting adaptation had occurred. Bacteria recovered from chickens had retained their aerotolerance, indicating this trait is stable. Whole genome sequencing enabled comparison with the wild-type sequence. Twenty-three point mutations were present, none of which were in genes known to affect oxidative stress resistance. Insertions or deletions caused frame shifts in several genes including, phosphoglycerate kinase and the b subunit of pyruvate carboxylase that suggest modification of central and carbohydrate metabolism in response to aerobic growth. Other genes affected include those encoding putative carbonic anhydrase, motility accessory factor, filamentous haemagglutinin, and aminoacyl dipeptidase proteins. Aerotolerance has the potential to affect environmental success and survival. Increased environmental survival outside of the host intestinal tract may allow opportunities for transmission between hosts. Resistance to oxidative stress may equate to increased virulence by virtue of reduced susceptibility to oxidative free radicals produced by host immune responses. Finally, resistance to ambient atmospheric oxygen may allow increased survival on chicken skin, and therefore constitutes an increased risk to public health.

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Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Gupta

Maurya

Verma

et al. 2019

J of Cellular Biochemistry

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Helicobacter pylori and humans have one of the most complex relationships in nature. How a bacterium manages to live in one of the harshest and hostile environments is a topic of unraveling mysteries. H. pylori is a prevalent species and it colonizes the human gut of more than 50% of the world population. It infects the epithelial region of antrum and persists there for a long period. Over the time of evolution, H. pylori has developed complex strategies to extend the degree of inflammation in gastric mucosa. H. pylori needs specific adaptations for initial colonization into the host environment like helical shape, flagellar movement, chemotaxis, and the production of urease enzyme that neutralizes acidic environment of the stomach. There are several factors from the bacterium as well as from the host that participate in these complex interactions. On the other hand, to establish the persistent infection, H. pylori escapes the immune system by mimicking the host antigens. This pathogen has the ability to dodge the immune system and then persist there in the form of host cell, which leads to immune tolerance. H. pylori has an ability to manipulate its own pathogen‐associated molecular patterns, which leads to an inhibition in the binding with specific pattern recognition receptors of the host to avoid immune cell detection. Also, it manipulates the host metabolic homeostasis in the gastric epithelium. Besides, it has several genes, which may get involved in the acquisition of nutrition from the host to survive longer in the host. Due to the persistence of H. pylori, it causes chronic inflammation and raises the chances of gastric cancer. This review highlights the important elements, which are certainly responsible for the persistence of H. pylori in the human host.

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Oxidative and nitrosative stress defences ofHelicobacterandCampylobacterspecies that counteract mammalian immunity

Cited by 45 publications

References 274 publications

Comparative Genomic Analysis of the Class Epsilonproteobacteria and Proposed Reclassification to Epsilonbacteraeota (phyl. nov.)

Comparative Genomic Analysis of the Class Epsilonproteobacteria and Proposed Reclassification to Epsilonbacteraeota (phyl. nov.)

Characterisation of Aerotolerant Forms of a Robust Chicken Colonizing Campylobacter coli

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

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