The Interaction of a Histidine‐Rich Protein <scp>H</scp>pn with the Membrane Mimics: Implications for Pathologic Roles of <scp>H</scp>pn in <i><scp>H</scp>elicobacter pylori</i>

Zhou, Qinglu; Qi, Shuang; Sun, Xia; Ge, Ruiguang

doi:10.1111/hel.12109

Cited by 4 publications

(3 citation statements)

References 28 publications

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“…Secretory proteins such as gingipains from P. gingivalis and Hpn from H. pylori are known to activate cytokine secretion (mainly IL-6 and IL-8). 39–41 Similarly, the CD-14 binding protein of S. sanguinis also results in secretion of host cytokines IL-6 and IL-8. 42 Further, the protein SerbB secreted by P. gingivalis modulates host cytoskeleton, thus aiding microbes to enter host tissues.…”

Section: Resultsmentioning

confidence: 99%

Linkages between oral commensal bacteria and atherosclerotic plaques in coronary artery disease patients

Chhibber‐Goel

Singhal

Bhowmik

et al. 2016

npj Biofilms Microbiomes

130

100

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Coronary artery disease is an inflammatory disorder characterized by narrowing of coronary arteries due to atherosclerotic plaque formation. To date, the accumulated epidemiological evidence supports an association between oral bacterial diseases and coronary artery disease, but has failed to prove a causal link between the two. Due to the recent surge in microbial identification and analyses techniques, a number of bacteria have been independently found in atherosclerotic plaque samples from coronary artery disease patients. In this study, we present meta-analysis from published studies that have independently investigated the presence of bacteria within atherosclerotic plaque samples in coronary artery disease patients. Data were collated from 63 studies covering 1791 patients spread over a decade. Our analysis confirms the presence of 23 oral commensal bacteria, either individually or in co-existence, within atherosclerotic plaques in patients undergoing carotid endarterectomy, catheter-based atherectomy, or similar procedures. Of these 23 bacteria, 5 (Campylobacter rectus, Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella intermedia, Prevotella nigrescens) are unique to coronary plaques, while the other 18 are additionally present in non-cardiac organs, and associate with over 30 non-cardiac disorders. We have cataloged the wide spectrum of proteins secreted by above atherosclerotic plaque-associated bacteria, and discuss their possible roles during microbial migration via the bloodstream. We also highlight the prevalence of specific poly-microbial communities within atherosclerotic plaques. This work provides a resource whose immediate implication is the necessity to systematically catalog landscapes of atherosclerotic plaque-associated oral commensal bacteria in human patient populations.

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Section: Resultsmentioning

confidence: 99%

Linkages between oral commensal bacteria and atherosclerotic plaques in coronary artery disease patients

Chhibber‐Goel

Singhal

Bhowmik

et al. 2016

npj Biofilms Microbiomes

130

100

View full text Add to dashboard Cite

show abstract

“…In solution, Hpn exists predominantly as a 20-mer [ 35 ] and each monomer binds 5 Ni(II) with a K d of 7.1 μM. Purified Hpn can assemble in vitro into amyloid-like fibers, interact with membrane mimics and is cytotoxic to gastric epithelial cell cultures [ 36 ] [ 37 ]. The actual existence of such fibers in H .…”

Section: Introductionmentioning

confidence: 99%

Evolution of Helicobacter: Acquisition by Gastric Species of Two Histidine-Rich Proteins Essential for Colonization

et al. 2015

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Metal acquisition and intracellular trafficking are crucial for all cells and metal ions have been recognized as virulence determinants in bacterial pathogens. Virulence of the human gastric pathogen Helicobacter pylori is dependent on nickel, cofactor of two enzymes essential for in vivo colonization, urease and [NiFe] hydrogenase. We found that two small paralogous nickel-binding proteins with high content in Histidine (Hpn and Hpn-2) play a central role in maintaining non-toxic intracellular nickel content and in controlling its intracellular trafficking. Measurements of metal resistance, intracellular nickel contents, urease activities and interactomic analysis were performed. We observed that Hpn acts as a nickel-sequestration protein, while Hpn-2 is not. In vivo, Hpn and Hpn-2 form homo-multimers, interact with each other, Hpn interacts with the UreA urease subunit while Hpn and Hpn-2 interact with the HypAB hydrogenase maturation proteins. In addition, Hpn-2 is directly or indirectly restricting urease activity while Hpn is required for full urease activation. Based on these data, we present a model where Hpn and Hpn-2 participate in a common pathway of controlled nickel transfer to urease. Using bioinformatics and top-down proteomics to identify the predicted proteins, we established that Hpn-2 is only expressed by H. pylori and its closely related species Helicobacter acinonychis. Hpn was detected in every gastric Helicobacter species tested and is absent from the enterohepatic Helicobacter species. Our phylogenomic analysis revealed that Hpn acquisition was concomitant with the specialization of Helicobacter to colonization of the gastric environment and the duplication at the origin of hpn-2 occurred in the common ancestor of H. pylori and H. acinonychis. Finally, Hpn and Hpn-2 were found to be required for colonization of the mouse model by H. pylori. Our data show that during evolution of the Helicobacter genus, acquisition of Hpn and Hpn-2 by gastric Helicobacter species constituted a decisive evolutionary event to allow Helicobacter to colonize the hostile gastric environment, in which no other bacteria persistently thrives. This acquisition was key for the emergence of one of the most successful bacterial pathogens, H. pylori.

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“…Laurdan was successfully used in the study of protein/membrane interactions in systems ranging from solutions to live cells . Bulk spectroscopic analysis of Laurdan emission has also been used for investigation of membrane interactions of several amyloid proteins and peptides, such as amyloid-β peptide, lysozyme, histidine-rich protein, and β 2 -microglubin along with studies on αSN. Specifically, Zhu et al initially reported an increased fluidity of mixed anionic/zwitterionic membranes upon addition of protofibrils and fibrillated αSN .…”

Section: Introductionmentioning

confidence: 99%

Protein/Lipid Coaggregates are Formed During α-Synuclein-Induced Disruption of Lipid Bilayers

et al. 2014

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Amyloid formation is associated with neurodegenerative diseases such as Parkinson's disease (PD). Significant α-synuclein (αSN) deposition in lipid-rich Lewy bodies is a hallmark of PD. Nonetheless, an unraveling of the connection between neurodegeneration and amyloid fibrils, including the molecular mechanisms behind potential amyloid-mediated toxic effects, is still missing. Interaction between amyloid aggregates and the lipid cell membrane is expected to play a key role in the disease progress. Here, we present experimental data based on hybrid analysis of two-photon-microscopy, solution small-angle X-ray scattering and circular dichroism data. Data show in real time changes in liposome morphology and stability upon protein addition and reveal that membrane disruption mediated by amyloidogenic αSN is associated with dehydration of anionic lipid membranes and stimulation of protein secondary structure. As a result of membrane fragmentation, soluble αSN:-lipid coaggregates are formed, hence, suggesting a novel molecular mechanism behind PD amyloid cytotoxicity.

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The Interaction of a Histidine‐Rich Protein Hpn with the Membrane Mimics: Implications for Pathologic Roles of Hpn in Helicobacter pylori

Abstract: The present data indicated that Hpn may take part in the pathological roles of Helicobacter pylori through membrane interactions.

Cited by 4 publications

References 28 publications

Linkages between oral commensal bacteria and atherosclerotic plaques in coronary artery disease patients

Linkages between oral commensal bacteria and atherosclerotic plaques in coronary artery disease patients

Evolution of Helicobacter: Acquisition by Gastric Species of Two Histidine-Rich Proteins Essential for Colonization

Protein/Lipid Coaggregates are Formed During α-Synuclein-Induced Disruption of Lipid Bilayers

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