Pathogen control at the intestinal mucosa – H2O2to the rescue

Knaus, Ulla G.; Hertzberger, Rosanne; Pîrcălăbioru, Grațiela Grădișteanu; Yousefi, S Parsa M; Santos, Filipe Branco dos

doi:10.1080/19490976.2017.1279378

Cited by 54 publications

(39 citation statements)

References 52 publications

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“…Here, orally administered PtNPs were found to reduce the phylotype richness and the Firmicutes/Bacteroidetes ratio, and to increase proinflammatory bacteria, which is similar to the results of gold and silver nanoparticles in previous studies. 47,49 H 2 O 2 generation by host epithelial and innate immune system and commensal lactic acid bacteria contributes to the maintenance of gut-microbiota homeostasis, 53 and therefore, we hypothesize that noble metal nanoparticles might induce gut dysbiosis by catalytic elimination of intraluminal H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

Platinum Nanoparticles As A Therapeutic Agent Against Dextran Sodium Sulfate-Induced Colitis In Mice

Zhu

Zeng²,

Feng³

et al. 2019

IJN

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Purpose: This study aimed to evaluate the anti-colitis potential of platinum nanoparticles (PtNPs). Materials and methods: 5-, 30-and 70-nm PtNPs were administered to C57BL/6 mice once daily by intragastric gavage for 8 d during and after 5-d dextran sodium sulfate treatment. Results: According to body weight change, stool blood and consistency, and colon length and histopathology, PtNPs size-dependently alleviated DSS-induced murine colitis. PtNPs enhanced gut-barrier function by upregulating the colonic expressions of heat-shock protein 25 and tight junction proteins. Based on colonic myeloperoxidase activity, colonic and peripheral levels of interleukin-6 and tumor necrosis factor-α, and peripheral counts of white blood cells, PtNPs attenuated colonic and systemic inflammation. By suppressing lipopolysaccharide-triggered production of proinflammatory mediators, including nitric oxide, tumor necrosis factor-α and interleukin-6, PtNPs exerted direct anti-inflammatory activities in RAW264.7 macrophages through a mechanism involving intracellular reactive oxygen species scavenging and Toll-like receptor 4/NF-κB signaling suppression. High-throughput 16S rRNA sequencing of fecal samples unveiled that PtNPs induced gut dysbiosis by unfavorably altering α-diversity, Firmicutes/Bacteroidetes ratio, and richness of certain specific bacteria. Conclusion: PtNPs are a promising anti-colitis agent, but may negatively impact gut-microbiota.

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Section: Discussionmentioning

confidence: 99%

Platinum Nanoparticles As A Therapeutic Agent Against Dextran Sodium Sulfate-Induced Colitis In Mice

Zhu

Zeng²,

Feng³

et al. 2019

IJN

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“…S. gordonii can adhere to carbohydrate receptors on epithelial cells (85,86), which, similarly, could stimulate signal transduction events. Moreover, oral streptococci, such as S. gordonii, produce hydrogen peroxide, which is capable of impacting host cell physiology (87).…”

Section: Discussionmentioning

confidence: 99%

Streptococcus gordonii programs epithelial cells to resist ZEB2 induction by Porphyromonas gingivalis

Ohshima

Wang

Fitzsimonds

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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The polymicrobial microbiome of the oral cavity is a direct precursor of periodontal diseases, and changes in microhabitat or shifts in microbial composition may also be linked to oral squamous cell carcinoma. Dysbiotic oral epithelial responses provoked by individual organisms, and which underlie these diseases, are widely studied. However, organisms may influence community partner species through manipulation of epithelial cell responses, an aspect of the host microbiome interaction that is poorly understood. We report here thatPorphyromonas gingivalis, a keystone periodontal pathogen, can up-regulate expression of ZEB2, a transcription factor which controls epithelial–mesenchymal transition and inflammatory responses. ZEB2 regulation byP. gingivaliswas mediated through pathways involving β-catenin and FOXO1. Among the community partners ofP. gingivalis,Streptococcus gordoniiwas capable of antagonizing ZEB2 expression. Mechanistically,S. gordoniisuppressed FOXO1 by activating the TAK1-NLK negative regulatory pathway, even in the presence ofP. gingivalis. Collectively, these results establishS. gordoniias homeostatic commensal, capable of mitigating the activity of a more pathogenic organism through modulation of host signaling.

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“…The multifaceted property of Ent is further exemplified by our findings that it could inhibit an array of neutrophil functions, including ROS generation, NETs formation, degranulation, phagocytosis and bacterial killing activity. Besides conferring a survival advantage to E. coli , the Ent-mediated inhibition of mucosal ROS generation may also be of advantage to other gut commensals in achieving a stable colonization (44). Such notion is exemplified by the intricate Ent-dependent crosstalk between microbial community (41, 45, 46) and the fact that various non-Ent-producing bacteria have, nonetheless, evolved to express the receptor for Ent (47).…”

Section: Discussionmentioning

confidence: 99%

Bacterial Siderophores Hijack Neutrophil Functions

Saha

Yeoh

Olvera

et al. 2017

The Journal of Immunology

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Neutrophils are the primary immune cells that respond to inflammation and combat microbial transgression. In order to thrive, the bacteria residing in their mammalian host have to withstand the anti-bactericidal responses of neutrophils. We report that enterobactin (Ent), a catecholate siderophore expressed by E. coli, inhibited PMA-induced generation of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in both mouse and human neutrophils. Ent also impaired the degranulation of primary granules, inhibited phagocytosis and bactericidal activity of neutrophils, but without affecting their migration and chemotaxis. Molecular analysis revealed that Ent can chelate intracellular labile iron that is required for neutrophil oxidative responses. Other siderophores (pyoverdine, ferrichrome, deferoxamine) likewise inhibited ROS and NETs in neutrophils, thus indicating that the chelation of iron may largely explain their inhibitory effects. To counter iron theft by Ent, neutrophils rely on the siderophore-binding protein lipocalin 2 (Lcn2) in a ‘tug-of-war’ for iron. The inhibition of neutrophil ROS and NETs by Ent was augmented in Lcn2-deficient neutrophils when compared to WT neutrophils, but rescued by the exogenous addition of recombinant Lcn2. Taken together, our findings illustrate the novel concept that microbial siderophore’s iron scavenging property may serve as an anti-radical defense system, that neutralizes immune functions of neutrophils.

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Pathogen control at the intestinal mucosa – H₂O₂to the rescue

Cited by 54 publications

References 52 publications

<p>Platinum Nanoparticles As A Therapeutic Agent Against Dextran Sodium Sulfate-Induced Colitis In Mice</p>

<p>Platinum Nanoparticles As A Therapeutic Agent Against Dextran Sodium Sulfate-Induced Colitis In Mice</p>

Streptococcus gordonii programs epithelial cells to resist ZEB2 induction by Porphyromonas gingivalis

Bacterial Siderophores Hijack Neutrophil Functions

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