Academic literature on the topic 'Pathobiont'
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Journal articles on the topic "Pathobiont":
1
Gilliland, A., Y. Chen, D. Tertigas, M. Surette, B. Bressler, and B. Vallance. "A24 AN ULCERATIVE COLITIS-ISOLATED PATHOBIONT CAN DEGRADE MUCUS PRODUCED BY UC PATIENT-DERIVED COLONOIDS." Journal of the Canadian Association of Gastroenterology 7, Supplement_1 (February 14, 2024): 13–14. http://dx.doi.org/10.1093/jcag/gwad061.024.
Abstract:
Abstract Background Inflammatory bowel disease (IBD) pathobionts are commensal microbes with pathogenic potential that may cause or exacerbate IBD symptoms. Some pathobionts (ex. Escherichia coli) reside at low levels in the lumen of a healthy gut but can rapidly grow in the inflamed colons of ulcerative colitis (UC) patients. To promote disease, these pathobionts must cross the colonic mucus barrier (comprised of MUC2) that separates the epithelium from luminal microbes. It is currently unclear how bacterial pathobionts cross the mucus barrier of UC patients. Aims Using healthy and UC patient biopsy-derived colonic organoids (colonoids) and an air liquid interface (ALI) monolayer model, we investigated how the UC-isolated E. coli pathobiont p19A crosses the mucus barrier. Methods Apical out healthy and UC patient biopsy-derived colonoids were infected with p19A to confirm this pathobiont exerts direct cytopathic effects on human colonocytes. Sequencing p19A’s genome, we found it contains two mucus degrading proteins (mucinases). Healthy human and UC colonoids, as well as mouse colonoids, were used to generate mucus-producing ALI monolayers. To detect p19A-mediated mucus degradation, concentrated p19A supernatant was incubated with ALI-derived mucus and degraded MUC2 proteins were detected by protein gel and MUC2 Western blot. MUC2 glycosylation was analyzed by protein gel and PAS staining. ALI monolayers were infected with p19A to evaluate mucus degradation and p19A localization by immunostaining. Results The UC-isolated pathobiont p19A infected and exerted cytotoxic effects on apical out healthy and UC patient colonoids. By day 14, ALI monolayers were differentiated and covered by a thick mucus layer as assessed using brightfield microscopy. Mucus removed for mucinase assays was replenished within 7 days. p19A harbours proteins capable of degrading human ALI-, but not mouse ALI-derived mucus, in vitro, suggesting the presence of host-specific mucinases. Mucus produced by UC ALI monolayers showed reduced glycosylation and increased degradation both over time and by p19A proteins. Day 21 ALI-monolayers infected with p19A for 18 hours exhibited overt mucus degradation allowing p19A to infect the underlying epithelium. Conclusions Patient-derived ALI monolayers produce a thick mucus layer that can be used to study pathobiont-mucus interactions. The UC pathobiont p19A disrupts apical out organoids and produces proteins that degrade ALI-derived mucus in vitro, with UC mucus being more susceptible to degradation than mucus from healthy controls. The results from our model suggest a potential mechanism for pathobiont-mediated mucosal barrier disruption in UC patients. Patient-derived ALI monolayer (blue/white) produces a thick mucus layer (green) that can be degraded by the pathobiont p19A (red). Funding Agencies CCC, CIHR
2
Jones, Josh, Qiaojuan Shi, Rahul R. Nath, and Ilana L. Brito. "Keystone pathobionts associated with colorectal cancer promote oncogenic reprograming." PLOS ONE 19, no. 2 (February 16, 2024): e0297897. http://dx.doi.org/10.1371/journal.pone.0297897.
Abstract:
Fusobacterium nucleatum (Fn) and enterotoxigenic Bacteroides fragilis (ETBF) are two pathobionts consistently enriched in the gut microbiomes of patients with colorectal cancer (CRC) compared to healthy counterparts and frequently observed for their direct association within tumors. Although several molecular mechanisms have been identified that directly link these organisms to features of CRC in specific cell types, their specific effects on the epithelium and local immune compartment are not well-understood. To fill this gap, we leveraged single-cell RNA sequencing (scRNA-seq) on wildtype mice and mouse model of CRC. We find that Fn and ETBF exacerbate cancer-like transcriptional phenotypes in transit-amplifying and mature enterocytes in a mouse model of CRC. We also observed increased T cells in the pathobiont-exposed mice, but these pathobiont-specific differences observed in wildtype mice were abrogated in the mouse model of CRC. Although there are similarities in the responses provoked by each organism, we find pathobiont-specific effects in Myc-signaling and fatty acid metabolism. These findings support a role for Fn and ETBF in potentiating tumorigenesis via the induction of a cancer stem cell-like transit-amplifying and enterocyte population and the disruption of CTL cytotoxic function.
3
Minton, Kirsty. "Pathobiont peacekeepers." Nature Reviews Immunology 18, no. 3 (February 16, 2018): 152. http://dx.doi.org/10.1038/nri.2018.11.
4
Yang, H., H. Mirsepasi-Lauridsen, C. Struve, J. M. Allaire, A. Sivignon, W. Vogl, E. S. Bosman, et al. "A21 ULCERATIVE COLITIS-ASSOCIATED E. COLI PATHOBIONTS POTENTIATE COLITIS IN SUSCEPTIBEL HOSTS." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (March 1, 2021): 142–44. http://dx.doi.org/10.1093/jcag/gwab002.020.
Abstract:
Abstract Background Ulcerative colitis (UC) is a chronic inflammatory condition linked to intestinal microbial dysbiosis, including the expansion of E. coli strains related to extra-intestinal pathogenic E. coli. These “pathobionts” exhibit pathogenic properties, but their potential to promote UC is unclear due to the lack of relevant animal models. Aims We explored the potential to establish a mouse model of GI infection by the UC-associated E. coli strain p19A, as well as characterize the pathogenic features of p19A. Methods We used a representative UC pathobiont strain (p19A), and mice lacking single immunoglobulin and toll-interleukin 1 receptor domain (SIGIRR), a deficiency increasing susceptibility to gut infections. Vancomycin-pretreated Sigirr-/- mice were subsequently gavaged with the control E. coli DH10B (a derivative of commensal strain K-12) or p19A. One day after infection, mice were exposed to 2.5% dextran sodium sulfate (DSS) in their drinking water for another 4 days. Results Strain p19A was found to adhere to the cecal mucosa of Sigirr-/- mice, causing modest inflammation. Moreover, it dramatically worsened DSS-induced colitis. This potentiation was attenuated using a p19A strain lacking α-hemolysin genes, or when we targeted pathobiont adherence using a p19A strain lacking the adhesin FimH, or following treatment with FimH antagonists. Conclusions Thus, UC pathobionts adhere to the intestinal mucosa, and worsen the course of colitis in susceptible hosts in a manner dependent on specific virulence factors, including α-hemolysin and FimH. Funding Agencies CCC, CIHR
5
Clayton, C., K. Ng, and C. Tropini. "A38 EXPLORING HOW BOWEL PREPARATION CAN AFFECT INFLAMMATORY BOWEL DISEASE VIA THE GUT MICROBIOTA." Journal of the Canadian Association of Gastroenterology 7, Supplement_1 (February 14, 2024): 21–22. http://dx.doi.org/10.1093/jcag/gwad061.038.
Abstract:
Abstract Background Inflammatory bowel disease (IBD) is a debilitating disorder that targets the gastrointestinal (GI) tract. Although its causes remain unknown, recent studies have identified changes to the gut microbiota associated with IBD. While most gut bacteria are essential for GI health, pathobionts are bacteria that are prevalent in IBD patients and that can act as pathogens and induce inflammation. IBD patients undergo routine endoscopies which require the administration of laxative-based bowel prep to clear out the luminal contents of the GI for the endoscope. It has been found that after bowel prep some IBD patients experience inflammatory flareups. IBD patients may experience adverse reactions following bowel prep, including increased inflammation, emergency room visits, and medication adjustments. Importantly, bowel prep perturbs the gut microbiota, depleting beneficial microorganisms, while allowing pathobiont strains to thrive, which could be the cause for worsened symptoms post-bowel prep in some patients. Aims We hypothesize that the altered intestinal microenvironment during bowel prep causes commensal bacteria depletion and favours osmotolerant pathogenic species that lead to increased inflammation in two systems: 1) in a model disease-causing microorganism, Salmonella enterica 2) in an IBD microbiota. Methods To investigate pathogen expansion after bowel prep a Salmonella mouse model was established. Microbiota changes were determined by 16S rRNA sequencing and spot plating. Changes to the gut environment and the mechanism for pathogen colonization were characterized using Salmonella mutants and confocal imaging. To identify changes to the IBD microbiota, a humanized mouse model was established, and microbiota changes were investigated as done in the Salmonella model. IBD-associated pathobiont growth was also characterized in in vitro conditions that were identified in our in vivo model. Results We have demonstrated that bowel prep increases GI osmolality and leads to increased Salmonella colonization in the gut and systemic organs following bowel prep unlike mice treated with vehicle, supporting our hypothesis. We then explored the effects of bowel prep in a humanized mouse model of IBD, which showed increased translocation of bacteria from the gut to internal organs post-prep. Additionally, IBD-associated pathobionts were able to grow much greater than commensal strains highlighting that IBD pathobionts can persist in the gut after bowel prep. Conclusions Our study highlights that bowel prep disrupts the gut microbiota and the intestinal environment allowing for pathogen colonization and bacterial translocation. Therefore, bacterial translocation could provide mechanistic insight for inflammatory flareups following bowel prep. Ultimately, our research underscores the importance of the gut environment in facilitating pathobiont exacerbation of IBD. Funding Agencies CIHR
6
Chapman, Timothy J., Matthew C. Morris, Lei Xu, and Michael E. Pichichero. "Nasopharyngeal colonization with pathobionts is associated with susceptibility to respiratory illnesses in young children." PLOS ONE 15, no. 12 (December 11, 2020): e0243942. http://dx.doi.org/10.1371/journal.pone.0243942.
Abstract:
Some children are more susceptible to viral and bacterial respiratory infections in the first few years of life than others. However, the factors contributing to this susceptibility are incompletely understood. In a retrospective analysis of clinical samples collected from a prospectively-enrolled cohort of 358 children we sought associations between physician-attended illness visits and bacterial colonization in the first five years of life. A subset of children was identified by unsupervised clustering analysis as infection and allergy prone (IAP). Several respiratory infection- and allergy-mediated illnesses co-occurred at higher rates in IAP children, while the rates of other illnesses were not significantly different between the groups. Analyses of nasopharyngeal (NP) pathobionts and microbiota commensals showed that early age of first colonization with pathobionts Streptococcus pneumonia, non-typeable Haemophilus influenzae, and Moraxella catarrhalis was associated with IAP children, and particularly Moraxella abundance was negatively associated with NP microbiome diversity. We conclude that mucosal pathobiont exposures in early life can influence susceptibility to respiratory illnesses in children.
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Yang, Hyungjun, Hengameh Chloé Mirsepasi-Lauridsen, Carsten Struve, Joannie M. Allaire, Else Bosman, Adeline Sivignon, Wayne Vogl, et al. "Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 192.3. http://dx.doi.org/10.4049/jimmunol.202.supp.192.3.
Abstract:
Abstract Ulcerative colitis (UC) is chronic inflammatory condition linked to intestinal microbial dysbiosis, including the expansion of E. coli strains related to extra-intestinal E. coli. These “pathobionts” exhibit pathogenic properties, but their potential to promote UC is unclear due to the lack of suitable animal models. Here, we established a mouse model using a representative UC pathobiont strain (p19A), and mice lacking single immunoglobulin and toll-interleukin 1 receptor domain (SIGIRR), a deficiency increasing susceptibility to gut infections. p19A was found to adhere to the cecal mucosa of Sigirr−/− mice, causing modest inflammation. Moreover, it dramatically worsened DSS induced colitis, in concert with adherence to, and penetration of the inflamed mucosa. This pathogenicity was lost in a p19A strain lacking the adhesin FimH; following treatment with FimH antagonists, or was attenuated when using a p19A strain lacking a-hemolysin genes. Thus UC pathobionts can worsen the course of colitis in susceptible hosts.
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Yang, H., X. Han, C. Ma, H. Yu, and B. Vallance. "A15 GENETIC OR DIET-ASSOCIATED DEFECTS IN MUCUS FACILITATE ULCERATIVE COLITIS PATHOBIONT-DRIVEN COLITIS." Journal of the Canadian Association of Gastroenterology 6, Supplement_1 (March 1, 2023): 8–9. http://dx.doi.org/10.1093/jcag/gwac036.015.
Abstract:
Abstract Background The Inflammatory Bowel Diseases (IBD), Crohn’s Disease (CD) and ulcerative colitis (UC) affect > 270,000 Canadians and are increasing in incidence. Ileal CD has been linked to the overgrowth of mucosal adherent E. coli. Recent studies have also implicated the adherence of Escherichia coli pathobionts to the colonic mucosa of UC patients. Using the representative UC E. coli pathobiont p19A, we recently demonstrated it aggravated chemical-induced colitis in susceptible mice, through the actions of the toxin alpha-hemolysin, and by adhering to the inflamed colonic mucosa via the adhesin FimH. It is less clear what host factors control susceptibility to the UC pathobionts. One of the potential candidates is the glycosylated mucin (Muc2) which forms the mucus layer that covers the colonic epithelium and is often impaired in UC patients. Purpose To define the role of mucus structure and function in determining susceptibility to the p19A pathobiont, and its ability to cause colitis in mice. Method In vitro growth was assessed to test p19A’s ability to utilize mucin-derived sugars as nutrients. Susceptibility to p19A was tested in two mouse models of colonic mucus impairment. The first is a mouse strain deficient in core 1 derived O-glycans in their intestinal epithelial cells (IEC C1galt1-/-), resulting in reduced Muc2 glycosylation, and thus a thin and impaired mucus barrier. The second model involves feeding wildtype (WT) C57BL/6CR mice a fiber-free (FF) diet, resulting in a significantly thinner colonic mucus layer. The mice were subsequently orally gavaged with p19A and their susceptibility determined by p19A burdens, intestinal histopathology, inflammatory cytokine and short chain fatty acid (SCFA) production. Result(s) When tested in vitro, the p19A pathobiont was found to use an array of mucin-derived sugars as sole carbon source to proliferate. Following oral gavage of WT mice fed a normal diet, immunostaining identified p19A within the colonic mucus but it did not reach the colonic mucosa or cause disease. In contrast, p19A was found at the colonic mucosal surface of mucus-defective IEC C1galt1-/- mice (as compared to IEC C1galt1flox/flox mice) and in WT mice fed a fiber-free diet. This mucosal adherence was associated with increased body weight loss during the course of infection, as well as increased p19A burdens, colonic pathology and pro-inflammatory cytokine expression. Especially fiber-free diet-fed mice showed reduced SCFA levels in their feces at baseline. When the mice were given exogenous SCFA (tributyrin) orally, p19A infection was reduced. Conclusion(s) Our results indicate that UC E. coli pathobionts are able to dwell within colonic mucus and utilize mucin sugars as nutrients. Moreover, they can reach the mucosal surface and induce colitis in hosts suffering genetic or diet-based mucus dysfunction. In part, this susceptibility reflects the important role played by mucus in the production of SCFA, suggesting potential therapeutic approaches for patients suffering UC. Please acknowledge all funding agencies by checking the applicable boxes below CCC, CIHR Disclosure of Interest None Declared
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Fine, Rebecca, Silvio Manfredo Vieira, Daniel Fernando Zegarra Ruiz, and Martin A. Kriegel. "Gut pathobiont translocation induces lymphocyte migration to internal organs in autoimmunity." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 102.16. http://dx.doi.org/10.4049/jimmunol.200.supp.102.16.
Abstract:
Abstract Gut commensal translocation to distant sites can drive autoimmunity. We have evidence that a gut pathobiont, Enterococcus gallinarum, translocates spontaneously to internal organs in the lupus-prone (NZWxBXSB)F1 mouse model to induce systemic autoimmune disease. Lymphocyte migration during commensal translocation to secondary lymphoid organs is not well characterized but may contribute to understanding host-microbiota interactions in autoimmunity. We thus investigated if gut-imprinted lymphocytes migrate to non-gut organs that are progressively colonized by a pathobiont in the (NZWxBXSB)F1 model. We longitudinally characterized gut homing markers on lymphocytes isolated from various tissues of autoimmune-prone F1 mice and monocolonized C57BL/6 mice. In F1 males, circulating CD4+α4β7+ and CD4+CCR9+ cells were increased with age. These subpopulations were reduced after administration of oral antibiotics that deplete the microbiota including E. gallinarum. Next, we monocolonized non-autoimmune prone C57BL/6 mice with E. gallinarum to track lymphocyte migration specifically due to this pathobiont that we have shown to translocate to liver and spleen, induce Th17 responses and autoantibody production. Aged monocolonized C57BL/6 mice harbored greater Peyer’s patch and splenic CD4+ T cells as well as splenic CD4+α4β7+ T cells, supporting that gut-imprinted lymphocytes follow E. gallinarum to non-gut sites. In summary, we linked gut-imprinted lymphocyte migration to internal organs in the setting of systemic autoimmunity that is induced by a translocating pathobiont. Ongoing studies are aimed at determining if these T cells are commensal-reactive and if blockade of gut homing can abrogate autoimmunity.
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Jochum, Lara, and Bärbel Stecher. "Label or Concept – What Is a Pathobiont?" Trends in Microbiology 28, no. 10 (October 2020): 789–92. http://dx.doi.org/10.1016/j.tim.2020.04.011.
Dissertations / Theses on the topic "Pathobiont":
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Jan, Alan. "Accélérer la restauration du microbiote intestinal pour renforcer la résistance à la colonisation contre les entérocoques résistants à la vancomycine." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASB087.
Abstract:
Le tractus gastro-intestinal est un réservoir d'agents pathogènes opportunistes ou de pathobiontes, qui profitent d'une dysbiose pour proliférer chez les patients fragilisés. Les ERV proviennent du tractus gastro-intestinal, où leur prolifération précède la dissémination dans la circulation sanguine et peut conduire à une infection systémique. La compréhension des mécanismes responsables de la résistance à la colonisation intestinale par les ERV est essentielle pour le contrôle des infections. Peu d'études ont identifié les bactéries commensales qui renforcent la résistance à la colonisation du microbiote par les ERV. J'ai cherché à identifier les bactéries commensales qui jouent un rôle clé dans l'effet barrière afin d'accélérer la restauration du microbiote intestinal après dysbiose antibiotique et de renforcer la résistance à la colonisation contre les ERV. J'ai effectué une analyse longitudinale de la composition du microbiote intestinal et des niveaux de portage d'ERV pendant la restauration du microbiote chez des souris colonisées par des ERV après dysbiose induite par des antibiotiques. En combinant les données biologiques et la modélisation mathématique, 15 espèces moléculaires (OTUs) à corrélation négative avec le portage d'ERV ont été identifiées. Six souches représentatives de ces OTU ont été collectées et utilisées en mélange avec une septième souche (Mix7) dans deux lignées de souris différentes colonisées avec l'ERV. Le Mix7 réduit le portage d'ERV et favorise une meilleure récupération du microbiote intestinal. Des différences dans l'effet du Mix7 entre les souris ont été observées avec des souris répondeuses et non répondeuses. Ces différences ont été associées à la variation de la composition pendant la récupération et du microbiote initial, fournissant des biomarqueurs potentiels pour prédire la réponse au Mix7. De plus, j'ai démontré que la souche du phylum Bacteroidota est nécessaire pour l'effet du Mix7 in vivo en présence d'au moins une des 6 autres souches. Dans un modèle murin de dysbiose persitante, des concentrations plus élevées d'acides gras à chaîne courte (acétate, propionate, butyrate) et d'un certain nombre de métabolites, y compris les acides biliaires, ont été observées chez les souris répondeuses par rapport aux souris non-répondeuses et aux souris témoins. Aucun des surnageants des 7 souches, seul ou en combinaison, n'inhibe la croissance de l'ERV in vitro. Il est intéressant de noter que 5 des 7 souches sont partagées entre l'homme et la souris et que 2 ont des équivalents fonctionnels. J'ai montré que la supplémentation avec un mélange de souches identifiées par modélisation mathématique améliore l'effet barrière contre les ERV par des mécanismes dépendant de la récupération et de la composition initiale du microbiote. A terme, ce travail permettra d'aller vers une médecine personnalisée en ciblant les patients à risque et susceptibles de répondre à la supplémentation avec des souches commensales anti-ERV, en fournissant de nouveaux produits biothérapeutiques vivants (LBP) et des biomarqueurs pour prédire la réponse au traitement. Les perspectives sont 1/ d'élargir l'effet à E. faecium pour lequel j'ai adapté un modèle de colonisation, 2/ de mieux comprendre le mécanisme à l'aide d'hypothèses basées sur la modélisation métabolique et en utilisant le milieu de culture que j'ai développé permettant la croissance des 7 souches et de l'ERV, 3/ d'explorer la représentation des espèces clés de l'effet barrière dans les bases de données du microbiome humain et 4/ d'isoler des souches humaines de ces espèces clésThe gastrointestinal tract is a reservoir of opportunistic pathogens or pathobionts, which benefit from dysbiosis to proliferate in fragilised patients. VRE originate from the gastrointestinal tract, where their proliferation precedes dissemination in the bloodstream, and may lead to systemic infection. Understanding the mechanisms responsible for resistance to intestinal colonisation by VRE is essential for infection control. Only few studies have identified commensal bacteria that enhance resistance to colonisation of the microbiota against VRE. I aimed to identify commensal bacteria, key in the barrier effect to accelerate gut microbiota recovery after antibiotic dysbiosis to enhance resistance to colonisation against VRE. I performed a longitudinal analysis of the gut microbiota composition and VRE carriage levels during microbiota recovery in mice colonised with VRE after antibiotic-induced dysbiosis. By combining biological data and mathematical modelling, I identified 15 molecular species (OTUs) that correlate negatively with VRE carriage. Six strains representative of these OTUs have been collected and used in mixture with a seventh strain (Mix7) in two different mice lines challenged with VRE. I found that Mix7 allows a reduction of VRE carriage and a better gut microbiota recovery. Differences in the effect of Mix7 between mice were observed with responder and non-responder mice. These differences were associated with variation in the composition during the recovery and of the initial microbiota, providing potential biomarkers to predict response to Mix7. Furthermore, the Bacteroidota strain is required for Mix7 effect in vivo in the presence of at least one of the 6 other strains. In a mice model of alternative stable state of dysbiosis, higher concentrations were observed in responder compared to non-responder and control mice for short-chain fatty acids (acetate, propionate, butyrate) and for a number of metabolites including bile acids. None of the supernatant of the 7 strains, alone or in combination, inhibits VRE growth in vitro. Interestingly, 5 of the 7 strains are shared between human and mice and 2 have human functional equivalents. I showed that supplementation with a mixture of strains identified through mathematical modelling improves the barrier effect against VRE through mechanisms dependent of the recovery and initial composition of the microbiota. Ultimately, this work will allow to move towards a personalised medicine by targeting patients at risk and susceptible to respond to the supplementation with commensal anti-VRE strains, providing novel lived biotherapeutic products and biomarkers to predict response to treatment. The perspectives are 1/ to extend the effect to E. faecium for which I have adapted a colonisation model, 2/ to better understand the mechanism by implementing hypotheses thanks to metabolic modelling and using the culture medium that I have developed allowing the growth of 7 strains and the VRE, 3/ to explore the representation of the key species in the barrier effect in human microbiome database and 4/ to isolate human strains of these key species
2
Larousse, Marie. "Étude de l’interaction entre Phytophthora parasitica et le microbiote rhizosphérique à la surface de la plante hôte Solanum lycopersicum." Thesis, Nice, 2016. http://www.theses.fr/2016NICE4038.
Abstract:
Les oomycètes phytopathogènes ont co-évolué avec les microbiotes des plantes hôtes. Il en résulte la formation de biofilms et des réseaux complexes d’interactions dont nous commençons juste à comprendre l’incidence sur la biologie et la virulence des oomycètes. Déterminer la nature de ces interactions et leur rôle dans le contexte d’une infection est aujourd’hui un enjeu cognitif qui concerne la caractérisation des mécanismes moléculaires et communautaires sous-jacents. C’est également une opportunité en termes d’innovation pour élaborer des méthodes de lutte alternative à l’usage de fongicides. Dans ce contexte, ce travail de thèse a consisté à étudier, d’une part, la formation de biofilm chez Phytophthora parasitica, un oomycète polyphage et tellurique, ainsi que, d’autre part, les interactions au sein de ce biofilm entre P. parasitica et le microbiote procaryote rhizosphérique de la plante hôte Solanum lycopersicum. L’analyse du génome de P. parasitica et du transcriptome du biofilm a conduit à la caractérisation d’une nouvelle famille de mucines restreinte à la lignée des oomycètes, les protéines MUCL. Ces 315 protéines sécrétées (25-30 kDa) sont réparties en 15 groupes et possèdent deux domaines : un domaine hautement conservé de fonction inconnue ; un domaine caractéristique des mucines, riche en résidus Sérine et Thréonine avec de très nombreux sites putatifs d’O-glycosylation. Chez P. parasitica, les 3 gènes PPMUCL1/2/3 sont exprimés et co-régulés spécifiquement au stade biofilmThe interactions between a pathogen and the host surface resident microbiota are critical to disease outbreak. These interactions shape the distribution, the density and the genetic diversity of inoculum. However for most plant pathogens how each of these interactions acts on disease as a single one or as a member of a functional network remains to be specified. This issue is addressed here through the analysis of two types of interactions involving the polyphagous oomycete P.parasitica : (i) the intraspecific interaction that leads to monospecific biofilm formation by P. parasitica zoospores on plant surface; (ii) the interspecific interactions that occur between P. parasitica biofilm and the prokaryotic microbiota of Solanum lycopersicum rhizosphere. The biology of monospecific biofilm is investigated through the characterization of MUCL, a new oomycete-specific Mucin-like Protein family. Gene profiling, biochemical and immunohistological analyses define the extent of this family and lead to identify three members, PPMUCL1/2/3, as residing in P. parasitica biofilm. The Phytophthora parasitica-Microbiota interaction is explored using first a metagenomic approach. Two microbial metagenomes derived from a soil of a tomato greenhouse is defined and compared after 16S RNA gene sequencing: M1 which corresponds to the sub-rhizospheric microbiota able to colonize the roots of axenic tomato seedlings; M2, the sub-microbiota able to colonize the tomato seedling roots previously coated with P. parasitica monospecific biofilm. A representative collection of microorganisms from M2 were also obtained through in vitro selection on a medium prepared from P. parasitica extract
3
Larousse, Marie. "Étude de l’interaction entre Phytophthora parasitica et le microbiote rhizosphérique à la surface de la plante hôte Solanum lycopersicum." Electronic Thesis or Diss., Nice, 2016. http://www.theses.fr/2016NICE4038.
Abstract:
Les oomycètes phytopathogènes ont co-évolué avec les microbiotes des plantes hôtes. Il en résulte la formation de biofilms et des réseaux complexes d’interactions dont nous commençons juste à comprendre l’incidence sur la biologie et la virulence des oomycètes. Déterminer la nature de ces interactions et leur rôle dans le contexte d’une infection est aujourd’hui un enjeu cognitif qui concerne la caractérisation des mécanismes moléculaires et communautaires sous-jacents. C’est également une opportunité en termes d’innovation pour élaborer des méthodes de lutte alternative à l’usage de fongicides. Dans ce contexte, ce travail de thèse a consisté à étudier, d’une part, la formation de biofilm chez Phytophthora parasitica, un oomycète polyphage et tellurique, ainsi que, d’autre part, les interactions au sein de ce biofilm entre P. parasitica et le microbiote procaryote rhizosphérique de la plante hôte Solanum lycopersicum. L’analyse du génome de P. parasitica et du transcriptome du biofilm a conduit à la caractérisation d’une nouvelle famille de mucines restreinte à la lignée des oomycètes, les protéines MUCL. Ces 315 protéines sécrétées (25-30 kDa) sont réparties en 15 groupes et possèdent deux domaines : un domaine hautement conservé de fonction inconnue ; un domaine caractéristique des mucines, riche en résidus Sérine et Thréonine avec de très nombreux sites putatifs d’O-glycosylation. Chez P. parasitica, les 3 gènes PPMUCL1/2/3 sont exprimés et co-régulés spécifiquement au stade biofilmThe interactions between a pathogen and the host surface resident microbiota are critical to disease outbreak. These interactions shape the distribution, the density and the genetic diversity of inoculum. However for most plant pathogens how each of these interactions acts on disease as a single one or as a member of a functional network remains to be specified. This issue is addressed here through the analysis of two types of interactions involving the polyphagous oomycete P.parasitica : (i) the intraspecific interaction that leads to monospecific biofilm formation by P. parasitica zoospores on plant surface; (ii) the interspecific interactions that occur between P. parasitica biofilm and the prokaryotic microbiota of Solanum lycopersicum rhizosphere. The biology of monospecific biofilm is investigated through the characterization of MUCL, a new oomycete-specific Mucin-like Protein family. Gene profiling, biochemical and immunohistological analyses define the extent of this family and lead to identify three members, PPMUCL1/2/3, as residing in P. parasitica biofilm. The Phytophthora parasitica-Microbiota interaction is explored using first a metagenomic approach. Two microbial metagenomes derived from a soil of a tomato greenhouse is defined and compared after 16S RNA gene sequencing: M1 which corresponds to the sub-rhizospheric microbiota able to colonize the roots of axenic tomato seedlings; M2, the sub-microbiota able to colonize the tomato seedling roots previously coated with P. parasitica monospecific biofilm. A representative collection of microorganisms from M2 were also obtained through in vitro selection on a medium prepared from P. parasitica extract
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Romano, Sara. "Dynamique des populations et communautés bactériennes au cours de l’hospitalisation et des infections associées aux soins : cas particulier de la chirurgie cardiaque." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONT3515.
Abstract:
Les microbiotes humains sont considérés comme des organes supplémentaires impliqués dans des pathologies diverses, y compris infectieuses. Les déséquilibres des microbiotes, ou dysbioses, créent des niches écologiques pathologiques ou pathobiomes. Ce nouveau paradigme de l'infection s'applique tout particulièrement aux infections opportunistes. Dans ce travail, nous considérons des infections associées aux soins (IAS), les infections du site opératoire en chirurgie cardiaque, comme le résultat d'une pathologie de niche et nous étudions la dynamique des communautés et des populations microbiennes comme conditions d'émergence et de succès de l'agent infectieux. La diversité et la dynamique du microbiote chirurgical superficiel et profond de patients opérés pour pontage aorto-coronarien montrent un remplacement partiel du microbiote pré-opératoire par un microbiote spécifique avec une résilience partielle lors de la cicatrisation. Un lien significatif est observé entre la composition microbiotique et les marqueurs de risque infectieux. Le suivi de la structure de population d'un agent pathogène reconnu en chirurgie cardiaque, Propionibacterium acnes, montre des fréquences différentielles de phylotypes selon les phases opératoires. La spécificité du microbiote opératoire consiste en une forte diversité de bactéries à Gram négatif dont certaines ont été décrites dans le microbiote de la peau saine. Nous avons réalisé une identification au niveau de l'espèce de ces bactéries de la peau saine qui s'avèrent atypiques parmi les bactéries humaines connues car elles évoquent une origine environnementale. Le réservoir cutané et non environnemental d'un pathogène opportuniste, Roseomonas mucosa, est démontré et trois populations de pathogène opportuniste à réservoir environnemental et/ou humain (Pseudomonas aeruginosa, Ochrobactrum antropi, O. intermedium) sont étudiés en termes de structure de population pour préciser les conditions de leur transmission et leur succès infectieux dans le contexte général du pathobiome et des niches écologiques perturbées. Ce contexte général permet d'organiser les résultats obtenus à diverses échelles (communauté, populations, espèces, phylotypes) pour proposer une vision intégrée et originale de la microbiologie des IASHuman microbiota are now considered as supplementary organs involved in diseases such as infections. Microbiota disequilibrium named dysbiosis creates impaired ecological niches (pathobiomes). This new paradigm of infection is particularly relevant for opportunistic infections. In this study, we consider one major type of healthcare associated infection (HAI), the surgical site infections after cardiothoracic surgery as a pathology of niche. We study the dynamics of microbial communities and populations as conditions for emergence and success of infectious agents.The diversity and dynamics of superficial and deep surgical microbiota in patients undergoing coronary artery bypass grafting show a partial replacement of the pre-operative microbiota by a specific surgical microbiota with partial resilience during healing. Significant links are found between microbiota composition and scores for infectious risk. The population structure of Propionibacterium acnes, a pathogen complicating cardiac surgery, shows variable frequencies of phylotypes according to operative stages. Surgical microbiota appears specific with high diversity of Gram-negative bacteria, some of them being previously described in healthy skin microbiota. At the species-level, these bacteria appear atypical among known human bacteria because they are related to environmental bacteria. We demonstrate the cutaneous reservoir of the opportunistic pathogen Roseomonas mucosa deemed, until now, to be environmental. Three populations of opportunistic pathogens (Pseudomonas aeruginosa, Ochrobactrum anthropi, O. intermedium) are structured in order to precise their transmission and their infectivity in the general context of impaired ecological niche and pathobiome.The results obtained at various microbiological scale (community, population, species, phylotype) are organized in this general context in order to delineate an original integrative vision of HAI
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Pauvert, Charlie. "Comparaison et évaluation d’approches bioinformatiques et statistiques pour l'analyse du pathobiome des plantes cultivées." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0214/document.
Abstract:
Les interactions entre micro-organismes sous-tendent de nombreux services écosystémiques, y compris la régulation des maladies des plantes cultivées. Un acteur de cette régulation est le pathobiome, défini comme le sous-ensemble des micro-organismes associés à une plante hôte en interaction avec un agent pathogène. L'un des défis actuels consiste à reconstruire les pathobiomes à partir de données de metabarcoding, pour identifier des agents potentiels de biocontrôle et pour surveiller en temps réel leurs réponses aux changements environnementaux. Plusieurs verrous méthodologiques doivent cependant être levés pour atteindre ces objectifs. Tout d’abord, il n’existe pas de consensus concernant l’approche bioinformatique la plus fiable pour déterminer l’identité et l’abondance des micro-organismes présents dans les échantillons végétaux. De plus, les réseaux microbiens construits avec les méthodes actuellement disponibles sont des réseaux d’associations statistiques entre des comptages de séquences, non directement superposables aux réseaux d’interactions (ex : compétition, parasitisme) entre micro-organismes. L’objectif de la thèse était donc de déterminer les approches bioinformatiques et statistiques les plus pertinentes pour reconstruire des réseaux d’interactions microbiennes à partir de données de metabarcoding. Le modèle d’étude était la vigne (Vitis vinifera L. cv. Merlot noir) et l’oïdium de la vigne, Erysiphe necator. Nous avons tout d’abord déterminé l’approche bioinformatique la plus adaptée pour identifier la communauté fongique associée à ce pathogène, en comparant la capacité de 360 pipelines à retrouver la composition d’une communauté artificielle de 189 souches fongiques. DADA2 est apparu comme l’outil le plus performant. Nous avons ensuite évalué l’influence de la pratique culturale (viticulture conventionnelle vs. biologique) sur les communautés fongiques des feuilles et évalué le niveau de réplicabilité des réseaux microbiens construits avec une méthode d’inférence classique, SparCC. La réplicabilité était très faible, jetant ainsi un doute sur l’utilité de ces réseaux pour le biocontrôle et la biosurveillance. Nous avons donc utilisé une nouvelle approche statistique, le modèle PLN, qui permet de prendre en compte la variabilité environnementale, pour explorer finement le pathobiome d’Erysiphe necator. Les interactions microbiennes prédites par le modèle sont en cours de comparaison avec des expériences de confrontations de levures en co-cultures. Une approche alternative, HMSC, a également été testée sur un autre modèle biologique et certaines prédictions ont été confrontées avec succès aux données de la littérature. Les réseaux microbiens, sous réserve d’amélioration des méthodes de reconstruction, pourraient donc être utilisés pour capturer les signaux des interactions biotiques dans le pathobiomeInteractions between microorganisms underpin many ecosystem services, including the regulation of crop diseases. An actor in this regulation is the pathobiome, defined as the subset of microorganisms associated with a host plant in interaction with a pathogen. One of the current challenges is to reconstruct pathobiomes from metabarcoding data, in order to identify potential biocontrol agents and to monitor in real time their responses to environmental changes. However, several methodological hurdles must be overcomed to achieve these objectives. First, there is no consensus on the most reliable bioinformatics approach to determine the identity and abundance of microorganisms present in plant samples. In addition, microbial networks built with currently available methods are networks of statistical associations between sequence counts, not directly related to networks of interactions (e. g. competition, parasitism) between microorganisms. The objective of the thesis was therefore to determine the most relevant bioinformatics and statistical approaches to reconstruct microbial interaction networks from metabarcoding data. The study system was grapevine (Vitis vinifera L. cv. Merlot noir) and the fungal agent of grapevine powdery mildew Erysiphe necator. First, we determined the most appropriate bioinformatics approach to identify the fungal community associated with this pathogen, by comparing the ability of 360 pipelines to recover the composition of an artificial community of 189 fungal strains. DADA2 has emerged as the most powerful tool. We then evaluated the influence of the cropping system (conventional vs. organic viticulture) on foliar fungal communities and assessed the level of replicability of microbial networks built with a standard inference method, SparCC. Replicability was very low, casting doubt on the usefulness of these networks for biocontrol and biomonitoring We therefore used a new statistical approach, the PLN model, which allows us to take into account environmental variability, to finely explore the pathobiome of Erysiphe necator. The microbial interactions predicted by the model are being compared with experiments confronting yeasts in co-cultures. An alternative approach, HMSC, was also tested on another biological model and some predictions were successfully compared with the data in the literature. Microbial networks, provided improved reconstruction methods, could therefore be used to capture signals of biotic interactions in the pathobiome
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Tröger, Hanno [Verfasser]. "Wirkungsweise von Pathogenen, Pathobionten und Probiotika auf die epitheliale Transport- und Barrierefunktion des Darms / Hanno Tröger." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1123071632/34.
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Chow, Janet. "A Pathobiont of the Mammalian Microbiota Balances Intestinal Inflammation and Colonization." Thesis, 2011. https://thesis.library.caltech.edu/6368/1/Chow%2C_Janet_Thesis.pdf.
Abstract:
Humans and mammals are colonized by a multitude of microbial organisms that have co‐evolved with their hosts for millions of years. The majority of these microbes reside in the gastrointestinal (GI) tract as a complex and dynamic consortium. Though most associations with the host are symbiotic or commensal, some resident bacteria have the potential to cause disease under certain conditions. We refer to these bacteria as ‘pathobionts.’ Pathobionts are distinct from opportunistic pathogens, which are often acquired from the environment and cause acute infections. Bacterial type VI secretion systems (T6SSs) are one mechanism for mediating close host‐microbial interactions. Herein we report that the T6SS of H. hepaticus, a pathobiont of the murine intestinal microbiota, mediates critical protective functions during association with its mammalian host. In cell cultures, infection of intestinal epithelial cells (IECs) with H. hepaticus T6SS mutants results in increased bacterial association compared to wild‐type bacteria. In animals, T6SS mutants colonize the lower GI tract to a higher degree. Most importantly, H. hepaticus defective in type VI secretion is unable to restrain potent innate and adaptive immune responses in an animal model of experimental colitis. In addition, the H. hepaticus T6SS directs an anti‐inflammatory gene expression profile in IECs, and CD4+ T cells from mice colonized with T6SS mutants produce increased proinflammatory interleukin‐17 cytokine in response to IECs presenting H. hepaticus antigens. Thus, our findings reveal that H. hepaticus has evolved a T6SS as a mechanism to actively maintain a non‐pathogenic, symbiotic relationship in the GI tract by regulating bacterial colonization and host inflammation. Disturbances in the dynamic interaction between gut bacteria and the intestinal immune system may lead to exacerbated host inflammation. As intestinal bacteria profoundly influence host biology, our findings support an emerging hypothesis that alterations in the composition of the microbiota, known as dysbiosis, is a critical factor in various human disorders such as inflammatory bowel disease and colon cancer.
Books on the topic "Pathobiont":
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Spatz, Linda Ann, Judith A. James, and Gregg Joshua Silverman, eds. Pathogens, Pathobionts and Autoimmunity. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-546-6.
Book chapters on the topic "Pathobiont":
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Dimkić, Ivica, Aleksandra Jelušić, Katarina Kruščić, and Tamara Janakiev. "Pathobiome and Microbial Community Shifts Associated with Vegetable, Fruit, and Cereal Crops." In Plant Pathogen Interaction, 237–58. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-4890-1_9.
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Bez, Cristina, Hang Dinh Thuy, Minh Nguyen Hong, Iris Bertani, and Vittorio Venturi. "Pathobiome Studies as a Way to Identify Microbial Co-operators and/or Antagonists of the Incoming Plant Pathogen." In Innovations in Land, Water and Energy for Vietnam’s Sustainable Development, 53–65. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51260-6_6.
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Stewart, Jane E., Mee-Sook Kim, Bradley Lalande, and Ned B. Klopfenstein. "Pathobiome and microbial communities associated with forest tree root diseases." In Forest Microbiology, 277–92. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-822542-4.00004-8.
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Bateman, Kelly S., Stephen W. Feist, John P. Bignell, David Bass, and Grant D. Stentiford. "Marine pathogen diversity and disease outcomes." In Marine Disease Ecology, 3–44. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198821632.003.0001.
Abstract:
This chapter provides an introduction to important marine pathogens, providing an overview of the diversity of pathogen types and how they affect different hosts in the marine environment. The chapter focuses on wild and cultured species and highlights that single infections are relatively rare, with co- and secondary infections being commonplace. The authors highlight the importance of understanding “normal” host tissue structure prior to interpreting pathological changes and outline the role of histology to assess pathogenicity of emerging diseases, linking presence of individual pathogens and co-infections with degree of host response. Fact sheets focus on the pathology (i.e., interaction of a specific pathogen group with the host cell/system) with high-quality histology and TEM images, emphasizing tissue changes caused by pathogens, and point the reader to presumptive diagnosis via histology while highlighting the need for confirmatory testing via other means. The pathobiome concept is introduced and explained, and the utility for predicting outcomes at the individual and population levels discussed.
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Coates, Christopher J. "Diseases of chelicerates." In Invertebrate Pathology, 219–48. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780198853756.003.0009.
Abstract:
Chelicerates represent one of the oldest and second most speciose groups within the Phylum Arthropoda. Often referred to as ‘living fossils’, extant chelicerates inhabit terrestrial and aquatic ecosystems. Spiders, scorpions, ticks, and mites are usually mistaken for insects, just as horseshoe crabs are misidentified as crustaceans. The biological and commercial importance of chelicerates cannot be overstated; members represent vectors of devastating animal and plant diseases (acarids), wielders of poisons and venoms (arachnids), and critical for the detection of bacterial contaminants in pharmaceuticals (horseshoe crabs). For many of the chelicerates (e.g. pycnogonids), there is a knowledge deficit with respect to host-pathogen antibiosis and histopathological condition. From the available literature, the book lungs and book gills are critical sites of pathogen dissemination throughout the haemocoel. Recent data gathered using high throughput sequencing reveals spiders as rich sources of endosymbionts and pathobionts. More broadly, research efforts are focussed on integrated pest management strategies using acaropathogenic and araneogenous fungi for controlling terrestrial chelicerate pests. This chapter represents the first extensive review of the diseases and pathobiology of chelicerates in the context of their innate immune defences. Much information has been accrued from captive settings, such as scorpions from zoological collections and horseshoe crabs in aquaria.
Conference papers on the topic "Pathobiont":
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Azzouz, Doua F., Jill P. Buyon, and Gregg J. Silverman. "AI-26 Intestinal IGA as pathfinders to identify microbiome pathobiont candidates in SLE." In Abstracts of the Third Biannual Scientific Meeting of the North and South American Lupus Community, Armonk, New York, USA, September 29 – October 1, 2016. Lupus Foundation of America, 2016. http://dx.doi.org/10.1136/lupus-2016-000179.26.
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Silverman, Gregg J., Macintosh Cornwell, Peter Izmirly, Jill Buyon, Doua F. Azzouz, and Kelly Ruggles. "1103 Lupus clinical flares in patients with gut pathobiont blooms share a novel peripheral blood transcriptomic immune activation profile." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.68.
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Pereira, M. S., K. Stuhlträger, N. Effelsberg, A. Rajput Khokhar, S. Redanz, H. Ebid, B. Hansen, et al. "OP0047 FASTING MODULATES THE HUMAN GUT MICROBIOME AND REDUCES AN IL-17+/IFNG+ T CELL-INDUCING GUT PATHOBIONT IN PATIENTS WITH RHEUMATOID ARTHRITIS." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.3302.
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Khomyakova, T. I., and Yu N. Khomyakov. "PATHOBIOM: STAGES OF FORMATION AND WAYS OF MANAGEMENT." In INNOVATIVE TECHNOLOGIES IN SCIENCE AND EDUCATION. DSTU-Print, 2020. http://dx.doi.org/10.23947/itno.2020.306-310.
Abstract:
An increase in the incidence and mortality of the population from pathologies associated with the formation of the pathobiome as a stable community of microorganisms occurs simultaneously with an increase in the proportion of antibiotic-resistant microorganisms in these communities. The formation of a pathobiome inevitably leads to the development of an immunodeficiency state and an increase in sensitivity to viral infections. The paper describes the stages of pathobiome formation and its main characteristics. Approaches have been formulated to prevent its pathobiome formation or reduce its stability, ensuring the effectiveness of correction. Experimental studies of pathobiome formation are described.
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Li, L., M. Mac Aogáin, T. Xu, T. Jaggi, L. L Y Chan, J. Qu, L. Wei, et al. "Neisseria species as pathobionts in bronchiectasis." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1566.
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Jaggi, T., M. Mac Aogáin, H. R. Keir, A. Dicker, T. Xu, M. S. Koh, T. H. Ong, et al. "Neisseria Species as Novel Respiratory Pathobionts in Bronchiectasis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3903.
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Aogáin, Micheál Mac, Li Liang, Tengfei Xu, Tavleen Jaggi, Louisa L. Y. Chan, Holly R. Keir, Alison J. Dicker, et al. "Characterizing Neisseria spp. as novel respiratory pathobionts in bronchiectasis." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2060.
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Fernandez-Barat, L., R. López-Aladid, V. Alcaraz, N. Vázquez, L. Bueno, R. Pastor, L. Lingren, et al. "The Mucoid Pathobiome and Its Clinical Implications in Non-Cystic Fibrosis Bronchiectasis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2001.
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"Actinidia host genetic background dictates oomycete pattern in the Kiwifruit Vine Decline Syndrome pathobiome." In IS-MPMI Congress. IS-MPMI, 2023. http://dx.doi.org/10.1094/ismpmi-2023-12.
Abstract:
Kiwifruit Vine Decline Syndrome (KVDS) is the most important soil-borne disease within Italian kiwifruit industry, causing €300,000 of economic losses in 2020 alone. So far, the KVDS’ aetiological agents belong primarily to the oomycetes. Since no effective management strategies exist yet, the most promising approach to overcoming KVDS is therefore the use of resistant species as rootstocks or for breeding programmes. Several Actinidia genotypes showing different resistance’ rates to KVDS were grown in disease-promoting soils. A metabarcoding approach was set up to identify the oomycetes associated with KVDS and investigate whether the primary involved specie(s) can vary according to plant genotype. Our results clearly showed significant differences between genotypes in terms of oomycetes detected in both plant rhizosphere and endosphere, which correlated strongly with the symptoms displayed. We found that the resistance of A. macrosperma to KVDS is related to its ability to shape the pathobiome, particularly as far as the endosphere is concerned. Under our conditions, Phytophthora sp. subclade7b (Yang et al., 2017) was found predominantly in sensitive genotypes; whilst Globisporangium intermedium was detected mainly in asymptomatic plants, suggesting that the latter might compete with Phytophthora sp. recruitment in resistant plants, and explain the occurrence of symptoms and resistance.