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Автор: Grafiati
Опубліковано: 7 липня 2024
Оновлено: 7 липня 2024

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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.

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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.

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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.

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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.

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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.

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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.

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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.
7

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.

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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.
8

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.

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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
9

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.

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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.
10

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.

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11

Chassaing, Benoit, and Andrew T. Gewirtz. "Pathobiont hypnotises enterocytes to promote tumour development." Gut 63, no. 12 (April 29, 2014): 1837–38. http://dx.doi.org/10.1136/gutjnl-2014-306890.

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12

Meghil, Mohamed M., and Christopher W. Cutler. "Oral Microbes and Mucosal Dendritic Cells, “Spark and Flame” of Local and Distant Inflammatory Diseases." International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1643. http://dx.doi.org/10.3390/ijms21051643.

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Mucosal health and disease is mediated by a complex interplay between the microbiota (“spark”) and the inflammatory response (“flame”). Pathobionts, a specific class of microbes, exemplified by the oral microbe Porphyromonas gingivalis, live mostly “under the radar” in their human hosts, in a cooperative relationship with the indigenous microbiota. Dendritic cells (DCs), mucosal immune sentinels, often remain undisturbed by such microbes and do not alert adaptive immunity to danger. At a certain tipping point of inflammation, an “awakening” of pathobionts occurs, wherein their active growth and virulence are stimulated, leading to a dysbiosis. Pathobiont becomes pathogen, and commensal becomes accessory pathogen. The local inflammatory outcome is the Th17-mediated degenerative bone disease, periodontitis (PD). In systemic circulation of PD subjects, inflammatory DCs expand, carrying an oral microbiome and promoting Treg and Th17 responses. At distant peripheral sites, comorbid diseases including atherosclerosis, Alzheimer’s disease, macular degeneration, chronic kidney disease, and others are reportedly induced. This review will review the immunobiology of DCs, examine the complex interplay of microbes and DCs in the pathogenesis of PD and its comorbid inflammatory diseases, and discuss the role of apoptosis and autophagy in this regard. Overall, the pathophysiological mechanisms of DC-mediated chronic inflammation and tissue destruction will be summarized.
13

Hecht, Aaron, and Juliane Bubeck Wardenburg. "975 Pathobiont Colonization Resistance by Type VI Secretion." Gastroenterology 150, no. 4 (April 2016): S198. http://dx.doi.org/10.1016/s0016-5085(16)30743-0.

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14

Pereira, Márcia S., and Martin A. Kriegel. "Evolving concepts of host–pathobiont interactions in autoimmunity." Current Opinion in Immunology 80 (February 2023): 102265. http://dx.doi.org/10.1016/j.coi.2022.102265.

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15

Siak, Jay, Anthony St. Leger, Kumarkrishna Raychaudhuri, Mary Mattapallil, Ivan J. Fuss, Raphaela Goldbach-Mansky, Warren Strober, and Rachel R. Caspi. "Commensal microbiota as possible pathobiont in autoinflammatory disease." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 120.26. http://dx.doi.org/10.4049/jimmunol.202.supp.120.26.

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Abstract The ocular surface has an associated microbiome that contributes to maintenance of local immune homeostasis and protects the ocular surface from fungal and bacterial infections. However, in individuals with a dysregulated immune response, commensal flora could cause pathology. In this study, we seek to understand how an ocular commensal colonizing humans and mice, C. mastitidis (C. mast), stimulates immunity in the immunologically perturbed host. Cryopyrin Associated Periodic Syndrome (CAPS) patients suffer from systemic and ocular autoinflammatory disease caused by a hyperactive NLRP3 inflammasome. Knock-in mice bearing a mutated NLRP3 gene cloned from a CAPS patient responded to ocular colonization with C. mast by increased conjunctival neutrophilia, which progressed to overt ocular surface disease. Compared to wild type (WT) controls, their BM dendritic cells produced elevated IL-1 in response to C. mast. Additionally, gd T cells, which were primarily the Vg4 subset, isolated from eye-draining lymph nodes of C. mast-associated mutant mice were more activated and produced more IL-17, suggesting a qualitatively analogous but quantitatively amplified response compared to WT. Importantly, the same commensal elicited strongly elevated IL-17 production from leukocytes of inflammasome disease patients when compared with healthy controls. Our results suggest that C. mast induces an abnormal immune response in the NLRP3 mutant and acts as a pathobiont, in contrast to its behavior in the immunologically normal host. Based on these data, we hypothesize that the recurrent non-infectious conjunctivitis observed in CAPS patients may be driven by a hyperactive immune response to their own ocular surface bacteria.
16

Guerrini, Matteo M., Alexis Vogelzang, and Sidonia Fagarasan. "A Hen in the Wolf Den: A Pathobiont Tale." Immunity 48, no. 4 (April 2018): 628–31. http://dx.doi.org/10.1016/j.immuni.2018.04.003.

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17

Kim, Donghyun, and Wan-Uk Kim. "Editorial: CanPrevotella copriBe a Causative Pathobiont in Rheumatoid Arthritis?" Arthritis & Rheumatology 68, no. 11 (October 27, 2016): 2565–67. http://dx.doi.org/10.1002/art.39807.

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18

A. James, Stephen, Sarah Phillips, Andrea Telatin, David Baker, Rebecca Ansorge, Paul Clarke, Lindsay J. Hall, and Simon R. Carding. "Preterm Infants Harbour a Rapidly Changing Mycobiota That Includes Candida Pathobionts." Journal of Fungi 6, no. 4 (November 9, 2020): 273. http://dx.doi.org/10.3390/jof6040273.

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Fungi and the mycobiome are a fundamental part of the human microbiome that contributes to human health and development. Despite this, relatively little is known about the mycobiome of the preterm infant gut. Here, we have characterised faecal fungal communities present in 11 premature infants born with differing degrees of prematurity and mapped how the mycobiome develops during early infancy. Using an ITS1 sequencing-based approach, the preterm infant gut mycobiome was found to be often dominated by a single species, typically a yeast. Candida was the most abundant genus, with the pathobionts C.albicans and C.parapsilosis highly prevalent and persistent in these infants. Gestational maturity at birth affected the distribution and abundance of these Candida, with hospital-associated C.parapsilosis more prevalent and abundant in infants born at less than 31 weeks. Fungal diversity was lowest at 6 months, but increased with age and change of diet, with food-associated Saccharomycescerevisiae most abundant in infants post weaning. This study provides a first insight into the fungal communities present within the preterm infant gut, identifying distinctive features including the prominence of pathobiont species, and the influence age and environmental factors play in shaping the development of the mycobiome.
19

Lau, Trevor C., Aline A. Fiebig-Comyn, Christopher R. Shaler, Joseph B. McPhee, Brian K. Coombes, and Jonathan D. Schertzer. "Low dietary fiber promotes enteric expansion of a Crohn’s disease-associated pathobiont independent of obesity." American Journal of Physiology-Endocrinology and Metabolism 321, no. 3 (September 1, 2021): E338—E350. http://dx.doi.org/10.1152/ajpendo.00134.2021.

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It is commonly thought that obesity or a high-fat diet alters pathogenic bacteria and promotes inflammatory gut diseases. We found that lower dietary fiber is a key factor that expands a gut pathobiont linked to Crohn’s disease, independent of obesity status in mice.
20

Singh, Shivani, and Leopoldo N. Segal. "A lung pathobiont story: Thinking outside the Koch’s postulate box." Cell Host & Microbe 30, no. 9 (September 2022): 1196–98. http://dx.doi.org/10.1016/j.chom.2022.08.012.

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21

Jellbauer, Stefan, and Manuela Raffatellu. "An intestinal arsonist: pathobiont ignites IBD and flees the scene." Gut 63, no. 7 (September 11, 2013): 1034–35. http://dx.doi.org/10.1136/gutjnl-2013-305589.

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22

Meisner, Jeffrey, Toni Bransford, Kelsey Miller, Jackson Lee, Adarsh Jose, Michael Giuggio, Megan McComb, et al. "THE SYNTHETIC GLYCAN KB295 OPTIMIZES MICROBIOME COMPOSITION AND FUNCTION IN ULCERATIVE COLITIS – RESULTS FROM A PROOF OF PRINCIPLE HUMAN STUDY." Inflammatory Bowel Diseases 28, Supplement_1 (January 22, 2022): S70—S71. http://dx.doi.org/10.1093/ibd/izac015.114.

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Abstract The pathogenesis of ulcerative colitis (UC) involves genetic susceptibility, immune-mediated tissue injury and environmental factors including disturbances of the gut microbiota. Nearly all current approved therapies modify host immunity, rather than directly targeting the microbiota. Fecal microbiota transplantation provides encouraging evidence for the therapeutic potential of gut microbiome modulation. Bacteria in the GI tract are ecologically differentiated by their ability to use specific glycans as growth substrates, making glycans a promising and safe alternative to target the microbiome. To explore this, we used an ex vivo fecal microbiota culture system to identify a synthetic glycan (KB295) with desirable microbiological activity and conducted a proof of principle study of safety and tolerability of KB295 in patients with UC. Fecal microbial communities from healthy subjects were incubated anaerobically with and without (negative control) KB295. KB295 increased short chain fatty acid (SCFA) production across ten fecal samples to a median concentration of 47.0 mM compared to 15.2 mM with the negative control in culture supernatants, including increases in acetate, propionate, and butyrate in all cases. Metagenomic sequencing of the ex vivo fecal pellets revealed that KB295 depleted pathobionts in the family Enterobacteriaceae to a median relative abundance of 10.8% compared to 38.2% with the negative control. Pathobiont depletion was associated with enrichments of diverse genera in the phyla Bacteroidetes and Firmicutes. Twelve patients with mild to moderate UC were enrolled in an open-label single-arm study with an 8-week intake of KB295. KB295 was well tolerated with generally mild adverse events, and only one AE resulted in discontinuation. The most frequently occurring adverse events were changes in bowel habit, flatulence, and headache. Fecal calprotectin and lactoferrin decreased by median values of 69.0% (n=11) and 86.0% (n=6), respectively, from screening to the end of the KB295 intake. Consistent with the ex vivo preclinical findings, of the subjects for whom we have data to date, the relative abundance of the fecal pathobiont family Enterobacteriaceae decreased from five participants, and the commensal genus Parabacteroides was enriched in four of five participants. These results establish a proof of principle for the glycobiological modulation of gut microbiome composition and function and provide insight into the potential utility of this strategy in patients with ulcerative colitis. The safety, tolerability, and encouraging evidence for reduced inflammation with KB295 call for a Phase 2 study, which is planned.
23

Manfredo Vieira, S., M. Hiltensperger, V. Kumar, D. Zegarra-Ruiz, C. Dehner, N. Khan, F. R. C. Costa, et al. "Translocation of a gut pathobiont drives autoimmunity in mice and humans." Science 359, no. 6380 (March 8, 2018): 1156–61. http://dx.doi.org/10.1126/science.aar7201.

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24

Chow, Janet, and Sarkis K. Mazmanian. "A Pathobiont of the Microbiota Balances Host Colonization and Intestinal Inflammation." Cell Host & Microbe 7, no. 4 (April 2010): 265–76. http://dx.doi.org/10.1016/j.chom.2010.03.004.

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25

Vieira, Silvio Manfredo, Michael Hiltensperger, Varun Kumar, Daniel Zegarra-Ruiz, Carina Anja Dehner, Andrea Barbieri, Dhanpat Jain, Andrew Goodman, and Martin A. Kriegel. "Spontaneous translocation of a human enterococcal gut pathobiont drives systemic autoimmunity." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 162.10. http://dx.doi.org/10.4049/jimmunol.200.supp.162.10.

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Abstract Host-microbiota interactions in the pathogenesis of autoimmunity remain poorly understood. Here, we show that a gut commensal, Enterococcus gallinarum, reaches lymphocytes beyond the gut barrier in the mesenteric lymph node, liver and spleen of lupus-prone (NZWxBXSB)F1 mice. Oral vancomycin treatment suppressed growth of E. gallinarum in tissues of these mice, prevented organ manifestations and mortality by lowering pathogenic autoantibodies, Th17 and Tfh cells. Hepatocyte-commensal cocultures revealed induction of the lupus signature cytokine IFN-α as well as the AhR pathway (AhR, Cyp1a1, Cyp1a2) that could be linked to Th17 induction in vivo. E. gallinarum monocolonization in germ-free C57BL/6 animals allowed for translocation to internal organs and induction of autoantibodies as well as increase of lamina propria plasmacytoid dendritic cells (pDCs) and systemic Th17 cells. Additionally, RNA-Seq of short-term ileum E. gallinarum-monocolonized mice demonstrated induction of molecules related to barrier function (occludin, claudins, Plvap, Axin2), the mucus layer (mucin, Fut2), antimicrobial defence (Reg3b, Defa2), and inflammation and pDC induction (AhR/Cyp1a1, Enpp3). Species-specific PCR of sterilely obtained liver tissue from autoimmune hepatitis and lupus patients revealed also E. gallinarum, suggesting similar processes in humans. Accordingly, human hepatocyte-commensal coculture demonstrated production of the same autoimmune-promoting factors as with murine hepatocytes. Collectively, these data indicate that a human pathobiont translocates spontaneously to promote autoimmunity in genetically predisposed hosts, broadening our understanding of autoimmune host-microbiota interactions.
26

Zeng, Melody. "Regulation of the gut microbiota and intestinal homeostasis by phagocyte NADPH oxdiase (INC1P.351)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 54.8. http://dx.doi.org/10.4049/jimmunol.194.supp.54.8.

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Abstract The phagocyte NADPH oxidase generates reactive oxygen species (ROS) for microbial killing, and its impairment gives rise to Chronic Granulomatous Disease (CGD), a primary immunodeficiency characterized by recurrent infections and granulomatous lesions. Mutations in Nox2 (Cybb), a critical subunit of the oxidase, contribute 66% of CGD. In our study, we found spontaneous inflammation in the intestine of naïve Cybb-/- mice, indicated by higher levels of IL-1b, IL-6 and TNFα in lamina propria macrophages, as well as increased levels of IFNγ and IL-17A in CD4+ T cells. In addition, Klebsiella pneumoniae, a bacterium frequently found in granulomatous lesions in CGD patients, were detected in the spleens and mesenteric lymph nodes (MLNs) of naïve Cybb-/- mice, and IP administration of this pathobiont strain of K. pneumonia led to rapid mortality of wild-type mice. Oral administration of this K. pneumoniae induced intestinal inflammation in wild-type and Cybb-/- mice, but translocation of K. pneumoniae to MLNs was drastically enhanced in Cybb-/- mice and bone marrow chimeras with a neutrophil-specific deficiency in NOX2. Thus, our results demonstrate the importance of neutrophil-derived ROS in restricting dissemination of pathobionts from the intestine under steady-state conditions. Therefore, our study underscores a critical role for the NADPH oxidase in regulating intestinal homeostasis and provides insights into intestinal complications in CGD patients.
27

Cezar-de-Mello, Paula Fernandes Tavares, Stanthia Ryan, and Raina N. Fichorova. "The microRNA Cargo of Human Vaginal Extracellular Vesicles Differentiates Parasitic and Pathobiont Infections from Colonization by Homeostatic Bacteria." Microorganisms 11, no. 3 (February 21, 2023): 551. http://dx.doi.org/10.3390/microorganisms11030551.

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The disturbed vaginal microbiome defined as bacterial vaginosis (BV) and the parasitic infection by Trichomonas vaginalis (TV), the most common non-viral sexually transmitted pathogen, have well-established adverse effects on reproductive outcomes and susceptibility to infection and cancer. Molecular mechanisms underlying these associations and the failure of antibiotic therapy to mitigate adverse consequences are not fully elucidated. In an in vitro human vaginal colonization model, we tested the hypothesis that responses to TV and/or BV-bacteria will disrupt the micro(mi)RNA cargo of extracellular vesicles (EV) with the potential to modify pathways associated with reproductive function, cancer, and infection. miRNAs were quantified by HTG EdgeSeq. MiRNA differential expression (DE) was established in response to TV, the BV signature pathobiont Prevotella bivia and a homeostatic Lactobacillus crispatus with adjusted p < 0.05 using R. Validated gene targets, pathways, protein-protein interaction networks, and hub genes were identified by miRWalk, STRING, Cytoscape, and CytoHubba. In contrast to L. crispatus, TV and the BV pathobiont dysregulated a massive number of EV-miRNAs, over 50% shared by both pathogens. Corresponding target pathways, protein interaction clusters and top hub genes were related to cancer, infectious disease, circadian rhythm, steroid hormone signaling, pregnancy, and reproductive tissue terms. These data support the emerging concept that bacteria and parasitic eukaryotes disturbing the human vaginal microbiome may impact reproductive health through EV-miRNA dysregulation.
28

Lee, June-Chul, Hae-Youn Lee, Tae Kang Kim, Min-Soo Kim, Young Mi Park, Jinyoung Kim, Kihyoun Park, et al. "Obesogenic diet-induced gut barrier dysfunction and pathobiont expansion aggravate experimental colitis." PLOS ONE 12, no. 11 (November 6, 2017): e0187515. http://dx.doi.org/10.1371/journal.pone.0187515.

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29

Chassaing, Benoit, Omry Koren, Frederic A. Carvalho, Ruth E. Ley, and Andrew T. Gewirtz. "AIEC pathobiont instigates chronic colitis in susceptible hosts by altering microbiota composition." Gut 63, no. 7 (July 29, 2013): 1069–80. http://dx.doi.org/10.1136/gutjnl-2013-304909.

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30

Devkota, Suzanne, and Eugene B. Chang. "Interactions between Diet, Bile Acid Metabolism, Gut Microbiota, and Inflammatory Bowel Diseases." Digestive Diseases 33, no. 3 (2015): 351–56. http://dx.doi.org/10.1159/000371687.

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The composite human gut microbiomes of Western populations have changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Diets high in saturated fats and refined sugars and low in fiber are leading candidates for these events and for triggering the increased prevalence of immune-mediated diseases like inflammatory bowel disease (IBD). Our studies have shown that consumption of a ‘Western' diet high in saturated (milk-derived) fat (MF) or n-6 polyunsaturated (safflower oil) fat have similar effects on the structure of the colonic microbiome of wild-type and IL- 10-/- mice, characterized by increased Bacteroidetes and decreased Firmicutes. However, the MF diet uniquely promotes the expansion of an immunogenic sulfite-reducing pathobiont, Bilophila wadsworthia, a member of the Deltaproteobacteria and minor component of the gut microbiome. This bacterial bloom results from a MF diet-induced shift in hepatic conjugation of bile acids, from glycocholic to taurocholic (TC) acid, which is important for solubilizing the more hydrophobic MF diet. However, it is also responsible for delivery of taurine-derived sulfur to the distal bowel, promoting the assemblage of bile-tolerant microbes such as B. wadsworthia. The bloom of this species promotes a Th1-mediated immune response and the development of colitis in IL-10-/- mice. A similar bloom of B. wadsworthia is seen when IL-10-/- mice are fed a low-fat diet supplemented with TC. B. wadsworthia colonization of monoassociated germ-free IL-10-/- mice was dependent on the host consuming either a high-saturated MF diet or the gavage with TC. Together, these data provide a plausible explanation for the link between diseases such as IBD and dietary-mediated selection of gut microbial pathobionts in genetically susceptible hosts. With this knowledge, it may be possible to mitigate the bloom of these types of pathobionts by modifying the conjugation states of bile acids.
31

Liang, Shen-Huan, and Richard J. Bennett. "The Impact of Gene Dosage and Heterozygosity on the Diploid Pathobiont Candida albicans." Journal of Fungi 6, no. 1 (December 27, 2019): 10. http://dx.doi.org/10.3390/jof6010010.

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Candida albicans is a fungal species that can colonize multiple niches in the human host where it can grow either as a commensal or as an opportunistic pathogen. The genome of C. albicans has long been of considerable interest, given that it is highly plastic and can undergo a wide variety of alterations. These changes play a fundamental role in determining C. albicans traits and have been shown to enable adaptation both to the host and to antifungal drugs. C. albicans isolates contain a heterozygous diploid genome that displays variation from the level of single nucleotides to largescale rearrangements and aneuploidy. The heterozygous nature of the genome is now increasingly recognized as being central to C. albicans biology, as the relative fitness of isolates has been shown to correlate with higher levels of overall heterozygosity. Moreover, loss of heterozygosity (LOH) events can arise frequently, either at single polymorphisms or at a chromosomal level, and both can alter the behavior of C. albicans cells during infection or can modulate drug resistance. In this review, we examine genome plasticity in this pathobiont focusing on how gene dosage variation and loss of heterozygosity events can arise and how these modulate C. albicans behavior.
32

Cavallucci, Virve, Ivana Palucci, Marco Fidaleo, Antonella Mercuri, Letizia Masi, Valeria Emoli, Giada Bianchetti, et al. "Proinflammatory and Cancer-Promoting Pathobiont Fusobacterium nucleatum Directly Targets Colorectal Cancer Stem Cells." Biomolecules 12, no. 9 (September 7, 2022): 1256. http://dx.doi.org/10.3390/biom12091256.

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Intestinal bacterial communities participate in gut homeostasis and are recognized as crucial in bowel inflammation and colorectal cancer (CRC). Fusobacterium nucleatum (Fn), a pathobiont of the oral microflora, has recently emerged as a CRC-associated microbe linked to disease progression, metastasis, and a poor clinical outcome; however, the primary cellular and/or microenvironmental targets of this agent remain elusive. We report here that Fn directly targets putative colorectal cancer stem cells (CR-CSCs), a tumor cell subset endowed with cancer re-initiating capacity after surgery and chemotherapy. A patient-derived CSC line, highly enriched (70%) for the stem marker CD133, was expanded as tumor spheroids, dissociated, and exposed in vitro to varying amounts (range 100–500 MOI) of Fn. We found that Fn stably adheres to CSCs, likely by multiple interactions involving the tumor-associated Gal-GalNac disaccharide and the Fn-docking protein CEA-family cell adhesion molecule 1 (CEACAM-1), robustly expressed on CSCs. Importantly, Fn elicited innate immune responses in CSCs and triggered a growth factor-like, protein tyrosine phosphorylation cascade largely dependent on CEACAM-1 and culminating in the activation of p42/44 MAP kinase. Thus, the direct stimulation of CSCs by Fn may contribute to microbiota-driven colorectal carcinogenesis and represent a target for innovative therapies.
33

Xu, Mo, Maria Pokrovskii, Yi Ding, Ren Yi, Christy Au, Oliver J. Harrison, Carolina Galan, Yasmine Belkaid, Richard Bonneau, and Dan R. Littman. "c-MAF-dependent regulatory T cells mediate immunological tolerance to a gut pathobiont." Nature 554, no. 7692 (February 2018): 373–77. http://dx.doi.org/10.1038/nature25500.

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34

Devkota, Suzanne, Yunwei Wang, Mark W. Musch, Vanessa Leone, Hannah Fehlner-Peach, Anuradha Nadimpalli, Dionysios A. Antonopoulos, Bana Jabri, and Eugene B. Chang. "Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice." Nature 487, no. 7405 (June 13, 2012): 104–8. http://dx.doi.org/10.1038/nature11225.

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35

Kitamoto, Sho, Hiroko Nagao-Kitamoto, Yizu Jiao, Merritt G. Gillilland, Atsushi Hayashi, Jin Imai, Kohei Sugihara, et al. "The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis." Cell 182, no. 2 (July 2020): 447–62. http://dx.doi.org/10.1016/j.cell.2020.05.048.

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36

Wagner, V. E., N. Dey, J. Guruge, A. Hsiao, P. P. Ahern, N. P. Semenkovich, L. V. Blanton, et al. "Effects of a gut pathobiont in a gnotobiotic mouse model of childhood undernutrition." Science Translational Medicine 8, no. 366 (November 23, 2016): 366ra164. http://dx.doi.org/10.1126/scitranslmed.aah4669.

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37

shulzhenko, Natalia, Xiaoxi Dong, Dariia Vyshenska, Renee Greer, Manoj Gurung, Stephany Vasquez-Perez, Kate Peremyslova, et al. "Low Intestinal IGA Production in CVID Facilitates Pathobiont-Mediated IFN Responses and Enteropathy." Gastroenterology 152, no. 5 (April 2017): S997—S998. http://dx.doi.org/10.1016/s0016-5085(17)33381-4.

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38

Jiao, Yizu, Youssef Darzi, Kazuki Tawaratsumida, Julie T. Marchesan, Mizuho Hasegawa, Henry Moon, Grace Y. Chen, et al. "Induction of Bone Loss by Pathobiont-Mediated Nod1 Signaling in the Oral Cavity." Cell Host & Microbe 13, no. 5 (May 2013): 595–601. http://dx.doi.org/10.1016/j.chom.2013.04.005.

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39

Meisner, J., K. Miller, J. Lee, A. Jose, M. Giuggio, M. McComb, E. Humphries, et al. "P493 The synthetic glycan KB295 optimises microbiome composition and function in ulcerative colitis: Results from a proof of principle human study." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i458. http://dx.doi.org/10.1093/ecco-jcc/jjab232.620.

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Abstract Background Ulcerative colitis (UC) pathogenesis involves genetic susceptibility, immune-mediated tissue injury, and gut microbiota disturbances. Most approved therapies modify host immunity, rather than directly targeting the microbiota. Faecal microbiota transplantation provides encouraging evidence for the therapeutic potential of gut microbiome modulation. Gastrointestinal tract bacteria are ecologically differentiated by their ability to use specific glycans as growth substrates, making glycans a promising and safe alternative to target the microbiome. To explore this, we used an ex vivo faecal microbiota culture system to identify a synthetic glycan (KB295) with desirable microbiological activity and conducted a proof of principle study (NCT04508413) of safety and tolerability of KB295 in patients with UC. Methods In ex vivo studies, faecal microbial communities from healthy subjects were incubated anaerobically (negative control) ± KB295. Taxa counts from shotgun metagenomic sequencing data were used to evaluate microbial response to KB295. Short-chain fatty acid (SCFA) levels were also assessed. KB295 was evaluated in an open-label single-arm study in adult patients with mild to moderate UC. KB295 was ingested over an 8-wk period. Objectives included KB295 safety (primary) and effect on gut microbiota composition and faecal biomarkers. Results In ex vivo studies, KB295 increased SCFA levels across 10 faecal samples to a median of 47.0 vs 15.2 mM with negative control, including increases in acetate, propionate, and butyrate levels. Metagenomic sequencing showed pathobiont depletion in the family Enterobacteriaceae with KB295 to a median relative abundance of 10.8% vs 38.2% with negative control. Pathobiont depletion was associated with enrichments of diverse genera in the phyla Bacteroidetes and Firmicutes. In patients with UC (n=12), KB295 was well tolerated with generally mild adverse events (AEs). The most frequently occurring AEs were bowel habit changes, flatulence, and headache. Median faecal calprotectin and lactoferrin levels decreased by 69.0% (n=11) and 86.0% (n=6), respectively, from screening to end of the KB295 intake. Consistent with our ex vivo results, of the patients for whom we have data to date, the relative abundance of the faecal pathobiont family Enterobacteriaceae decreased in 5 of 5 participants, and the commensal genus Parabacteroides was enriched in 4 of 5 participants. Conclusion Our results establish a proof of principle for the glycan modulation of gut microbiome composition and function and provide insight into the potential utility of this strategy in patients with UC. The safety and tolerability of KB295, along with evidence of reduced inflammation, support a phase 2 study, which is planned.
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Ayres, Janelle S., Norver J. Trinidad, and Russell E. Vance. "Lethal inflammasome activation by a multidrug-resistant pathobiont upon antibiotic disruption of the microbiota." Nature Medicine 18, no. 5 (April 22, 2012): 799–806. http://dx.doi.org/10.1038/nm.2729.

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41

Amanda, Ramer-Tait, Gomes Neto Joao Carlos, Kittana Hatem, and Hostetter Jesse. "O-036 Role of the Resident Microbiota in Pathobiont-Mediated Susceptibility to Intestinal Inflammation." Inflammatory Bowel Diseases 20 (December 2014): S19. http://dx.doi.org/10.1097/01.mib.0000456694.40363.8d.

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42

Imai, Jin, Sho Kitamoto, Kohei Sugihara, Hiroko Nagao-Kitamoto, Atsushi Hayashi, Tina L. Morhardt, Peter Kuffa, Peter D. R. Higgins, Nicolas Barnich, and Nobuhiko Kamada. "Flagellin-mediated activation of IL-33-ST2 signaling by a pathobiont promotes intestinal fibrosis." Mucosal Immunology 12, no. 3 (February 11, 2019): 632–43. http://dx.doi.org/10.1038/s41385-019-0138-4.

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43

Musharrafieh, Rami, Luca Tacchi, Joshua Trujeque, Scott LaPatra, and Irene Salinas. "Staphylococcus warneri, a resident skin commensal of rainbow trout (Oncorhynchus mykiss) with pathobiont characteristics." Veterinary Microbiology 169, no. 1-2 (February 2014): 80–88. http://dx.doi.org/10.1016/j.vetmic.2013.12.012.

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44

AKO, Simon Eyongabane, Eric Achidi AKUM, Céline Nguefeu NKENFOU, Jules Clement N. ASSOB, and Thumamo Benjamin POKAM. "In-vitro susceptibility of gut pathobiont associated with microbial translocation to cotrimoxazole and antiretroviral." Scientific African 6 (November 2019): e00192. http://dx.doi.org/10.1016/j.sciaf.2019.e00192.

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45

Brand, Meghan Wymore, Albert Jergens, Alexandra Proctor, Gregory Phillips, Jesse M. Hostetter, and Michael J. Wannemuehler. "Sa1753 Vertical Transmission of AIEC Pathobiont Increases Severity of DSS-Induced Colitis in Offspring." Gastroenterology 146, no. 5 (May 2014): S—288. http://dx.doi.org/10.1016/s0016-5085(14)61024-6.

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46

Vieira, Silvio Manfredo, Michael Hiltensperger, Varun Kumar, Carina Dehner, Daniel Zegarra-Ruiz, William Ruff, Nafeesa Khan, Andrew Goodman, and Martin A. Kriegel. "Spontaneous Translocation of a Gut Pathobiont Drives Autoimmunity that is Preventable by Intramuscular Vaccination." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 199.20. http://dx.doi.org/10.4049/jimmunol.198.supp.199.20.

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Abstract The gut microbiota contributes to the pathogenesis of autoimmunity. The mechanisms and sites of host-microbiota interactions are, however, largely unknown. Dietary antigens reach the mesenteric lymph node (MLN) via the lymphatics and the liver via the portal vein. We hypothesized that commensals reach lymphocytes beyond the gut barrier in autoimmune-prone hosts. We first altered the gut microbiota with single antibiotics in the (NZWxBXSB)F1 model of systemic autoimmunity that is characterized by a leaky barrier based on oral gavage with FITC-dextran. To test commensal translocation, we cultured anaerobically MLN and livers. Compared to controls, vancomycin alone lowered autoantibodies, Th17 and Tfh cells, and protected mice from autoimmune deaths. Cultures of MLN and liver of (NZWxBXSB)F1 mice revealed significant anaerobic growth, which was suppressed by vancomycin. Sequencing of colonies identified E. gallinarum, a human gut commensal, that grew uniquely in tissues of autoimmune but not control mice. Species-specific PCR of liver tissues from autoimmune hepatitis patients also revealed E. gallinarum. 16S rDNA sequencing confirmed the presence of Enterococcus genus in the gut of (NZWxBXSB)F1 mice. Germ-free C57BL/6 mice monocolonized with E. gallinarum also led to translocation and induction of autoantibodies as well as Th1/Th17 responses. Remarkably, an intramuscular vaccine against E. gallinarum prevented autoimmune deaths in (NZWxBXSB)F1 mice. These data support that an innocuous gut commensal translocates spontaneously to initiate autoimmunity that is preventable by a vaccine targeted at the translocating pathobiont. This approach represents a novel therapeutic avenue for immune-mediated diseases.
47

Wymore Brand, Meghan, Alexandra L. Proctor, Jesse M. Hostetter, Naihui Zhou, Iddo Friedberg, Albert E. Jergens, Gregory J. Phillips, and Michael J. Wannemuehler. "Vertical transmission of attaching and invasive E. coli from the dam to neonatal mice predisposes to more severe colitis following exposure to a colitic insult later in life." PLOS ONE 17, no. 4 (April 5, 2022): e0266005. http://dx.doi.org/10.1371/journal.pone.0266005.

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The gastrointestinal microbiota begins to be acquired at birth and continually matures through early adolescence. Despite the relevance for gut health, few studies have evaluated the impact of pathobiont colonization of neonates on the severity of colitis later in life. LF82 is an adherent invasive E. coli strain associated with ileal Crohn’s disease. The aim of this study was to evaluate the severity of dextran sodium sulfate (DSS)-induced colitis in mice following E. coli LF82 colonization. Gnotobiotic mice harboring the altered Schaedler flora (ASF) were used as the model. While E. coli LF82 is neither adherent nor invasive, it was been demonstrated that adult ASF mice colonized with E. coli LF82 develop more severe DSS-induced colitis compared to control ASF mice treated with DSS. Therefore, we hypothesized that E. coli LF82 colonization of neonatal ASF mice would reduce the severity of DSS-induced inflammation compared to adult ASF mice colonized with E. coli LF82. To test this hypothesis, adult ASF mice were colonized with E. coli LF82 and bred to produce offspring (LF82N) that were vertically colonized with LF82. LF82N and adult-colonized (LF82A) mice were given 2.0% DSS in drinking water for seven days to trigger colitis. More severe inflammatory lesions were observed in the LF82N + DSS mice when compared to LF82A + DSS mice, and were characterized as transmural in most of the LF82N + DSS mice. Colitis was accompanied by secretion of proinflammatory cytokines (IFNγ, IL-17) and specific mRNA transcripts within the colonic mucosa. Using 16S rRNA gene amplicon sequencing, LF82 colonization did not induce significant changes in the ASF community; however, minimal changes in spatial redistribution by fluorescent in situ hybridization were observed. These results suggest that the age at which mice were colonized with E. coli LF82 pathobiont differentially impacted severity of subsequent colitic events.
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B, Ashwath, Adline Vadhana D, Anitha V, and Shanmugam M. "Aggregatibacter actinomycetemcomitans- A periodontopathogen." IP International Journal of Periodontology and Implantology 6, no. 2 (July 15, 2021): 61–67. http://dx.doi.org/10.18231/j.ijpi.2021.011.

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is a gram-negative oral pathobiont that is associated with severe form of periodontitis. This bacterium has various virulence factors which enables the bacterium to colonize the oral cavity, invade and evade the host defences. Leukotoxin and cytolethal distending toxin are the important virulence factors that causes periodontal destruction. Periodontal infections with seems to be refractory to conventional therapy and systemic antibiotics. Hence, leukotoxin represents an ideal anti-virulence target and inhibition of its immunosuppressive activity would eliminate the colonization advantage provided to the bacteria by the toxin. This review provides a comprehensive update of with an emphasis on its virulence factors leukotoxin and cytolethal distending toxin and its role in periodontal destruction and recent developments in the management.
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Nørskov-Lauritsen, Claesson, Birkeholm Jensen, Åberg, and Haubek. "Aggregatibacter Actinomycetemcomitans: Clinical Significance of a Pathobiont Subjected to Ample Changes in Classification and Nomenclature." Pathogens 8, no. 4 (November 18, 2019): 243. http://dx.doi.org/10.3390/pathogens8040243.

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Aggregatibacter actinomycetemcomitans is a Gram-negative bacterium that is part of the oral microbiota. The aggregative nature of this pathogen or pathobiont is crucial to its involvement in human disease. It has been cultured from non-oral infections for more than a century, while its portrayal as an aetiological agent in periodontitis has emerged more recently. A. actinomycetemcomitans is one species among a plethora of microorganisms that constitute the oral microbiota. Although A. actinomycetemcomitans encodes several putative toxins, the complex interplay with other partners of the oral microbiota and the suppression of host response may be central for inflammation and infection in the oral cavity. The aim of this review is to provide a comprehensive update on the clinical significance, classification, and characterisation of A. actinomycetemcomitans, which has exclusive or predominant host specificity for humans.
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Shawki, Ali, Marianne R. Spalinger, Alina N. Santos, Vinicius Canale, Anica Sayoc-Becerra, Jonathan Mitchell, John Macbeth, et al. "A Novel IBD‐Associated Mouse Pathobiont E. coli Causes Disease and Prevents Recovery from Colitis." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06961.

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