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Journal articles on the topic 'Pathobiont'

Author: Grafiati

Published: 7 July 2024

Last updated: 31 July 2025

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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 (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

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2

Ryder, Mark I., Daniel H. Fine, and Annelise E. Barron. "From Global to Nano: A Geographical Perspective of Aggregatibacter actinomycetemcomitans." Pathogens 13, no. 10 (2024): 837. http://dx.doi.org/10.3390/pathogens13100837.

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The periodontal disease pathobiont Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) may exert a range of detrimental effects on periodontal diseases in general and, more specifically, with the initiation and progression of Localized Stage III Grade C periodontitis (molar–incisor pattern). In this review of the biogeography of this pathobiont, the full range of geographical scales for A. actinomycetemcomitans, from global origins and transmission to local geographical regions, to more locally exposed probands and families, to the individual host, down to the oral cavity, and fin

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3

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 (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 mi

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4

Minton, Kirsty. "Pathobiont peacekeepers." Nature Reviews Immunology 18, no. 3 (2018): 152. http://dx.doi.org/10.1038/nri.2018.11.

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5

Catalan, Eduardo A., Emilio Seguel-Fuentes, Brandon Fuentes, et al. "Oral Pathobiont-Derived Outer Membrane Vesicles in the Oral–Gut Axis." International Journal of Molecular Sciences 25, no. 20 (2024): 11141. http://dx.doi.org/10.3390/ijms252011141.

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Oral pathobionts are essential in instigating local inflammation within the oral cavity and contribute to the pathogenesis of diseases in the gastrointestinal tract and other distant organs. Among the Gram-negative pathobionts, Porphyromonas gingivalis and Fusobacterium nucleatum emerge as critical drivers of periodontitis, exerting their influence not only locally but also as inducers of gut dysbiosis, intestinal disturbances, and systemic ailments. This dual impact is facilitated by their ectopic colonization of the intestinal mucosa and the subsequent mediation of distal systemic effects by

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6

Yang, H., H. Mirsepasi-Lauridsen, C. Struve, et al. "A21 ULCERATIVE COLITIS-ASSOCIATED E. COLI PATHOBIONTS POTENTIATE COLITIS IN SUSCEPTIBEL HOSTS." Journal of the Canadian Association of Gastroenterology 4, Supplement_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 lack

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7

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 (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

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8

Kim, Byeongguk, and Nana Han. "Periodontal Pathobionts and Respiratory Diseases: Mechanisms of Interaction and Implications for Interdisciplinary Care." Biomedicines 13, no. 7 (2025): 1741. https://doi.org/10.3390/biomedicines13071741.

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Periodontitis is a prevalent chronic inflammatory disease that has been increasingly recognized for its systemic impacts, including its connection to respiratory diseases such as pneumonia, chronic obstructive pulmonary disease (COPD), Obstructive Sleep Apnea (OSA), asthma, lung cancer, and COVID-19. This review explores the potential role of periodontal pathobionts, particularly Porphyromonas gingivalis (Pg), Treponema denticola (Td), Fusobacterium nucleatum (Fn), Aggregatibacter actinomycetemcomitans (Aa), and Tannerella forsythia (Tf), in respiratory health. These pathobionts contribute to

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9

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 (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-

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10

Yang, Hyungjun, Hengameh Chloé Mirsepasi-Lauridsen, Carsten Struve, et al. "Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts." Journal of Immunology 202, no. 1_Supplement (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 m

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11

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 (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 &gt; 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 mucos

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12

Yang, H., W. Kim, c. ma, H. Yu, and B. vallance. "A172 GENETIC AND DIET-ASSOCIATED MUCUS IMPAIRMENTS INCREASE SUSCEPTIBILITY TO ULCERATIVE COLITIS PATHOBIONT-DRIVEN COLITIS." Journal of the Canadian Association of Gastroenterology 8, Supplement_1 (2025): i70. https://doi.org/10.1093/jcag/gwae059.172.

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Abstract Background The Inflammatory Bowel Diseases (IBD), Crohn’s Disease (CD) and ulcerative colitis (UC) affect &gt; 320,000 Canadians and are increasing in incidence. Ileal CD has been linked to the overgrowth of mucosal adherent-invasive Escherichia coli. Recent studies have also implicated the adherence of E. 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 colo

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13

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 (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 (NZWxBX

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14

Jochum, Lara, and Bärbel Stecher. "Label or Concept – What Is a Pathobiont?" Trends in Microbiology 28, no. 10 (2020): 789–92. http://dx.doi.org/10.1016/j.tim.2020.04.011.

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15

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

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16

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 (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 an

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17

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

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18

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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19

Siak, Jay, Anthony St. Leger, Kumarkrishna Raychaudhuri, et al. "Commensal microbiota as possible pathobiont in autoinflammatory disease." Journal of Immunology 202, no. 1_Supplement (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 NLRP

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20

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

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21

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

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22

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 (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.

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23

A. James, Stephen, Sarah Phillips, Andrea Telatin, et al. "Preterm Infants Harbour a Rapidly Changing Mycobiota That Includes Candida Pathobionts." Journal of Fungi 6, no. 4 (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 pathobiont

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24

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

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25

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

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26

Meisner, Jeffrey, Toni Bransford, Kelsey Miller, 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 (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

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Manfredo Vieira, S., M. Hiltensperger, V. Kumar, et al. "Translocation of a gut pathobiont drives autoimmunity in mice and humans." Science 359, no. 6380 (2018): 1156–61. http://dx.doi.org/10.1126/science.aar7201.

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28

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

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29

Vieira, Silvio Manfredo, Michael Hiltensperger, Varun Kumar, et al. "Spontaneous translocation of a human enterococcal gut pathobiont drives systemic autoimmunity." Journal of Immunology 200, no. 1_Supplement (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, Cy

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30

Zeng, Melody. "Regulation of the gut microbiota and intestinal homeostasis by phagocyte NADPH oxdiase (INC1P.351)." Journal of Immunology 194, no. 1_Supplement (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, Klebsie

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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 (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 extrace

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

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33

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 (2013): 1069–80. http://dx.doi.org/10.1136/gutjnl-2013-304909.

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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

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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 (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 rear

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Cavallucci, Virve, Ivana Palucci, Marco Fidaleo, et al. "Proinflammatory and Cancer-Promoting Pathobiont Fusobacterium nucleatum Directly Targets Colorectal Cancer Stem Cells." Biomolecules 12, no. 9 (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 che

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Xu, Mo, Maria Pokrovskii, Yi Ding, et al. "c-MAF-dependent regulatory T cells mediate immunological tolerance to a gut pathobiont." Nature 554, no. 7692 (2018): 373–77. http://dx.doi.org/10.1038/nature25500.

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Devkota, Suzanne, Yunwei Wang, Mark W. Musch, et al. "Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice." Nature 487, no. 7405 (2012): 104–8. http://dx.doi.org/10.1038/nature11225.

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39

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

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40

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

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

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

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43

Franz, Mathias, Roland R. Regoes, and Jens Rolff. "How infection-triggered pathobionts influence virulence evolution." Philosophical Transactions of the Royal Society B: Biological Sciences 379, no. 1901 (2024). http://dx.doi.org/10.1098/rstb.2023.0067.

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Host–pathogen interactions can be influenced by the host microbiota, as the microbiota can facilitate or prevent pathogen infections. In addition, members of the microbiota can become virulent. Such pathobionts can cause co-infections when a pathogen infection alters the host immune system and triggers dysbiosis. Here we performed a theoretical investigation of how pathobiont co-infections affect the evolution of pathogen virulence. We explored the possibility that the likelihood of pathobiont co-infection depends on the evolving virulence of the pathogen. We found that, in contrast to the exp

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Kelly, Matthew S., Pixu Shi, Sifelane C. Boiditswe, et al. "Role of the upper airway microbiota in respiratory virus and bacterial pathobiont dynamics in the first year of life." Nature Communications 16, no. 1 (2025). https://doi.org/10.1038/s41467-025-60552-4.

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Abstract The mechanisms by which respiratory viruses predispose to secondary bacterial infections remain poorly characterized. Using 2,409 nasopharyngeal swabs from 300 infants enrolled in a prospective cohort study in Botswana, we perform a detailed analysis of factors that influence the dynamics of bacterial pathobiont colonization during infancy. We quantify the extent to which viruses increase the acquisition of Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae. We provide evidence of cooperative interactions between these pathobionts while identifying host charac

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Gronke, Konrad, Mytien Nguyen, Helen Fuhrmann, et al. "Translocating gut pathobiont Enterococcus gallinarum induces T _H 17 and IgG3 anti-RNA–directed autoimmunity in mouse and human." Science Translational Medicine 17, no. 784 (2025). https://doi.org/10.1126/scitranslmed.adj6294.

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Chronic autoimmune diseases often lead to long-term sequelae and require lifelong immunosuppression because of an incomplete understanding of the triggers and drivers in genetically predisposed patients. Gut bacteria that escape the gut barrier, known as translocating gut pathobionts, have been implicated as instigators and perpetuators of extraintestinal autoimmune diseases in mice. The gut microbial contributions to autoimmunity in humans remain largely unclear, including whether specific pathological human adaptive immune responses are triggered by such pathobionts. Here, we show that the t

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Harris, Onywera, A. Mabunda Sikhumbuzo, Williamson Anna-Lise, and Z. A. Mbulawa Zizipho. "Microbiological and Behavioural Determinants of Genital HPV Infections among Adolescent Girls and Young Women in South Africa." December 4, 2021. https://doi.org/10.5281/zenodo.5759110.

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<strong>Patterns of bacterial pathobiont infections according to vaginal HPV status among 192 AGYW.</strong> HPV-positive AGYW with (<strong>a</strong>) single infections, (<strong>b</strong>) dual infections, (<strong>c</strong>) triple infections; and HPV-negative AGYW with (<strong>d</strong>) single infections, (<strong>e</strong>) dual infections, (<strong>f</strong>) triple infections. The number of AGYW in each group is in parentheses. Of all the AGYW with information on HPV status, 193 had any detectable pathobiont (<em>M. genitalium</em>, <em>M. hominis</em>, <em>U. parvum</em>, or <e

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Higashi, Dustin L., Hua Qin, Christina Borland, Jens Kreth, and Justin Merritt. "An inflammatory paradox: strategies inflammophilic oral pathobionts employ to exploit innate immunity via neutrophil manipulation." Frontiers in Oral Health 5 (June 11, 2024). http://dx.doi.org/10.3389/froh.2024.1413842.

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Inflammatory dysbiotic diseases present an intriguing biological paradox. Like most other infectious disease processes, the alarm bells of the host are potently activated by tissue-destructive pathobionts, triggering a cascade of physiological responses that ultimately mobilize immune cells like neutrophils to sites of active infection. Typically, these inflammatory host responses are critical to inhibit and/or eradicate infecting microbes. However, for many inflammatory dysbiotic diseases, inflammophilic pathobiont-enriched communities not only survive the inflammatory response, but they actu

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Centeno-Delphia, Ruth Eunice, Erica A. Long, Audrey C. Ellis, et al. "Nasal pathobiont abundance does not differ between dairy cattle with or without clinical symptoms of bovine respiratory disease." Animal Microbiome 7, no. 1 (2025). https://doi.org/10.1186/s42523-025-00382-3.

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Abstract Background Bovine respiratory disease (BRD) remains a significant health and economic problem to the dairy cattle industry. Multiple risk factors contribute to BRD susceptibility including the bacterial pathobionts Mannheimia haemolytica, Pasteurella multocida, Histophilus somni, and Mycoplasma bovis. Studies have characterized and quantified the abundance of these bacteria in the nasal cavity of cattle to infer and help disease diagnosis; nonetheless, there is still discrepancy in the results observed of when these microbes are commensal or pathogenic. Additionally, some of these stu

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Tanaka, Rika, Jin Imai, Hitoshi Tsugawa, et al. "Adherent-invasive E. coli – induced specific IgA limits pathobiont localization to the epithelial niche in the gut." Frontiers in Microbiology 14 (February 23, 2023). http://dx.doi.org/10.3389/fmicb.2023.1031997.

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Background and aimAdherent-invasive E. coli (AIEC) has been identified as a pathobiont associated with Crohn’s disease (CD), that prefers to grow in inflammatory conditions. Although the colonization by AIEC is implicated in the progression of the disease and exacerbates inflammation in murine colitis models, the recognition and response of host immunity to AIEC remains elusive.MethodsAntibiotic treated female C57BL/6 mice were inoculated by commensal E. coli and LF82 AIEC strains. Luminal-IgA fractions were prepared from feces and their binding to AIEC and other strains was assessed to confir

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Joshi, C., A. Mezincescu, M. Gunasekara, et al. "Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study." Scientific Reports 12, no. 1 (2022). http://dx.doi.org/10.1038/s41598-022-19154-z.

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AbstractTo establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes’ expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8 × 10–6, 95% CI = 1.1 × 10–7–2.1 × 10–5), one-fold increased expressions of fimA (β = 14.3,

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