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Journal articles on the topic 'Nucleatum'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Nurfitri, Azzara, Hedijanti Joenoes, and Boy M. Bachtiar. "ANALYSIS OF THE POTENTIAL OF STREPTOCOCCUS SALIVARIUS ISOLATED FROM THE SALIVA AND TONGUE DORSUM TO INHIBIT THE GROWTH OF FUSOBACTERIUM NUCLEATUM." International Journal of Applied Pharmaceutics 9 (October 30, 2017): 8. http://dx.doi.org/10.22159/ijap.2017.v9s1.06.

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Objective: Analyzing the potential of S. salivarius isolated from the saliva and tongue dorsum of adults to inhibit the growth of Fusobacteriumnucleatum.Methods: Polymerase chain reaction, deferred antagonism test, and well-diffused agar test.Results: Inhibition of the growth F. nucleatum by S. salivarius isolated from the tongue dorsum (p>0.05). No inhibition to the growth of F. nucleatumby S. salivarius isolated from the saliva. No inhibition to the growth of F. nucleatum by the protein produced by S. salivarius.Conclusions: The growth of F. nucleatum was not inhibited by S. salivarius isolated from the saliva but by S. salivarius isolated from the dorsum of thetongue.

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2

Allen-Vercoe, Emma, Jaclyn Strauss, and Kris Chadee. "Fusobacterium nucleatum." Gut Microbes 2, no. 5 (September 2011): 294–98. http://dx.doi.org/10.4161/gmic.2.5.18603.

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3

Bashir, Arif, Abid Y. Miskeen, Ashaqullah Bhat, Khalid M. Fazili, and Bashir A. Ganai. "Fusobacterium nucleatum." European Journal of Cancer Prevention 24, no. 5 (September 2015): 373–85. http://dx.doi.org/10.1097/cej.0000000000000116.

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4

Yocum, Denise. "Fusobacterium nucleatum." Journal of the American Academy of Physician Assistants 29, no. 12 (December 2016): 1–4. http://dx.doi.org/10.1097/01.jaa.0000508216.58368.74.

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5

Jewett, Anahid, Wyatt R. Hume, Ho Le, Tri N. Huynh, Yiping W. Han, Genhong Cheng, and Wenyuan Shi. "Induction of Apoptotic Cell Death in Peripheral Blood Mononuclear and Polymorphonuclear Cells by an Oral Bacterium,Fusobacterium nucleatum." Infection and Immunity 68, no. 4 (April 1, 2000): 1893–98. http://dx.doi.org/10.1128/iai.68.4.1893-1898.2000.

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ABSTRACT It is largely unknown why a variety of bacteria present in the oral cavity are capable of establishing themselves in the periodontal pockets of nonimmunocompromised individuals in the presence of competent immune effector cells. In this paper we present evidence for the immunosuppressive role of Fusobacterium nucleatum, a gram-negative oral bacterium which plays an important role in the generation of periodontal disease. Our studies indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organism to induce apoptotic cell death in peripheral blood mononuclear cells (PBMCs) and in polymorphonuclear cells (PMNs). F. nucleatum treatment induced apoptosis of PBMCs and PMNs as assessed by an increase in subdiploid DNA content determined by DNA fragmentation and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling assays. The ability of F. nucleatum to induce apoptosis was abolished by either heat treatment or proteinase digestion but was retained after formaldehyde treatment, suggesting that a heat-labile surface protein component is responsible for bacterium-mediated cell apoptosis. The data also indicated that F. nucleatum-induced cell apoptosis requires activation of caspases and is protected by NF-κB. Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal disease are discussed.

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Beavers, Bruce R. "FUSOBACTERIUM NUCLEATUM PYOMYOSITIS." Orthopedics 15, no. 2 (February 1992): 208–11. http://dx.doi.org/10.3928/0147-7447-19920201-17.

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Lee, H. R., I. C. Rhyu, H. D. Kim, H. K. Jun, B. M. Min, S. H. Lee, and B. K. Choi. "In-vivo-induced antigenic determinants of Fusobacterium nucleatum subsp. nucleatum." Molecular Oral Microbiology 26, no. 2 (January 10, 2011): 164–72. http://dx.doi.org/10.1111/j.2041-1014.2010.00594.x.

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Wang, James C., Joehassin Cordero, Yan Sun, Mayank Aranke, Randall Wolcott, Jane A. Colmer-Hamood, and Abdul N. Hamood. "Planktonic Growth ofPseudomonas aeruginosaaround a Dual-Species Biofilm Supports the Growth ofFusobacterium nucleatumwithin That Biofilm." International Journal of Otolaryngology 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/3037191.

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Purpose.The goal of this study was to understand the potential interaction betweenPseudomonas aeruginosaandFusobacterium nucleatumwithin the middle ear.Methods.We examined the microbiota of ear fluid and tympanostomy tubes (TTs) obtained from patients with posttympanostomy tube otorrhea. We also examined biofilms formed byP. aeruginosaandF. nucleatum, singly or together, under aerobic or anaerobic conditions.Results.While the facultative anaerobeP. aeruginosadominated the bacterial population within the ear fluid, strict anaerobes, includingF. nucleatum,dominated bacterial populations within the TTs.F. nucleatumwas able to grow under aerobic conditions only in the presence ofP. aeruginosa, whose growth reduced the level of dissolved oxygen within the broth to nearly anoxic condition within 4 h after inoculation. The presence ofP. aeruginosaallowedF. nucleatumto maintain its growth for 72 h within the dual-species biofilm but not within the planktonic growth. Visualization of the biofilms revealed coaggregation ofP. aeruginosaandF. nucleatum.Conclusion.Extrapolation of these results suggests that, within the middle ear fluid, the growth ofP. aeruginosaproduces the anaerobic conditions required for the growth ofF. nucleatum, both within effusion and within biofilms.

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Könönen, E., A. Kanervo, K. Salminen, and H. Jousimies-Somer. "β-Lactamase Production and Antimicrobial Susceptibility of Oral Heterogeneous Fusobacterium nucleatum Populations in Young Children." Antimicrobial Agents and Chemotherapy 43, no. 5 (May 1, 1999): 1270–73. http://dx.doi.org/10.1128/aac.43.5.1270.

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ABSTRACT Oral Fusobacterium nucleatum populations from 20 young, healthy children were examined for β-lactamase production. Ten children (50%) harbored, altogether, 25 β-lactamase-positiveF. nucleatum isolates that were identified as F. nucleatum subsp. polymorphum, F. nucleatum subsp. nucleatum, and F. nucleatum subsp. vincentii (J. L. Dzink, M. T. Sheenan, and S. S. Socransky, Int. J. Syst. Bacteriol. 40:74–78, 1990). In vitro susceptibility of these β-lactamase-producing and 26 non-β-lactamase-producing F. nucleatum isolates was tested with penicillin G, amoxicillin-clavulanic acid, tetracycline hydrochloride, metronidazole, trovafloxacin, and azithromycin. Except for penicillin G, the antimicrobials exhibited good activity against all F. nucleatum isolates.

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Lai, Yue, Jun Mi, and Qiang Feng. "Fusobacterium nucleatum and Malignant Tumors of the Digestive Tract: A Mechanistic Overview." Bioengineering 9, no. 7 (June 28, 2022): 285. http://dx.doi.org/10.3390/bioengineering9070285.

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Fusobacterium nucleatum (F. nucleatum) is an oral anaerobe that plays a role in several oral diseases. However, F. nucleatum is also found in other tissues of the digestive tract, and several studies have recently reported that the level of F. nucleatum is significantly elevated in malignant tumors of the digestive tract. F. nucleatum is proposed as one of the risk factors in the initiation and progression of digestive tract malignant tumors. In this review, we summarize recent reports on F. nucleatum and its role in digestive tract cancers and evaluate the mechanisms underlying the action of F. nucleatum in digestive tract cancers.

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Gharbia, S. E., and H. N. Shah. "Fusobacterium nucleatum subsp. fusiforme subsp. nov. and Fusobacterium nucleatum subsp. animalis subsp. nov. as Additional Subspecies within Fusobacterium nucleatum." International Journal of Systematic Bacteriology 42, no. 2 (April 1, 1992): 296–98. http://dx.doi.org/10.1099/00207713-42-2-296.

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Engevik, Melinda, Heather Danhof, Robert Britton, and James Versalovic. "20 ELUCIDATING THE ROLE OF FUSOBACTERIUM NUCLEATUM IN INTESTINAL INFLAMMATION." Inflammatory Bowel Diseases 26, Supplement_1 (January 2020): S29. http://dx.doi.org/10.1093/ibd/zaa010.070.

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Abstract Background While the direct cause of inflammatory bowel disease (IBD) is unknown, the gut microbiota is speculated to play a key role. The complexity of the microbiome has made it difficult to pinpoint whether bacterial species are specifically associated with IBD exacerbations; although select microbes have emerged as compelling candidates. Several groups have identified increased abundance in Fusobacterium in IBD patients. Fusobacterium nucleatum drives inflammation in the oral cavity, but few studies have examined the potential for F. nucleatum to promote intestinal inflammation. We hypothesize that F. nucleatum secretes Outer Membrane Vesicles (OMVs) that activate epithelial Toll-like receptor 4 (TLR4) to drive inflammation. Methods & Results Given the prevalence of F. nucleatum in IBD specimens, we sought to determine if this pathobiont could promote pro-inflammatory responses in human epithelial cultures. Using fluorescently tagged F. nucleatum, we demonstrate that F. nucleatum subspecies polymorphum adheres to the mucus layer of human colonic HT29-MTX cells. Application of F. nucleatum metabolites to HT29-MTX cells resulted in upregulation of pro-inflammatory cytokines IL-8 and TNF by qPCR and ELISA. Purified OMVs from F. nucleatum alone were able to stimulate IL-8 and TNF production. This demonstrates the robust response of colonic epithelial cells to F. nucleatum. Additionally, we used human jejunum and colon enteroid monolayers treated with F. nucleatum metabolites in an anti-oxidant free enteroid media and found that F. nucleatum secreted products promoted TNF secretion by ELISA. Using the Luminex Magpix Platform we further queried the enteroid system to assess which pathways were activated. Enteroid monolayers treated with F. nucleatum metabolites exhibited increased phosphorylated ERK and CREB, downstream effectors of TLRs. We next sought to address whether F. nucleatum alone could elicit pro-inflammatory responses in a mouse model. Mice harboring a human microbiota, or humanized mice, were treated for 5 days with a cocktail of antibiotics and treated with F. nucleatum (108 CFU) by oral gavage; a regimen designed to mimic IBD patient treatment. Compared to control mice that received antibiotics and PBS vehicle control, mice treated with F. nucleatum exhibited disruption of the colonic architecture, with increased immune infiltrate and depleted mucus layer, resulting in a closer proximity of luminal contents to the epithelium. Analysis of mucosal gene expression revealed increased levels of epithelial TNF and KC (mouse homolog of IL-8), in addition to immune cell derived IL-6 in F. nucleatum-treated mice compared for controls. Conclusions These data provide evidence that F. nucleatum is capable of driving a pro-inflammatory signaling cascade in vitro and in vivo and F. nucleatum may represent a specific target for drug therapy.

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Mandal, Devi Prasad, Neeta Mohanty, Paresh Kumar Behera, Divya Gopinath, Sasmita Panda, Abdulaziz A. Al-Kheraif, Darshan Devang Divakar, Sukumaran Anil, and Swagatika Panda. "A Plausible Proposition of CCL20-Related Mechanism in Fusobacterium nucleatum-Associated Oral Carcinogenesis." Life 11, no. 11 (November 10, 2021): 1218. http://dx.doi.org/10.3390/life11111218.

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Objective: The objective of this prospective observational case–control study is to evaluate the prevalence of Fusobacterium nucleatum in the tissues of oral squamous cell carcinoma (OSCC). Reconnoitering the CCL20-related mechanism of carcinogenesis in Fusobacterium nucleatum-positive OSCC is another objective. Methodology: Tissues from 50 OSCC patients and 30 healthy oral tissues were collected. The prevalence of Fusobacterium nucleatum was evaluated in both tumour and healthy tissue by polymerase chain reaction. The immunohistochemistry of OSCC tissues was conducted to evaluate the difference in the expression of CCL20 between Fusobacterium nucleatum-positive and -negative OSCC tissues. Results: Fusobacterium nucleatum was significantly (p < 0.001) prevalent in OSCC tissues (74%), compared to healthy tissues (26%). No association of Fusobacterium nucleatum or CCL20 immuno-expression with any clinical or histopathological features of OSCC was observed. While the intensity of CCL20 immuno-expression did not differ (p = 0.053), the CCL20-positive cell population was significantly different (p = 0.034) between Fusobacterium nucleatum-positive and -negative OSCC. Conclusion: Fusobacterium nucleatum is possibly prevalent in oral cancer tissues in the Indian population. By using immunohistochemistry, this is the first study to propose that the carcinogenesis in Fusobacterium nucleatum-positive OSCC may be CCL20-related. The findings enrich the knowledge of mechanisms involved in Fusobacterium nucleatum-mediated oral carcinogenesis.

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Kang, Wenyan, Zhilong Jia, Di Tang, Zhanwei Zhang, Hui Gao, Kunlun He, and Qiang Feng. "Fusobacterium nucleatum Facilitates Apoptosis, ROS Generation, and Inflammatory Cytokine Production by Activating AKT/MAPK and NF-κB Signaling Pathways in Human Gingival Fibroblasts." Oxidative Medicine and Cellular Longevity 2019 (October 13, 2019): 1–22. http://dx.doi.org/10.1155/2019/1681972.

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Fusobacterium nucleatum (F. nucleatum) plays key roles in the initiation and progression of periodontitis. However, the pathogenic effect of F. nucleatum on human oral tissues and cells has not been fully evaluated. In this study, we aimed to analyze the pathogenic effects of F. nucleatum on human gingival fibroblasts (GFs) and clarify the potential mechanisms. RNA-sequencing analysis confirmed that F. nucleatum significantly altered the gene expression of GF as the stimulation time increased. Cell counting and EdU-labeling assays indicated that F. nucleatum inhibited GF proliferation and promoted cell apoptosis in a time- and dose-dependent manner. In addition, cell apoptosis, intracellular reactive oxygen species (ROS) generation, and proinflammatory cytokine production were dramatically elevated after F. nucleatum stimulation. Furthermore, we found that the AKT/MAPK and NF-κB signaling pathways were significantly activated by F. nucleatum infection and that a large number of genes related to cellular proliferation, apoptosis, ROS, and inflammatory cytokine production downstream of AKT/MAPK and NF-κB signaling pathways were significantly altered in F. nucleatum-stimulated GFs. These findings suggest that F. nucleatum inhibits GF proliferation and promotes cell apoptosis, ROS generation, and inflammatory cytokine production partly by activating the AKT/MAPK and NF-κB signaling pathways. Our study opens a new window for understanding the pathogenic effects of periodontal pathogens on the host oral system.

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Varela Barca, Laura, Javier Miguelena Hycka, Javier Cobo Reinoso, and Jose Romero Vivas. "Endocarditis por Fusobacterium nucleatum." Revista Colombiana de Cardiología 24, no. 5 (September 2017): 539–40. http://dx.doi.org/10.1016/j.rccar.2017.05.009.

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Hockensmith, M. L., D. L. Mellman, and E. L. Aronsen. "Fusobacterium nucleatum Empyema Necessitans." Clinical Infectious Diseases 29, no. 6 (December 1, 1999): 1596–98. http://dx.doi.org/10.1086/313553.

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17

Haake, Susan Kinder, Sean C. Yoder, Gwynne Attarian, and Kara Podkaminer. "Native Plasmids of Fusobacterium nucleatum: Characterization and Use in Development of Genetic Systems." Journal of Bacteriology 182, no. 4 (February 15, 2000): 1176–80. http://dx.doi.org/10.1128/jb.182.4.1176-1180.2000.

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ABSTRACT Three native plasmids of Fusobacterium nucleatum were characterized, including DNA sequence analysis of one plasmid, pFN1. A shuttle plasmid, pHS17, capable of transforming Escherichia coli and F. nucleatum ATCC 10953 was constructed with pFN1. pHS17 was stably maintained in the F. nucleatum transformants, and differences in the transformation efficiencies suggested the presence of a restriction-modification system in F. nucleatum.

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Kim, Younghoon, Nam Yun Cho, and Gyeong Hoon Kang. "Prognostic and clinicopathological significance of Fusobacterium nucleatum in colorectal cancer: a systemic review and meta-analysis." Journal of Pathology and Translational Medicine 56, no. 3 (May 15, 2022): 144–51. http://dx.doi.org/10.4132/jptm.2022.03.13.

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Background: Fusobacterium nucleatum has been identified to promote tumor progression in colorectal cancer (CRC). However, association between F. nucleatum and prognostic or clinicopathological features has been diverse among studies, which could be affected by type of biospecimen (formalin-fixed paraffin-embedded or fresh frozen [FF]).Methods: Articles were systemically reviewed for studies that included the correlation between F. nucleatum and prognosis or clinicopathological features in CRC.Results: Ten articles, eight studies with survival-related features involving 3,199 patients and nine studies with clinical features involving 2,655 patients, were eligible for the meta-analysis. Overall survival, disease-free survival, and cancer-specific survival were all associated with worse prognosis in F. nucleatum–high patients (p<.05). In subgroup analysis, only studies with FF tissues retained prognostic significance with F. nucleatum. In meta-analysis of clinicopathological variables, F. nucleatum level was associated with location within colon, pT category, MLH1 hypermethylation, microsatellite instability status, and BRAF mutation regardless of type of biospecimen. However, lymph node metastasis and KRAS mutation was only associated with F. nucleatum level in FF-based studies.Conclusions: In conclusion, type of biospecimen could affect the role of F. nucleatum as a biomarker associated with clinicopathological features and prognosis.

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Ikegami, Akihiko, Peter Chung, and Yiping W. Han. "Complementation of the fadA Mutation in Fusobacterium nucleatum Demonstrates that the Surface-Exposed Adhesin Promotes Cellular Invasion and Placental Colonization." Infection and Immunity 77, no. 7 (April 27, 2009): 3075–79. http://dx.doi.org/10.1128/iai.00209-09.

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ABSTRACT Fusobacterium nucleatum is a gram-negative oral anaerobe implicated in periodontal disease and adverse pregnancy outcome. The organism colonizes the mouse placenta, causing localized infection and inflammation. The mechanism of placental colonization has not been elucidated. Previous studies identified a novel adhesin from F. nucleatum, FadA, as being involved in the attachment and invasion of host cells. The fadA deletion mutant F. nucleatum 12230 US1 was defective in host cell attachment and invasion in vitro, but it also exhibited pleiotropic effects with altered cell morphology and growth rate. In this study, a fadA-complementing clone, F. nucleatum 12230 USF81, was constructed. The expression of FadA on USF81 was confirmed by Western blotting and immunofluorescent labeling. USF81 restored host cell attachment and invasion activities. The ability of F. nucleatum 12230, US1, and USF81 to colonize the mouse placenta was examined. US1 was severely defective in placental colonization compared to the wild type and USF81. Thus, FadA plays an important role in F. nucleatum colonization in vivo. These results also represent the first complementation studies for F. nucleatum. FadA may be a therapeutic target for preventing F. nucleatum colonization of the host.

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Ganesan, Kumar, Songhe Guo, Sundaz Fayyaz, Ge Zhang, and Baojun Xu. "Targeting Programmed Fusobacterium nucleatum Fap2 for Colorectal Cancer Therapy." Cancers 11, no. 10 (October 18, 2019): 1592. http://dx.doi.org/10.3390/cancers11101592.

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Colorectal patients generally have the maximum counts of Fusobacterium nucleatum (F. nucleatum) in tumors and elevate colorectal adenomas and carcinomas, which show the lowest rate of human survival. Hence, F. nucleatum is a diagnostic marker of colorectal cancer (CRC). Studies demonstrated that targeting fusobacterial Fap2 or polysaccharide of the host epithelium may decrease fusobacteria count in the CRC. Attenuated F. nucleatum-Fap2 prevents transmembrane signals and inhibits tumorigenesis inducing mechanisms. Hence, in this review, we hypothesized that application of genetically programmed fusobacterium can be skillful and thus reduce fusobacterium in the CRC. Genetically programmed F. nucleatum is a promising antitumor strategy.

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Yu, Mi Ra, Hye Jung Kim, and Hae Ryoun Park. "Fusobacterium nucleatum Accelerates the Progression of Colitis-Associated Colorectal Cancer by Promoting EMT." Cancers 12, no. 10 (September 23, 2020): 2728. http://dx.doi.org/10.3390/cancers12102728.

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Recently, it has been reported that Fusobacterium nucleatum, a major pathogen involved in chronic periodontitis, may play an important role in colorectal cancer (CRC) progression. In addition, inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease represent major predisposing conditions for the development of CRC, and this subtype of cancer is called colitis-associated cancer (CAC). Although the importance of F. nucleatum in CRC has attracted attention, its exact role and related mechanism in CAC progression remain unclear. In this study, we investigated the effects of F. nucleatum in experimental colitis induced with dextran sodium sulfate (DSS), which is a well-known colitis-inducing chemical, on the aggressiveness of CAC and its related mechanism in both in vitro and in vivo models. F. nucleatum synergistically increased the aggressiveness and epithelial–mesenchymal transition (EMT) characteristics of CRC cells that were treated with DSS compared to those in non-treated CRC cells. The role of F. nucleatum in CAC progression was further confirmed in mouse models, as F. nucleatum was found to significantly increase the malignancy of azoxymethane (AOM)/DSS-induced colon cancer. This promoting effect of F. nucleatum was based on activation of the EGFR signaling pathways, including protein kinase B (AKT) and extracellular signal-regulated kinase (ERK), and epidermal growth factor receptor (EGFR) inhibition significantly reduced the F. nucleatum-induced EMT alteration. In conclusion, F. nucleatum accelerates the progression of CAC by promoting EMT through the EGFR signaling pathway.

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Ahn, Hyeok, Kyungchan Min, Eulgi Lee, Hyun Kim, Sujeong Kim, Yunjae Kim, Gihyeon Kim, et al. "Whole-Transcriptome Sequencing Reveals Characteristics of Cancer Microbiome in Korean Patients with GI Tract Cancer: Fusobacterium nucleatum as a Therapeutic Target." Microorganisms 10, no. 10 (September 23, 2022): 1896. http://dx.doi.org/10.3390/microorganisms10101896.

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Remarkable progress has occurred over the past two decades in identifying microbiomes affecting the human body in numerous ways. The microbiome is linked to gastrointestinal (GI) tract cancer. The purpose of this study was to determine if there is a common microbiome among GI tract cancers and how the microbiome affects the disease. To ensure ethnic consistency, Korean patients with GI tract cancer were selected. Fusobacterium nucleatum is an enriched bacteria in all cancer tissues. F. nucleatum is a Gram-negative obligate anaerobe that promotes colorectal cancer. Through Gene Set Enrichment Analysis (GSEA) and Differentially Expressed Genes (DEG) analyses, the upregulation of the G2M checkpoint pathway was identified in the F. nucleatum-high group. Cell viability and G2M checkpoint pathway genes were examined in MC 38 cells treated with F. nucleatum. F. nucleatum upregulated the expression of G2M checkpoint pathway genes and the cell proliferation of MC 38 cells. F. nucleatum facilitated cancer’s use of G2M checkpoint pathways and F. nucleatum could be a therapeutic target in Korean GI tract cancer.

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DZINK, J. L., M. T. SHEENAN, and S. S. SOCRANSKY. "Proposal of Three Subspecies of Fusobacterium nucleatum Knorr 1922: Fusobacterium nucleatum subsp. nucleatum subsp. nov., comb. nov.; Fusobacterium nucleatum subsp. polymorphum subsp. nov., nom. rev., comb. nov.; and Fusobacterium nucleatum subsp. vincentii subsp. nov., nom. rev., comb. nov." International Journal of Systematic Bacteriology 40, no. 1 (January 1, 1990): 74–78. http://dx.doi.org/10.1099/00207713-40-1-74.

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Ugai, Tomotaka, Hidetaka Kawamura, Yasutoshi Takashima, Kazuo Okadome, Takashi Shimizu, Kosuke Mima, Seyed Mostafa Mousavi Kahaki, et al. "Abstract B002: History of appendectomy and colorectal cancer oncidence, overall and by intratumoral fusobacterium nucleatum status." Cancer Research 82, no. 23_Supplement_1 (December 1, 2022): B002. http://dx.doi.org/10.1158/1538-7445.crc22-b002.

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Abstract Background: Evidence suggests that Fusobacterium nucleatum (F. nucleatum) plays a role in colorectal carcinogenesis by suppressing the host immune response to tumors. The appendix is an organ that may influence the intestinal microbiome. We hypothesized that appendectomy history might be associated with altered colorectal cancer incidence and that the association might differ by the amount of F. nucleatum in tumor tissue. Methods: Utilizing the Nurses’ Health Study and the Health Professionals Follow-up Study, we examined the association of appendectomy history with the incidence of colorectal cancer overall and tumor subtypes classified by the amount of intratumoral F. nucleatum. We used an inverse probability weighted multivariable Cox proportional hazards regression model to control for potential confounders and selection bias due to tissue availability and potential confounders. Results: During follow-up of 139,424 participants (2,894,345 person-years), we documented 2,819 colorectal cancer cases, including 1,069 cases with available intratumoral F. nucleatum data. While appendectomy history was not statistically significantly associated with the incidence of colorectal cancer [multivariable-adjusted hazard ratio (HR), 0.92; 95% confidence interval (CI), 0.84 to 1.01, P=0.068], the association of appendectomy history with colorectal cancer incidence differed by intratumoral F. nucleatum status (Pheterogeneity=0.013). Appendectomy history was associated with reduced incidence of F. nucleatum-positive tumors (multivariable-adjusted HR, 0.52; 95% CI, 0.33 to 0.84, P=0.0067), but not F. nucleatum-negative tumors (multivariable-adjusted HR, 0.98; 95% CI, 0.84 to 1.14, P=0.79). Conclusions: We found that appendectomy history was associated with reduced incidence of F. nucleatum-positive (but not F. nucleatum-negative) colorectal cancer. Our findings suggest that an appendectomy may change the intestinal microbiota, thereby altering potential pathogenic effect of F. nucleatum. Citation Format: Tomotaka Ugai, Hidetaka Kawamura, Yasutoshi Takashima, Kazuo Okadome, Takashi Shimizu, Kosuke Mima, Seyed Mostafa Mousavi Kahaki, Melissa Zhao, Juha P. Väyrynen, Xuehong Zhang, Kimmie Ng, Jonathan A. Nowak, Jeffrey A. Meyerhardt, Edward L. Giovannucci, Marios Giannakis, Andrew T. Chan, Curtis Huttenhower, Wendy S. Garrett, Mingyang Song, Shuji Ogino. History of appendectomy and colorectal cancer oncidence, overall and by intratumoral fusobacterium nucleatum status [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer; 2022 Oct 1-4; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_1):Abstract nr B002.

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Carlsson, J., J. T. Larsen, and M. B. Edlund. "Utilization of glutathione (l-γ-glutamyl-l-cysteinylglycine) by Fusobacterium nucleatum subspecies nucleatum." Oral Microbiology and Immunology 9, no. 5 (October 1994): 297–300. http://dx.doi.org/10.1111/j.1399-302x.1994.tb00074.x.

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Klees, Anne-Grit, Dietmar Linder, and Wolfgang Buckel. "2-Hydroxyglutaryl-CoA dehydratase from Fusobacterium nucleatum (subsp. nucleatum): an iron-sulfur flavoprotein." Archives of Microbiology 158, no. 4 (September 1992): 294–301. http://dx.doi.org/10.1007/bf00245248.

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Suehiro, Yutaka, Kouhei Sakai, Mitsuaki Nishioka, Shinichi Hashimoto, Taro Takami, Shingo Higaki, Yoshitaro Shindo, et al. "Highly sensitive stool DNA testing of Fusobacterium nucleatum as a marker for detection of colorectal tumours in a Japanese population." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 54, no. 1 (September 28, 2016): 86–91. http://dx.doi.org/10.1177/0004563216643970.

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Background Accumulating evidence shows an over-abundance of Fusobacterium nucleatum in colorectal tumour tissues. Although stool DNA testing of Fusobacterium nucleatum might be a potential marker for the detection of colorectal tumours, the difficulty in detecting Fusobacterium nucleatum in stool by conventional methods prevented further explorations. Therefore, we developed a droplet digital polymerase chain reaction (PCR) assay for detecting Fusobacterium nucleatum in stool and investigated its clinical utility in the management of colorectal tumours in a Japanese population. Methods Feces were collected from 60 healthy subjects (control group) and from 11 patients with colorectal non-advanced adenomas (non-advanced adenoma group), 19 patients with colorectal advanced adenoma/carcinoma in situ (advanced adenoma/carcinoma in situ (CIS) group) and 158 patients with colorectal cancer of stages I to IV (colorectal cancer group). Absolute copy numbers of Fusobacterium nucleatum were measured by droplet digital PCR. Results The median copy number of Fusobacterium nucleatum was 17.5 in the control group, 311 in the non-advanced adenoma group, 122 in the advanced adenoma/CIS group, and 317 in the colorectal cancer group. In comparison with that in the control group, the Fusobacterium nucleatum level was significantly higher in the non-advanced adenoma group, the advanced adenoma/CIS group and the colorectal cancer group. Conclusions This study illustrates the potential of stool DNA testing of Fusobacterium nucleatum by droplet digital PCR to detect individuals with colorectal tumours in a Japanese population.

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Novak, Karen F., William J. Diamond, Sreenatha Kirakodu, Rebecca Peyyala, Kimberly W. Anderson, Ronald C. Montelaro, and Timothy A. Mietzner. "Efficacy of the De Novo-Derived Antimicrobial Peptide WLBU2 against Oral Bacteria." Antimicrobial Agents and Chemotherapy 51, no. 5 (February 26, 2007): 1837–39. http://dx.doi.org/10.1128/aac.00924-06.

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ABSTRACT The efficacy of a novel synthetic antimicrobial peptide (WLBU2) was evaluated against three oral microorganisms (grown planktonically): Streptococcus gordonii, Fusobacterium nucleatum, and Porphyromonas gingivalis. WLBU2 killed all three species, with F. nucleatum being the most susceptible. WLBU2 also reduced the bacterial burden of S. gordonii and F. nucleatum biofilms.

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Hilmi, Marc, Cindy Neuzillet, Jérémie H. Lefèvre, Magali Svrcek, Sophie Vacher, Leonor Benhaim, Peggy Dartigues, et al. "Prognostic Value of Fusobacterium nucleatum after Abdominoperineal Resection for Anal Squamous Cell Carcinoma." Cancers 14, no. 7 (March 22, 2022): 1606. http://dx.doi.org/10.3390/cancers14071606.

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Main prognostic factors of anal squamous cell carcinoma (ASCC) are tumor size, differentiation, lymph node involvement, and male gender. However, they are insufficient to predict relapses after exclusive radiotherapy (RT) or chemoradiotherapy (CRT). Fusobacterium nucleatum has been associated with poor prognosis in several digestive cancers. In this study, we assessed the association between intratumoral F. nucleatum load and clinico-pathological features, relapse, and survival in patients with ASCC who underwent abdominoperineal resection (APR) after RT/CRT. We retrospectively analyzed surgical samples from a cohort of 166 patients with ASCC who underwent APR. F. nucleatum 16S rRNA gene sequences were quantified using real-time quantitative PCR. We associated F. nucleatum load with classical clinicopathological features, overall survival (OS), disease-free survival (DFS), and metastasis-free survival (MFS) using Cox regression univariate and multivariate analyses. Tumors harboring high loads of F. nucleatum (highest tercile) showed longer OS and DFS (median: not reached vs. 50.1 months, p = 0.01, and median: not reached vs. 18.3 months, p = 0.007, respectively). High F. nucleatum load was a predictor of longer OS (HR = 0.55, p = 0.04) and DFS (HR = 0.50, p = 0.02) in multivariate analysis. High F. nucleatum load is an independent favorable prognostic factor in patients with ASCC who underwent APR.

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Krome, Susanne. "Link zwischen Ernährung, Darmflora und Tumorentstehung." Onkologische Welt 08, no. 05 (September 2017): 225. http://dx.doi.org/10.1055/s-0038-1639637.

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Fusobacterium nucleatum kommt in Adenomen und Kolonkarzinomen teilweise angereichert vor Sein Nachweis war mit einer erhöhten Tumoraggressivität assoziiert. Eine Langzeitstudie weist nun darauf hin, dass eine ballaststoffarme Ernährung mit viel rotem Fleisch die Besiedlung mit F. nucleatum fördert. Das Bakterium ist eine wahrscheinliche Schnittstelle zwischen Ernährungstyp und F. nucleatum-positiven Kolonkarzinomen, so die Autoren.

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Edwards, Andrew M., Tracy J. Grossman, and Joel D. Rudney. "Fusobacterium nucleatum Transports Noninvasive Streptococcus cristatus into Human Epithelial Cells." Infection and Immunity 74, no. 1 (January 2006): 654–62. http://dx.doi.org/10.1128/iai.74.1.654-662.2006.

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ABSTRACT Analysis of human buccal epithelial cells frequently reveals an intracellular polymicrobial consortium of bacteria. Although several oral bacteria have been demonstrated to invade cultured epithelial cells, several others appear unable to internalize. We hypothesized that normally noninvasive bacteria may gain entry into epithelial cells via adhesion to invasive bacteria. Fusobacterium nucleatum is capable of binding to and invading oral epithelial cells. By contrast, Streptococcus cristatus binds weakly to host cells and is not internalized. F. nucleatum and S. cristatus coaggregate strongly via an arginine-sensitive interaction. Coincubation of KB or TERT-2 epithelial cells with equal numbers of F. nucleatum and S. cristatus bacteria led to significantly increased numbers of adherent and internalized streptococci. F. nucleatum also promoted invasion of KB cells by other oral streptococci and Actinomyces naeslundii. Dissection of fusobacterial or streptococcal adhesive interactions by using sugars, amino acids, or antibodies demonstrated that this phenomenon is due to direct attachment of S. cristatus to adherent and invading F. nucleatum. Inhibition of F. nucleatum host cell attachment and invasion with galactose, or fusobacterial-streptococcal coaggregation by the arginine homologue l-canavanine, abrogated the increased S. cristatus adhesion to, and invasion of, host cells. In addition, polyclonal antibodies to F. nucleatum, which inhibited fusobacterial attachment to both KB cells and S. cristatus, significantly decreased invasion by both species. Similar decreases were obtained when epithelial cells were pretreated with cytochalasin D, staurosporine, or cycloheximide. These studies indicate that F. nucleatum may facilitate the colonization of epithelial cells by bacteria unable to adhere or invade directly.

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Stokowa-Sołtys, Kamila, Kamil Wojtkowiak, and Karolina Jagiełło. "Fusobacterium nucleatum – Friend or foe?" Journal of Inorganic Biochemistry 224 (November 2021): 111586. http://dx.doi.org/10.1016/j.jinorgbio.2021.111586.

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Li, Rongrong, Jilu Shen, and Yuanhong Xu. "Fusobacterium nucleatum and Colorectal Cancer." Infection and Drug Resistance Volume 15 (March 2022): 1115–20. http://dx.doi.org/10.2147/idr.s357922.

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Haber, Stuart W. "Splenic Abscess from Fusobacterium nucleatum." Annals of Internal Medicine 110, no. 11 (June 1, 1989): 948. http://dx.doi.org/10.7326/0003-4819-110-11-948_1.

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Merritt, Justin, Guoqing Niu, Toshinori Okinaga, and Felicia Qi. "Autoaggregation Response of Fusobacterium nucleatum." Applied and Environmental Microbiology 75, no. 24 (October 16, 2009): 7725–33. http://dx.doi.org/10.1128/aem.00916-09.

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ABSTRACT Fusobacterium nucleatum is a gram-negative oral bacterial species associated with periodontal disease progression. This species is perhaps best known for its ability to adhere to a vast array of other bacteria and eukaryotic cells. Numerous studies of F. nucleatum have examined various coaggregation partners and inhibitors, but it is largely unknown whether these interactions induce a particular genetic response. We tested coaggregation between F. nucleatum ATCC strain 25586 and various species of Streptococcus in the presence of a semidefined growth medium containing saliva. We found that this condition could support efficient coaggregation but, surprisingly, also stimulated a similar degree of autoaggregation. We further characterized the autoaggregation response, since few reports have examined this in F. nucleatum. After screening several common coaggregation inhibitors, we identified l-lysine as a competitive inhibitor of autoaggregation. We performed a microarray analysis of the planktonic versus autoaggregated cells and found nearly 100 genes that were affected after only about 60 min of aggregation. We tested a subset of these genes via real-time reverse transcription-PCR and confirmed the validity of the microarray results. Some of these genes were also found to be inducible in cell pellets created by centrifugation. Based upon these data, it appears that autoaggregation activates a genetic program that may be utilized for growth in a high cell density environment, such as the oral biofilm.

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Tweedy, Charles R., and William B. White. "Multiple Fusobacterium Nucleatum Liver Abscesses." Journal of Clinical Gastroenterology 9, no. 2 (April 1987): 194–97. http://dx.doi.org/10.1097/00004836-198704000-00017.

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Gholizadeh, Pourya, Hosein Eslami, and Hossein Samadi Kafil. "Carcinogenesis mechanisms of Fusobacterium nucleatum." Biomedicine & Pharmacotherapy 89 (May 2017): 918–25. http://dx.doi.org/10.1016/j.biopha.2017.02.102.

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Hutton, J. "Sheep abortion outbreak - possiblyFusobacterium nucleatum." New Zealand Veterinary Journal 40, no. 1 (March 1992): 35. http://dx.doi.org/10.1080/00480169.1992.36514.

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Ang, Mia Yang, Avirup Dutta, Wei Yee Wee, David Dymock, Ian C. Paterson, and Siew Woh Choo. "Comparative Genome Analysis ofFusobacterium nucleatum." Genome Biology and Evolution 8, no. 9 (August 18, 2016): 2928–38. http://dx.doi.org/10.1093/gbe/evw199.

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FREDRIKSEN, GJERT, and TOR HOFSTAD. "CHEMOTYPES OF FUSOBACTERIUM NUCLEATUM LIPOPOLYSACCHARIDES." Acta Pathologica Microbiologica Scandinavica Section B Microbiology 86B, no. 1-6 (August 15, 2009): 41–46. http://dx.doi.org/10.1111/j.1699-0463.1978.tb00006.x.

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41

Ugai, Tomotaka, Takashi Shimizu, Hidetaka Kawamura, Yasutoshi Takashima, Juha P. Väyrynen, Seyed Mostafa Mousavi Kahaki, Kazuo Okadome, et al. "Abstract B001: Inverse relationship between tissue fusobacterium nucleatum amount and CD274 (PD-L1) expression of colorectal carcinoma." Cancer Research 82, no. 23_Supplement_1 (December 1, 2022): B001. http://dx.doi.org/10.1158/1538-7445.crc22-b001.

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Abstract Background: The CD274 (programmed cell death ligand 1, PD-L1)/PDCD1 (programmed cell death 1, PD-1) immune checkpoint axis is known to regulate the antitumor immune response. Evidence suggests that Fusobacterium nucleatum (F. nucleatum) promotes colorectal carcinogenesis through its suppressive effect on antitumor immunity. We hypothesized that tumor CD274 overexpression and intratumor abundance of F. nucleatum might tend to be mutually exclusive immune evasion mechanisms in colorectal cancer. Methods: We assessed tumor CD274 expression by immunohistochemistry and F. nucleatum DNA within tumor tissue by quantitative polymerase chain reaction in 812 cases among 4,465 incident colorectal cancer cases that had occurred in the Nurses’ Health Study and the Health Professionals Follow-up Study. To adjust for potential confounders and selection bias due to tissue data availability, inverse probability weighting was integrated into multivariable ordinal logistic regression analyses to examine the association of tumor CD274 expression with the amount of intratumor F. nucleatum. Results: Tumor CD274 expression was negative in 93 (11%), low in 231 (28%), intermediate in 210 (26%), and high in 278 (34%) of 812 cases. F. nucleatum DNA was detected in tumor tissue in 109 (13%) cases of 812 cases. Tumor CD274 expression level was inversely associated with the amount of F. nucleatum in colorectal cancer tissue. For one category increase in three ordinal F. nucleatum categories (negative, low, and high), multivariable-adjusted odds ratios (with 95% confidence intervals) of the low, middle, and high CD274 expression categories (vs. negative) were 0.78 (0.41-1.51), 0.64 (0.32-1.28), and 0.50 (0.25–0.99), respectively (Ptrend=0.032). Conclusions: We found that CD274 expression was inversely associated with the amount of F. nucleatum in colorectal cancer tissue. Our findings suggest that a colorectal tumor tends to have either of the immune evasion mechanisms, i.e., PDCD1 (PD-1) immune checkpoint activation and intratumor abundance of F. nucleatum. Citation Format: Tomotaka Ugai, Takashi Shimizu, Hidetaka Kawamura, Yasutoshi Takashima, Juha P. Väyrynen, Seyed Mostafa Mousavi Kahaki, Kazuo Okadome, Yohei Masugi, Annacarolina da Silva, Xuehong Zhang, Andrew T. Chan, Molin Wang, Jeffrey A. Meyerhardt, Jonathan A. Nowak, Mingyang Song, Marios Giannakis, Shuji Ogino. Inverse relationship between tissue fusobacterium nucleatum amount and CD274 (PD-L1) expression of colorectal carcinoma [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer; 2022 Oct 1-4; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_1):Abstract nr B001.

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Xie, H., R. J. Gibbons, and D. I. Hay. "Adhesive properties of strains of Fusobacterium nucleatum of the subspecies nucleatum, vincentii and polymorphum." Oral Microbiology and Immunology 6, no. 5 (October 1991): 257–63. http://dx.doi.org/10.1111/j.1399-302x.1991.tb00488.x.

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Grenier, D., and L. Grignon. "Response of human macrophage-like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide." Oral Microbiology and Immunology 21, no. 3 (June 2006): 190–96. http://dx.doi.org/10.1111/j.1399-302x.2006.00278.x.

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Beatrix, Birgitta, Klaus Bendrat, Sabine Rospert, and Wolfgang Buckel. "The biotin-dependent sodium ion pump glutaconyl-CoA decarboxylase from Fusobacterium nucleatum (subsp. nucleatum)." Archives of Microbiology 154, no. 4 (September 1990): 362–69. http://dx.doi.org/10.1007/bf00276532.

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Fukuda, Soichiro, Shunsuke Ito, Jun Nishikawa, Tatsuya Takagi, Naoto Kubota, Ken-ichiro Otsuyama, Hidehiro Tsuneoka, et al. "Deep Ultraviolet Light-Emitting Diode Light Therapy for Fusobacterium nucleatum." Microorganisms 9, no. 2 (February 19, 2021): 430. http://dx.doi.org/10.3390/microorganisms9020430.

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Background: Fusobacterium nucleatum, which is associated with periodontitis and gingivitis, has been detected in colorectal cancer (CRC). Methods: We evaluated the bactericidal effect of deep ultraviolet (DUV) light-emitting diode (LED) light therapy on F. nucleatum both qualitatively and quantitatively. Two DUV-LEDs with peak wavelengths of 265 and 280-nm were used. DNA damage to F. nucleatum was evaluated by the production of cyclobutane pyrimidine dimers (CPD) and pyrimidine (6–4) pyrimidone photoproducts (6–4PP). Results: DUV-LEDs showed a bactericidal effect on F. nucleatum. No colony growth was observed after 3 min of either 265 nm or 280 nm DUV-LED irradiation. The survival rates of F. nucleatum under 265 nm DUV-LED light irradiation dropped to 0.0014% for 10 s and to 0% for 20 s irradiation. Similarly, the survival rate of F. nucleatum under 280 nm DUV-LED light irradiation dropped to 0.00044% for 10 s and 0% for 20 s irradiation. The irradiance at the distance of 35 mm from the DUV-LED was 0.265 mW/cm2 for the 265 nm LED and 0.415 mW/cm2 for the 280 nm LED. Thus, the radiant energy for lethality was 5.3 mJ/cm2 for the 265 nm LED and 8.3 mJ/cm2 for the 280 nm LED. Amounts of CPD and 6–4PP in F. nucleatum irradiated with 265 nm DUV-LED light were 6.548 ng/µg and 1.333 ng/µg, respectively. Conclusions: DUV-LED light exerted a bactericidal effect on F. nucleatum by causing the formation of pyrimidine dimers indicative of DNA damage. Thus, DUV-LED light therapy may have the potential to prevent CRC.

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Darenfed, H., D. Grenier, and D. Mayrand. "Acquisition of Plasmin Activity byFusobacterium nucleatum subsp. nucleatum and Potential Contribution to Tissue Destruction during Periodontitis." Infection and Immunity 67, no. 12 (December 1, 1999): 6439–44. http://dx.doi.org/10.1128/iai.67.12.6439-6444.1999.

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ABSTRACT Fusobacterium nucleatum subsp. nucleatumhas been associated with a variety of oral and nonoral infections such as periodontitis, pericarditis, bone infections, and brain abscesses. Several studies have shown the role of plasmin, a plasma serine protease, in increasing the invasive capacity of microorganisms. In this study, we investigated the binding of human plasminogen toF. nucleatum subsp. nucleatum, and its subsequent activation into plasmin. Plasminogen-binding activity of bacterial cells was demonstrated by a solid-phase dot blot assay using an anti-plasminogen antibody. The binding activity was heat resistant and involved cell-surface lysine residues since it was abolished in the presence of the lysine analog ɛ-aminocaproic acid. Activation of plasminogen-coated bacteria occurred following incubation with either streptokinase, urokinase-type plasminogen activator (u-PA), or aPorphyromonas gingivalis culture supernatant. In the case of the P. gingivalis culture supernatant, a cysteine protease was likely involved in the activation. The plasmin activity generated on the cell surface of F. nucleatum subsp.nucleatum could be inhibited by aprotinin. Activation of plasminogen by u-PA was greatly enhanced when plasminogen was bound to bacteria rather than in a free soluble form. u-PA-activated plasminogen-coated F. nucleatum subsp.nucleatum was found to degrade fibronectin, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Tissue inhibitor of metalloproteinase-1 was also degraded by the plasmin activity generated on the bacterial cells. This study suggests a possible role for plasminogen, which is present in affected periodontal sites, in promoting tissue destruction and invasion by nonproteolytic bacteria such as F. nucleatum subsp. nucleatum.

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Jabra-Rizk, Mary Ann, William A. Falkler, William G. Merz, Jacqueline I. Kelley, A. A. M. A. Baqui, and Timothy F. Meiller. "Coaggregation of Candida dubliniensiswith Fusobacterium nucleatum." Journal of Clinical Microbiology 37, no. 5 (1999): 1464–68. http://dx.doi.org/10.1128/jcm.37.5.1464-1468.1999.

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The binding of microorganisms to each other and oral surfaces contributes to the progression of microbial infections in the oral cavity. Candida dubliniensis, a newly characterized species, has been identified in human immunodeficiency virus-seropositive patients and other immunocompromised individuals.C. dubliniensis phenotypically resembles Candida albicans in many respects yet can be identified and differentiated as a unique Candida species by phenotypic and genetic profiles. The purpose of this study was to determine oral coaggregation (CoAg) partners of C. dubliniensis and to compare these findings with CoAg of C. albicansunder the same environmental conditions. Fifteen isolates ofC. dubliniensis and 40 isolates of C. albicans were tested for their ability to coaggregate with strains of Fusobacterium nucleatum,Peptostreptococcus micros, Peptostreptococcus magnus, Peptostreptococcus anaerobius,Porphyromonas gingivalis, and Prevotella intermedia. When C. dubliniensis andC. albicans strains were grown at 37°C on Sabouraud dextrose agar, only C. dubliniensis strains coaggregated with F. nucleatum ATCC 49256 and noC. albicans strains showed CoAg. However, when theC. dubliniensis and C. albicansstrains were grown at 25 or 45°C, both C. dubliniensis and C. albicans strains demonstrated CoAg with F. nucleatum. Heating theC. albicans strains (grown at 37°C) at 85°C for 30 min or treating them with dithiothreitol allowed the C. albicans strains grown at 37°C to coaggregate withF. nucleatum. CoAg at all growth temperatures was inhibited by mannose and α-methyl mannoside but not by EDTA or arginine. The CoAg reaction between F. nucleatum and the Candida species involved a heat-labile component onF. nucleatum and a mannan-containing heat-stable receptor on the Candida species. The CoAg reactions betweenF. nucleatum and the Candida species may be important in the colonization of the yeast in the oral cavity, and the CoAg of C. dubliniensis by F. nucleatum when grown at 37°C provides a rapid, specific, and inexpensive means to differentiate C. dubliniensisfrom C. albicans isolates in the clinical laboratory.

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Liu, Kaixi, Xinran Yang, Mi Zeng, Yumeng Yuan, Jianhong Sun, Ping He, Jiayu Sun, et al. "The Role of Fecal Fusobacterium nucleatum and pks+ Escherichia coli as Early Diagnostic Markers of Colorectal Cancer." Disease Markers 2021 (November 22, 2021): 1–11. http://dx.doi.org/10.1155/2021/1171239.

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Background. Accurate analysis of intestinal microbiota will facilitate establishment of an evaluating system for assessing colorectal cancer (CRC) risk and prognosis. This study evaluates the potential role of Fusobacterium nucleatum (F. nucleatum) and Escherichia coli with a pks gene (pks+ E. coli) in early CRC diagnosis. Methods. We recruited 139 patients, including CRC ( n = 60 ), colorectal adenomatous polyposis (CAP) ( n = 37 ), and healthy individuals ( n = 42 ) based on their colonoscopy examinations. We collected stool and serum samples from the participants and measured the relative abundance of F. nucleatum and pks+ E. coli in fecal samples by quantitative PCR. Receiver operating characteristic curve (ROC) analyses were used to analyze the diagnostic value of single or combined biomarkers. Results. Fecal F. nucleatum and pks+ E. coli levels were higher in the CRC group in either the CAP group or healthy controls ( P = 0.02 ; 0.01). There was no statistical difference in the distribution of F. nucleatum and pks+ E. coli in patients with different tumor sites ( P > 0.05 ). The combination of F. nucleatum+pks+ E. coli+CEA+CA19-9+FOBT was chosen as the optimal panel in differentiating both CRC and CAP from the controls. The combination of F. nucleatum, pks+ E. coli, and FOBT improved diagnostic efficiency. However, there was difficulty in differentiating CRC from CAP. Conclusion. Our results suggested that combining bacterial markers with conventional tumor markers improves the diagnostic efficiency for noninvasive diagnosis of CRC.

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Sasaki-Imamura, Takako, Akira Yano, and Yasuo Yoshida. "Production of Indole from l-Tryptophan and Effects of These Compounds on Biofilm Formation by Fusobacterium nucleatum ATCC 25586." Applied and Environmental Microbiology 76, no. 13 (May 14, 2010): 4260–68. http://dx.doi.org/10.1128/aem.00166-10.

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ABSTRACT The l-tryptophan degradation product indole is a purported extracellular signaling molecule that influences biofilm formation in various bacteria. Here we analyzed the mechanisms of indole production in Fusobacterium nucleatum and the effects of tryptophan and indole on F. nucleatum planktonic and biofilm cells. The amino acid sequence deduced from the fn1943 gene in F. nucleatum ATCC 25586 was 28% identical to that deduced from tnaA in Escherichia coli, which encodes tryptophanase catalyzing the β-elimination of l-tryptophan to produce indole. The fn1943 gene was cotranscribed with the downstream gene fn1944, which is a homolog of tnaB encoding low-affinity tryptophan permease. The transcript started at position −68 or −153 from the first nucleotide of the fn1943 translation initiation codon. Real-time quantitative PCR showed that much more F. nucleatum fn1943 transcripts were obtained from log-phase cells than from stationary-phase cells. Indole production by the purified recombinant protein encoded by fn1943 was examined using high-performance liquid chromatography. The Km and k cat of the enzyme were 0.26 ± 0.03 mM and 0.74 ± 0.04 s−1, respectively. F. nucleatum biofilm formation and the biofilm supernatant concentration of indole increased dose dependently with increasing tryptophan concentrations. Exogenous indole also increased F. nucleatum biofilm formation in a dose-dependent manner. Even at very high concentrations, tryptophan did not affect fn1943 expression, whereas similar indole concentrations decreased expression. Thus, exogenous tryptophan and indole were suggested to increase F. nucleatum biofilms.

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Nakagaki, Hidetaka, Shinichi Sekine, Yutaka Terao, Masahiro Toe, Muneo Tanaka, Hiro-O. Ito, Shigetada Kawabata, Satoshi Shizukuishi, Kohtaro Fujihashi, and Kosuke Kataoka. "Fusobacterium nucleatum Envelope Protein FomA Is Immunogenic and Binds to the Salivary Statherin-Derived Peptide." Infection and Immunity 78, no. 3 (December 14, 2009): 1185–92. http://dx.doi.org/10.1128/iai.01224-09.

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ABSTRACT We have previously shown that one of the minimal active regions of statherin, a human salivary protein, for binding to Fusobacterium nucleatum is a YQPVPE amino acid sequence. In this study, we identified the FomA protein of F. nucleatum, which is responsible for binding to the statherin-derived YQPVPE peptide. Overlay analysis showed that a 40-kDa protein of the F. nucleatum cell envelope (40-kDa CE) specifically bound to the YQPVPE peptide. The equilibrium association constant between the affinity-purified 40-kDa CE and the YQPVPE peptide was 4.30 × 106. Further, the purity and amino acid sequence analyses of the purified 40-kDa CE revealed approximately 98.7% (wt/wt) purity and a high degree of homology with FomA, a major porin protein of F. nucleatum. Thus, a FomA-deficient mutant failed to bind to the YQPVPE peptide. In addition, increased levels of a FomA-specific mucosal IgA antibody (Ab) and plasma IgG and IgA Abs were seen only in mice immunized nasally with cholera toxin (CT) and the purified 40-kDa FomA protein. Interestingly, saliva from mice that received FomA plus CT as a mucosal adjuvant nasally prevented in vitro binding of F. nucleatum to statherin-coated polyvinyl chloride plates. Taken together, these results suggest that induction of specific immunity to the 40-kDa FomA protein of F. nucleatum, which specifically binds to the statherin-derived peptide, may be an effective tool for preventing the formation of F. nucleatum biofilms in the oral cavity.

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