Role of FAD-I in Fusobacterial Interspecies Interaction and Biofilm Formation

Shokeen, Bhumika; Park, Jane; Duong, Emily; Rambhia, Sonam; Paul, Manash K.; Weinberg, Aaron; Shi, Wenyuan; Lux, Renate

doi:10.3390/microorganisms8010070

Cited by 10 publications

(6 citation statements)

References 43 publications

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“…The lack of fad-I, a gene expressed immediately upstream from radD, increases the expression of radD, and then increases the coaggregation of F. nucleatum with S. gordonii and subsequent biofilm formation. These findings suggest that the lipoprotein Fad-I plays an important role in the regulation of RadD adhesion (Shokeen et al, 2020). Another small fusobacterial lipoprotein, Aid1, also participates in the interspecies interactions of F. nucleatum, especially with oral streptococci and related Gram-positive species (Kaplan et al, 2014).…”

Section: Structure and Formation Of Oral Microbial Biofilmsmentioning

confidence: 88%

The Oral Microbiota: Community Composition, Influencing Factors, Pathogenesis, and Interventions

et al. 2022

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The human oral cavity provides a habitat for oral microbial communities. The complexity of its anatomical structure, its connectivity to the outside, and its moist environment contribute to the complexity and ecological site specificity of the microbiome colonized therein. Complex endogenous and exogenous factors affect the occurrence and development of the oral microbiota, and maintain it in a dynamic balance. The dysbiotic state, in which the microbial composition is altered and the microecological balance between host and microorganisms is disturbed, can lead to oral and even systemic diseases. In this review, we discuss the current research on the composition of the oral microbiota, the factors influencing it, and its relationships with common oral diseases. We focus on the specificity of the microbiota at different niches in the oral cavity, the communities of the oral microbiome, the mycobiome, and the virome within oral biofilms, and interventions targeting oral pathogens associated with disease. With these data, we aim to extend our understanding of oral microorganisms and provide new ideas for the clinical management of infectious oral diseases.

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Section: Structure and Formation Of Oral Microbial Biofilmsmentioning

confidence: 88%

The Oral Microbiota: Community Composition, Influencing Factors, Pathogenesis, and Interventions

et al. 2022

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“…Fn species are known to induce the expression of β-defensin and TNF-α and invasion of heterogeneous human epithelial colorectal adenocarcinoma in the Caco-2 cell lines. 18 , 22 , 23 Also, these have been associated with increased chemotherapeutic resistance in tumors via regulation of tumor cell autophagy. 23 Akin to other gram-negative bacteria, Fn shed EVs (FnEVs) that are composed of bacterial outer membrane and periplasmic components.…”

Section: Introductionmentioning

confidence: 99%

Extracellular vesicles of Fusobacterium nucleatum compromise intestinal barrier through targeting RIPK1-mediated cell death pathway

et al. 2021

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Microbial factors that mediate microbes-host interaction in ulcerative colitis (UC), a chronic disease seriously affecting human health, are not fully known. The emerging oncobacterium Fusobacterium nucleatum (Fn) secretes extracellular vesicles carrying several types of harmful molecules in the intestine which can alter microbes-host interaction, especially the epithelial homeostasis in UC. However, the mechanism is not yet clear. Previously, we isolated EVs by the ultracentrifugation of Fn culture media and characterized them as the potent inducer of pro-inflammatory cytokines. Here, we examined the mechanism in detail. We found that in macrophage/Caco-2 co-cultures, FnEVs significantly promoted epithelial barrier loss and oxidative stress damage, which are related to epithelial necroptosis caused by the activation of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Furthermore, FnEVs promoted the migration of RIPK1 and RIPK3 into necrosome in Caco2 cells. Notably, these effects were reversed by TNF-α neutralizing antibody or Necrostatin-1 (Nec-1), a RIPK1 inhibitor. This suggested that FADD-RIPK1-caspase-3 signaling is involved in the process. Moreover, the observed effects were verified in the murine colitis model treated with FnEVs or by adoptive transfer of FnEVs-trained macrophages. In conclusion, we propose that RIPK1-mediated epithelial cell death promotes FnEVs-induced gut barrier disruption in UC and the findings can be used as the basis to further investigate this disease.

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“…to evade host defenses and induce abnormal host immune responses. [27][28][29] Fn was found to be present in colon cancer as well as in primary tumors and liver metastases and that its presence is correlated with poor patient prognosis. 30 Fn-positive colorectal tumors were transplanted in mice, and antibiotics delayed tumor growth.…”

Section: Dovepressmentioning

confidence: 99%

Airway Fusobacterium is Associated with Poor Response to Immunotherapy in Lung Cancer

Chu¹,

Cheng²,

Yin³

et al. 2022

OTT

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There is a major limitation in the immunotherapy for solid cancer is that it only benefited a minority of cancer patients. This study aims to investigate whether the differential composition of the lung microbiome could affect the sustained clinical responses in lung cancers treated with immunotherapy. Methods: Twenty-seven non-responders and 19 responders treated with anti-PD-1 therapy were included in the discovery set. Bacterial load in bronchoalveolar lavage from lung cancer patients was examined by quantitative PCR of 16S rRNA copies. Bacterial 16S rDNA was sequenced using the Illumina HiSeq on the 16S rDNA V3-V4 variable region. Operational taxonomic unit (OTU) analysis was performed using VSEARCH v2. The α-diversity and β-diversity were calculated using QIIME software. Results:The mean copy number of bacterial 16S DNA levels significantly decreased after anti-PD-1 treatment (after: 1.8 ± 0.6×10 4 copies per milliliter vs prior to treatment: 3.3 ± 1.1x10 4 , p = 0.0036). In addition, longitudinal analysis revealed that microbial diversity was reduced taxonomically after treatment compared to those prior to the treatment (Shannon values: before: 3.291 ± 0.067 vs after: 2.668 ± 0.168, p < 0.01). Further, we observed a reduction of Fusobacterium nucleatum, including phylum Fusobacteria (p < 0.01), class Fusobacteria (p < 0.01), order Fusobacteria (p < 0.01), family Fusobacteria (p < 0.01), genus Fusobacteria (p = 0.025) in the responders post anti-PD-1 treatment. However, there was no significant difference of Fusobacterium in non-responders. An independent cohort was used to validate the levels of Fusobacterium, demonstrating that patients with higher abundance of Fusobacterium prior to treatment were significantly more likely to have poor response to anti-PD-1 therapy (p < 0.001). Conclusion: Airway enriched Fusobacterium prior to anti-PD-1 therapy is associated with poor response in lung cancer, which indicated that potential resistance to immunotherapy can be attributed to lung microbiome.

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Role of FAD-I in Fusobacterial Interspecies Interaction and Biofilm Formation

Cited by 10 publications

References 43 publications

The Oral Microbiota: Community Composition, Influencing Factors, Pathogenesis, and Interventions

The Oral Microbiota: Community Composition, Influencing Factors, Pathogenesis, and Interventions

Extracellular vesicles of Fusobacterium nucleatum compromise intestinal barrier through targeting RIPK1-mediated cell death pathway

Airway Fusobacterium is Associated with Poor Response to Immunotherapy in Lung Cancer

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