Streptococcus cristatus modulates the Fusobacterium nucleatum-induced epithelial interleukin-8 response through the nuclear factor-kappa B pathway

Zhang, G.; Chen, R.; Rudney, Joel D.

doi:10.1111/j.1600-0765.2011.01373.x

Cited by 29 publications

(36 citation statements)

References 61 publications

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“…Thus, on the one hand, the observed decrease in prevalence of Streptococcus and increased abundance of Fusobacterium genera in pre-cancers could reflect the altered surface properties of the cancer cells and stroma, which might no longer support adhesion of streptococci . On the other hand, we can hypothesize that shifts in abundance of these two genera could result in an enhanced pro-inflammatory environment, since Streptococcus species have been reported to attenuate Fusobacterium nucleatum induced pro-inflammatory responses of oral epithelial cells [41], [42]. We also note that Fusobacterium nucleatum grown as a biofilm is capable of invading organotypic cultures [43], and secondly, that the organism has recently been reported in colon cancers [44], [45], further supporting a potential role in oral cancer.…”

Section: Discussionmentioning

confidence: 99%

Changes in Abundance of Oral Microbiota Associated with Oral Cancer

et al. 2014

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Individual bacteria and shifts in the composition of the microbiome have been associated with human diseases including cancer. To investigate changes in the microbiome associated with oral cancers, we profiled cancers and anatomically matched contralateral normal tissue from the same patient by sequencing 16S rDNA hypervariable region amplicons. In cancer samples from both a discovery and a subsequent confirmation cohort, abundance of Firmicutes (especially Streptococcus) and Actinobacteria (especially Rothia) was significantly decreased relative to contralateral normal samples from the same patient. Significant decreases in abundance of these phyla were observed for pre-cancers, but not when comparing samples from contralateral sites (tongue and floor of mouth) from healthy individuals. Weighted UniFrac principal coordinates analysis based on 12 taxa separated most cancers from other samples with greatest separation of node positive cases. These studies begin to develop a framework for exploiting the oral microbiome for monitoring oral cancer development, progression and recurrence.

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Section: Discussionmentioning

confidence: 99%

Changes in Abundance of Oral Microbiota Associated with Oral Cancer

et al. 2014

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“…In line with this, we demonstrate here that, in vitro , aggregation of tumor isolates C. showae CC57C with F. nucleatum CC53 [4] is evident (Figure 4). Co-aggregation of Streptococcus cristatus with F. nucleatum has previously been shown to facilitate invasion of the former into cultured host cells, and to alter the host response to F. nucleatum invasion [47,48]. Whether co-aggregation of F. nucleatum and C. showae is relevant to disease etiology remains to be tested and the influence of this co-aggregation on bacterial virulence in vitro is currently being investigated by our group.…”

Section: Discussionmentioning

confidence: 99%

Co-occurrence of anaerobic bacteria in colorectal carcinomas

et al. 2013

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BackgroundNumerous cancers have been linked to microorganisms. Given that colorectal cancer is a leading cause of cancer deaths and the colon is continuously exposed to a high diversity of microbes, the relationship between gut mucosal microbiome and colorectal cancer needs to be explored. Metagenomic studies have shown an association between Fusobacterium species and colorectal carcinoma. Here, we have extended these studies with deeper sequencing of a much larger number (n = 130) of colorectal carcinoma and matched normal control tissues. We analyzed these data using co-occurrence networks in order to identify microbe-microbe and host-microbe associations specific to tumors.ResultsWe confirmed tumor over-representation of Fusobacterium species and observed significant co-occurrence within individual tumors of Fusobacterium, Leptotrichia and Campylobacter species. This polymicrobial signature was associated with over-expression of numerous host genes, including the gene encoding the pro-inflammatory chemokine Interleukin-8. The tumor-associated bacteria we have identified are all Gram-negative anaerobes, recognized previously as constituents of the oral microbiome, which are capable of causing infection. We isolated a novel strain of Campylobacter showae from a colorectal tumor specimen. This strain is substantially diverged from a previously sequenced oral Campylobacter showae isolate, carries potential virulence genes, and aggregates with a previously isolated tumor strain of Fusobacterium nucleatum.ConclusionsA polymicrobial signature of Gram-negative anaerobic bacteria is associated with colorectal carcinoma tissue.

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“…Numerous cancer-associated microbes appear to activate NF-κΒ signaling within the tumor microenvironment [e.g., the colon cancer–associated F. nucleatum (23)]. The activation of NF-κΒ by F. nucleatum may be the result of pattern recognition receptor engagement (10, 34–37) or FadA engagement of E-cadherin (25). Other pattern recognition receptors, such as the nucleotide-binding oligomerization domain–like receptor (NLR) family members NOD-2, NLRP3, NLRP6, and NLRP12, may play a role in mediating colorectal cancer; mice deficient in these NLRs display an enhanced susceptibility to colitis-associated colorectal cancer (caCRC) (38–44).…”

Section: The Immune System Microbes Microbiota and Cancermentioning

confidence: 99%

Cancer and the microbiota

Garrett

2015

Science

1,065

839

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A host’s microbiota may increase, diminish, or have no effect at all on cancer susceptibility. Assigning causal roles in cancer to specific microbes and microbiotas, unraveling host-microbiota interactions with environmental factors in carcinogenesis, and exploiting such knowledge for cancer diagnosis and treatment are areas of intensive interest. This Review considers how microbes and the microbiota may amplify or mitigate carcinogenesis, responsiveness to cancer therapeutics, and cancer-associated complications.

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Streptococcus cristatus modulates the Fusobacterium nucleatum-induced epithelial interleukin-8 response through the nuclear factor-kappa B pathway

Abstract: The mechanism by which S. cristatus attenuates F. nucleatum-induced proinflammatory responses in oral epithelial cells appears to involve blockade of NF-κB nuclear translocation at the level of IκB-α degradation.

Cited by 29 publications

References 61 publications

Changes in Abundance of Oral Microbiota Associated with Oral Cancer

Changes in Abundance of Oral Microbiota Associated with Oral Cancer

Co-occurrence of anaerobic bacteria in colorectal carcinomas

Cancer and the microbiota

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