Differential Responses of Colorectal Cancer Cell Lines to Enterococcus faecalis’ Strains Isolated from Healthy Donors and Colorectal Cancer Patients

Almeida, Carolina Vieira De; Lulli, Matteo; Pilato, Vincenzo Di; Schiavone, Nicola; Russo, Edda; Nannini, Giulia; Baldi, Simone; Borrelli, Rossella; Bartolucci, Gianluca; Menicatti, Marta; Taddei, Antonio; Ringressi, Maria Novella; Niccolai, Elena; Prisco, Domenico; Rossolini, Gian María; Amedei, Amedeo

doi:10.3390/jcm8030388

Cited by 31 publications

(20 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown that MED13 could directly link a cyclin-dependent kinase 8 (CDK8) module to Mediator 81,82 , which is a colorectal cancer oncogene, amplified in colorectal tumours and activating transcription driving colon tumorigenesis leading to CRC 58 . This could explain a long suspected link between Enterococcus faecalis and development of CRC after having been found in higher concentrations in CRC patients than healthy individuals 51-55 . The suspected mode of action of E. faecalis on CRC development is currently unclear, but could be linked to extracellular free radical production directly leading to DNA break, point mutation and chromosomal instability in colorectal cells 56 .…”

Section: Discussionmentioning

confidence: 99%

Combined effects of host genetics and diet on human gut microbiota and incident disease in a single population cohort

Qin

Havulinna

Liu

et al. 2020

Preprint

View full text Add to dashboard Cite

Co-evolution between humans and the microbial communities colonizing them has resulted in an intimate assembly of thousands of microbial species mutualistically living on and in their body and impacting multiple aspects of host physiology and health. Several studies examining whether human genetic variation can affect gut microbiota suggest a complex combination of environmental and host factors. Here, we leverage a single large-scale population-based cohort of 5,959 genotyped individuals with matched gut microbial shotgun metagenomes, dietary information and health records up to 16 years post-sampling, to characterize human genetic variations associated with microbial abundances, and predict possible causal links with various diseases using Mendelian randomization (MR). Genome-wide association study (GWAS) identified 583 independent SNP-taxon associations at genome-wide significance (p<5.0×10-8), which included notable strong associations with LCT (p=5.02×10-35), ABO (p=1.1×10-12), and MED13L (p=1.84×10-12). A combination of genetics and dietary habits was shown to strongly shape the abundances of certain key bacterial members of the gut microbiota, and explain their genetic association. Genetic effects from the LCT locus on Bifidobacterium and three other associated taxa significantly differed according to dairy intake. Variation in mucin-degrading Faecalicatena lactaris abundances were associated with ABO, highlighting a preferential utilization of secreted A/B/AB-antigens as energy source in the gut, irrespectively of fibre intake. Enterococcus faecalis levels showed a robust association with a variant in MED13L, with putative links to colorectal cancer. Finally, we identified putative causal relationships between gut microbes and complex diseases using MR, with a predicted effect of Morganella on major depressive disorder that was consistent with observational incident disease analysis. Overall, we present striking examples of the intricate relationship between humans and their gut microbial communities, and highlight important health implications.

show abstract

Section: Discussionmentioning

confidence: 99%

Combined effects of host genetics and diet on human gut microbiota and incident disease in a single population cohort

Qin

Havulinna

Liu

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…The SCFAs in the samples were analyzed as free acid form using a Supelco Nukol column 30 m length, 0.25 mm internal diameter and 0.25 µm of film thickness with the temperatures program as follows: Initial temperature of 40 °C was held for 1 min, then it was increased to 150 °C at 30 °C/min, finally grow up to 220 °C at 20 °C/min[26]. A 1 µL aliquot of extracted sample was injected in splitless mode (splitless time 1 min) at 250 °C, while the transfer line temperature was 280 °C.…”

Section: Methodsmentioning

confidence: 99%

Evaluation and comparison of short chain fatty acids composition in gut diseases

Niccolai

Baldi

Ricci

et al. 2019

WJG

Self Cite

107

View full text Add to dashboard Cite

BACKGROUNDAn altered (dysbiosis) and unhealthy status of the gut microbiota is usually responsible for a reduction of short chain fatty acids (SCFAs) concentration. SCFAs obtained from the carbohydrate fermentation processes are crucial in maintaining gut homeostasis and their determination in stool samples could provide a faster, reliable and cheaper method to highlight the presence of an intestinal dysbiosis and a biomarker for various gut diseases. We hypothesize that different intestinal diseases, such as celiac disease (CD), adenomatous polyposis (AP) and colorectal cancer (CRC) could display a particular fecal SCFAs’ signature.AIMTo compare the fecal SCFAs’ profiles of CD, AP, CRC patients and healthy controls, using the same analytical method.METHODSIn this cross-sectional study, we defined and compared the SCFAs’ concentration in fecal samples of 9 AP, 16 CD, 19 CRC patients and 16 healthy controls (HC). The SCFAs’ analysis were performed using a gas-chromatography coupled with mass spectrometry method. Data analysis was carried out using Wilcoxon rank-sum test to assess pairwise differences of SCFAs’ profiles, partial least squares-discriminate analysis (PLS-DA) to determine the status membership based on distinct SCFAs’ profiles, and Dirichlet regression to determine factors influencing concentration levels of SCFAs.RESULTSWe have not observed any difference in the SCFAs’ amount and composition between CD and healthy control. On the contrary, the total amount of SCFAs was significantly lower in CRC patients compared to HC (P = 0.044) and CD (P = 0.005). Moreover, the SCFAs’ percentage composition was different in CRC and AP compared to HC. In detail, HC displayed higher percentage of acetic acid (P value = 1.3 × 10-6) and a lower amount of butyric (P value = 0.02192), isobutyric (P value = 7.4 × 10-5), isovaleric (P value = 0.00012) and valeric (P value = 0.00014) acids compared to CRC patients. AP showed a lower abundance of acetic acid (P value = 0.00062) and higher percentages of propionic (P value = 0.00433) and isovaleric (P value = 0.00433) acids compared to HC. Moreover, AP showed higher levels of propionic acid (P value = 0.03251) and a lower level of isobutyric acid (P value = 0.00427) in comparison to CRC. The PLS-DA model demonstrated a significant separation of CRC and AP groups from HC, although some degree of overlap was observed between CRC and AP.CONCLUSIONAnalysis of fecal SCFAs shows the potential to provide a non-invasive means of diagnosis to detect patients with CRC and AP, while CD patients cannot be discriminated from healthy subjects.

show abstract

“…Furthermore, the heat‐killed E. faecalis strain KH2 may attenuate NLRP3 inflammasome activation in macrophages and ameliorate the severity of dextran sulfate sodium‐induced colitis and the development of colitis‐associated CRC in mice 47 . These conflicting roles of E. faecalis in CRC development may be attributed to the different isolated and investigated strains 48,49 . Given that obesity leads to increased risk for CRC, the authors of the present study speculated that reduced E. faecalis in obese patients with CRC could be a promoting factor for the development of obesity‐related CRC.…”

Section: Discussionmentioning

confidence: 78%

“…47 These conflicting roles of E. faecalis in CRC development may be attributed to the different isolated and investigated strains. 48,49 Given that obesity leads to increased risk for CRC, the authors of the present study speculated that reduced E. faecalis in obese patients with CRC could be a promoting factor for the development of obesity-related CRC.…”

Section: Discussionmentioning

confidence: 80%

Characteristics of the gut microbiome profile in obese patients with colorectal cancer

et al. 2021

View full text Add to dashboard Cite

Background and Aim Obesity affects the gut microbiome, which in turn increases the risk for colorectal cancer. Several studies have shown the mechanisms by which some bacteria may influence the development of colorectal cancer; however, gut microbiome characteristics in obese patients with colorectal cancer remain unclear. Therefore, this study evaluated their gut microbiome profile and its relationship with metabolic markers. Methods The study assessed fecal samples from 36 consecutive patients with colorectal cancer and 38 controls without colorectal cancer. To identify microbiotic variations between patients with colorectal cancer and controls, as well as between nonobese and obese individuals, 16S rRNA gene amplicon sequencing was performed. Results Principal coordinate analysis showed significant differences in the overall structure of the microbiome among the study groups. The α‐diversity, assessed by the Chao1 index or Shannon index, was higher in patients with colorectal cancer versus controls. The relative abundance of the genera Enterococcus, Capnocytophaga, and Polaribacter was significantly altered in obese patients with colorectal cancer, whose serum low‐density lipoprotein concentrations were positively correlated with the abundance of the genus Enterococcus; among the most abundant species was Enterococcus faecalis, observed at lower levels in obese versus nonobese patients. Conclusions This study demonstrated several compositional alterations of the gut microbiome in patients with colorectal cancer and showed that a reduced presence of E. faecalis may be associated with obesity‐related colorectal cancer development. The gut microbiome may provide novel insights into the potential mechanisms in obesity‐related colorectal carcinogenesis.

show abstract

Differential Responses of Colorectal Cancer Cell Lines to Enterococcus faecalis’ Strains Isolated from Healthy Donors and Colorectal Cancer Patients

Cited by 31 publications

References 59 publications

Combined effects of host genetics and diet on human gut microbiota and incident disease in a single population cohort

Combined effects of host genetics and diet on human gut microbiota and incident disease in a single population cohort

Evaluation and comparison of short chain fatty acids composition in gut diseases

Characteristics of the gut microbiome profile in obese patients with colorectal cancer

Contact Info

Product

Resources

About