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

The metabolites produced by the host’s gut microbiota have an important role in the maintenance of intestinal homeostasis, but can also act as toxins and induce DNA damage in colorectal epithelial cells increasing the colorectal cancer (CRC) chance. In this scenario, the impact of some of the components of the natural human gastrointestinal microbiota, such as Enterococcus faecalis (E. faecalis), at the onset of CRC progression remains controversial. Since under dysbiotic conditions it could turn into a pathogen, the aim of this study was to compare the effect of E. faecalis’ strains (isolated from CRC patients and healthy subjects’ stools) on the proliferation of different colorectal cells lines. First, we isolated and genotyping characterized the Enterococcus faecalis’ strains. Then, we analyzed the proliferation index (by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay) of three tumor and one normal intestinal cell lines, previously exposed to E. faecalis strains pre-cultured medium. Stool samples of CRC patients demonstrated a reduced frequency of E. faecalis compared to healthy subjects. In addition, the secreted metabolites of E. faecalis’ strains, isolated from healthy donors, decreased the human ileocecal adenocarcinoma cell line HCT-8 and human colon carcinoma cell line HCT-116 cell proliferation without effects on human colorectal adenocarcinoma cell line SW620 and on normal human diploid cell line CLR-1790. Notably, the metabolites of the strains isolated from CRC patients did not influence the cell growth of CRC cell lines. Our results demonstrated a new point of view in the investigation of E. faecalis’ role in CRC development, which raises awareness of the importance of not only associating the presence/absence of a unique microorganism, but also in defining the specific characteristics of the different investigated strains

Crohn’s disease recurrence updates: first surgery vs. surgical relapse patients display different profiles of ileal microbiota and systemic microbial-associated inflammatory factors

Background and aimsCrohn’s disease (CD) pathogenesis is still unclear. Remodeling in mucosal microbiota and systemic immunoregulation may represent an important component in tissue injury. Here, we aim to characterize the ileal microbiota in both pathological and healthy settings and to evaluate the correlated systemic microbial-associated inflammatory markers comparing first-time surgery and relapse clinical conditions.MethodsWe enrolled 28 CD patients at surgery; we collected inflamed and non-inflamed mucosa tissues and blood samples from each patient. Bacterial wall adherence was observed histologically, while its composition was assessed through amplicon sequencing of the 16S rRNA gene. In addition, we evaluated the systemic microRNA (miRNA) using quantitative real-time PCR amplification and free fatty acids (FFAs) using gas chromatography–mass spectroscopy.ResultsThe total number of mucosal adherent microbiota was enriched in healthy compared to inflamed mucosa. In contrast, the phylum Tenericutes, the family Ruminococcaceae, and the genera Mesoplasma and Mycoplasma were significantly enriched in the pathological setting. Significant microbiota differences were observed between the relapse and first surgery patients regarding the families Bacillaceae 2 and Brucellaceae and the genera Escherichia/Shigella, Finegoldia, Antrobacter, Gemmatimonas, Moraxella, Anoxibacillus, and Proteus. At the systemic level, we observed a significant downregulation of circulating miR-155 and miR-223, as well as 2-methyl butyric, isobutyric, and hexanoic (caproic) acids in recurrence compared to the first surgery patients. In addition, the level of hexanoic acid seems to act as a predictor of recurrence risk in CD patients (OR 18; 95% confidence interval 1.24–261.81; p = 0.006).ConclusionsWe describe a dissimilarity of ileal microbiota composition comparing CD and healthy settings, as well as systemic microbial-associated inflammatory factors between first surgery and surgical relapse. We suggest that patterns of microbiota, associated with healthy ileal tissue, could be involved in triggering CD recurrence. Our findings may provide insight into the dynamics of the gut microbiota–immunity axis in CD surgical recurrence, paving the way for new diagnostics and therapeutics aimed not only at reducing inflammation but also at maintaining a general state of eubiosis in healthy tissue

The Gut–Brain Axis in the Neuropsychological Disease Model of Obesity: A Classical Movie Revised by the Emerging Director “Microbiome”

The worldwide epidemic of obesity has become an important public health issue, with serious psychological and social consequences. Obesity is a multifactorial disorder in which various elements (genetic, host, and environment), play a definite role, even if none of them satisfactorily explains its etiology. A number of neurological comorbidities, such as anxiety and depression, charges the global obesity burden, and evidence suggests the hypothesis that the brain could be the seat of the initial malfunction leading to obesity. The gut microbiome plays an important role in energy homeostasis regulating energy harvesting, fat deposition, as well as feeding behavior and appetite. Dietary patterns, like the Western diet, are known to be a major cause of the obesity epidemic, probably promoting a dysbiotic drift in the gut microbiota. Moreover, the existence of a “gut–brain axis” suggests a role for microbiome on hosts’ behavior according to different modalities, including interaction through the nervous system, and mutual crosstalk with the immune and the endocrine systems. In the perspective of obesity as a real neuropsychological disease and in light of the discussed considerations, this review focuses on the microbiome role as an emerging director in the development of obesity

Inflammatory Bowel Disease and Customized Nutritional Intervention Focusing on Gut Microbiome Balance

Inflammatory bowel disease (IBD) represents a chronic relapsing–remitting condition affecting the gastrointestinal system. The specific triggering IBD elements remain unknown: genetic variability, environmental factors, and alterations in the host immune system seem to be involved. An unbalanced diet and subsequent gut dysbiosis are risk factors, too. This review focuses on the description of the impact of pro- and anti-inflammatory food components on IBD, the role of different selected regimes (such as Crohn’s Disease Exclusion Diet, Immunoglobulin Exclusion Diet, Specific Carbohydrate Diet, LOFFLEX Diet, Low FODMAPs Diet, Mediterranean Diet) in the IBD management, and their effects on the gut microbiota (GM) composition and balance. The purpose is to investigate the potential positive action on IBD inflammation, which is associated with the exclusion or addition of certain foods or nutrients, to more consciously customize the nutritional intervention, taking also into account GM fluctuations during both disease flare-up and remission