Inflammatory Bowel Diseases: Host-Microbial-Environmental Interactions in Dysbiosis

Crohn’s Disease (CD) and Ulcerative Colitis (UC) are world-wide health problems in which intestinal dysbiosis or adverse functional changes in the microbiome are causative or exacerbating factors. The reduced abundance and diversity of the microbiome may be a result of a lack of exposure to vital commensal microbes or overexposure to competitive pathobionts during early life. Alternatively, many commensal bacteria may not find a suitable intestinal niche or fail to proliferate or function in a protective/competitive manner if they do colonize. Bacteria express a range of factors, such as fimbriae, flagella, and secretory compounds that enable them to attach to the gut, modulate metabolism, and outcompete other species. However, the host also releases factors, such as secretory IgA, antimicrobial factors, hormones, and mucins, which can prevent or regulate bacterial interactions with the gut or disable the bacterium. The delicate balance between these competing host and bacteria factors dictates whether a bacterium can colonize, proliferate or function in the intestine. Impaired functioning of NOD2 in Paneth cells and disrupted colonic mucus production are exacerbating features of CD and UC, respectively, that contribute to dysbiosis. This review evaluates the roles of these and other the host, bacterial and environmental factors in inflammatory bowel diseases.

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Intestinal Taxa Abundance and Diversity in Inflammatory Bowel Disease Patients: An Analysis including Covariates and Confounders

Nutrients ◽

10.3390/nu14020260 ◽

2022 ◽

Vol 14 (2) ◽

pp. 260

Author(s):

Adelaide Teofani ◽

Irene Marafini ◽

Federica Laudisi ◽

Daniele Pietrucci ◽

Silvia Salvatori ◽

...

Keyword(s):

Dairy Products ◽

Dietary Habits ◽

Rrna Gene ◽

Disease Extent ◽

Intestinal Dysbiosis ◽

Gene Sequence Analysis ◽

Bowel Diseases ◽

Inflammatory Bowel ◽

Abundance And Diversity ◽

The Impact

Intestinal dysbiosis has been widely documented in inflammatory bowel diseases (IBDs) and is thought to influence the onset and perpetuation of gut inflammation. However, it remains unclear whether such bacterial changes rely in part on the modification of an IBD-associated lifestyle (e.g., smoking and physical activity) and diet (e.g., rich in dairy products, cereals, meat and vegetables). In this study, we investigated the impact of these habits, which we defined as confounders and covariates, on the modulation of intestinal taxa abundance and diversity in IBD patients. 16S rRNA gene sequence analysis was performed using genomic DNA extracted from the faecal samples of 52 patients with Crohn’s disease (CD) and 58 with ulcerative colitis (UC), which are the two main types of IBD, as well as 42 healthy controls (HC). A reduced microbial diversity was documented in the IBD patients compared with the HC. Moreover, we identified specific confounders and covariates that influenced the association between some bacterial taxa and disease extent (in UC patients) or behaviour (in CD patients) compared with the HC. In particular, a PERMANOVA stepwise regression identified the variables “age”, “eat yogurt at least four days per week” and “eat dairy products at least 4 days per week” as covariates when comparing the HC and patients affected by ulcerative proctitis (E1), left-sided UC (distal UC) (E2) and extensive UC (pancolitis) (E3). Instead, the variables “age”, “gender”, “eat meat at least four days per week” and “eat bread at least 4 days per week” were considered as covariates when comparing the HC with the CD patients affected by non-stricturing, non-penetrating (B1), stricturing (B2) and penetrating (B3) diseases. Considering such variables, our analysis indicated that the UC extent differentially modulated the abundance of the Bifidobacteriaceae, Rikenellaceae, Christensenellaceae, Marinifilaceae, Desulfovibrionaceae, Lactobacillaceae, Streptococcaceae and Peptostreptococcaceae families, while the CD behaviour influenced the abundance of Christensenellaceae, Marinifilaceae, Rikenellaceae, Ruminococcaceae, Barnesiellaceae and Coriobacteriaceae families. In conclusion, our study indicated that some covariates and confounders related to an IBD-associated lifestyle and dietary habits influenced the intestinal taxa diversity and relative abundance in the CD and UC patients compared with the HC. Indeed, such variables should be identified and excluded from the analysis to characterize the bacterial families whose abundance is directly modulated by IBD status, as well as disease extent or behaviour.

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Early Life Environment and Natural History of Inflammatory Bowel Diseases

The American Journal of Gastroenterology ◽

10.14309/00000434-201410002-01639 ◽

2014 ◽

Vol 109 ◽

pp. S486

Author(s):

Abra Guo ◽

Robin Wilson ◽

Betsy Stevens ◽

Caitlin Russell ◽

Melissa Cohen ◽

...

Keyword(s):

Natural History ◽

Inflammatory Bowel Diseases ◽

Early Life ◽

Early Life Environment ◽

Bowel Diseases ◽

History Of ◽

Inflammatory Bowel

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Probiotics Can Cure Oral Aphthous-Like Ulcers in Inflammatory Bowel Disease Patients: A Review of the Literature and a Working Hypothesis

International Journal of Molecular Sciences ◽

10.3390/ijms20205026 ◽

2019 ◽

Vol 20 (20) ◽

pp. 5026 ◽

Cited By ~ 1

Author(s):

Francesco Cappello ◽

Francesca Rappa ◽

Federica Canepa ◽

Francesco Carini ◽

Margherita Mazzola ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Inflammatory Bowel Diseases ◽

Inflammatory Process ◽

Primary Role ◽

Extraintestinal Manifestations ◽

Review Of The Literature ◽

Chronic Inflammatory Process ◽

Intestinal Dysbiosis ◽

Bowel Diseases ◽

Inflammatory Bowel

Dysbiosis has been associated with the onset of several chronic autoimmune or inflammatory pathologies (e.g., inflammatory bowel diseases—IBD), because of its primary role in the establishment of a chronic inflammatory process leading to tissue damage. Inflammatory bowel diseases can even involve areas far away from the gut, such as the extraintestinal manifestations involving the oral cavity with the onset of aphthous-like ulcers (ALU). Studies carried out on animal models have shown that intestinal dysbiosis may be related to the development of autoimmune diseases, even if the mechanisms involved are not yet well known. The aim of this paper is to verify the hypothesis that in inflammatory bowel diseases patients, aphthous-like ulcers are the result of the concomitance of intestinal dysbiosis and other events, e.g., the microtraumas, occurring in the oral mucosa, and that ex adiuvantibus therapy with probiotics can be employed to modify the natural course of the aphthous-like ulcers.

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