Dataset Information

Inflammatory Bowel Disease-Associated Changes in the Gut: Focus on Kazan Patients.

ABSTRACT:

Background

Several studies have highlighted the role of host-microbiome interactions in the pathogenesis of inflammatory bowel disease (IBD), resulting in an increasing amount of data mainly focusing on Western patients. Because of the increasing prevalence of IBD in newly industrialized countries such as those in Asia, the Middle East, and South America, there is mounting interest in elucidating the gut microbiota of these populations. We present a comprehensive analysis of several IBD-related biomarkers and gut microbiota profiles and functions of a unique population of patients with IBD and healthy patients from Kazan (Republic of Tatarstan, Russia).

Methods

Blood and fecal IBD biomarkers, serum cytokines, and fecal short-chain fatty acid (SCFA) content were profiled. Finally, fecal microbiota composition was analyzed by 16S and whole-genome shotgun sequencing.

Results

Fecal microbiota whole-genome sequencing confirmed the presence of classic IBD dysbiotic features at the phylum level, with increased abundance of Proteobacteria, Actinobacteria, and Fusobacteria and decreased abundance of Firmicutes, Bacteroidetes, and Verrucomicrobia. At the genus level, the abundance of both fermentative (SCFA-producing and hydrogen (H2)-releasing) and hydrogenotrophic (H2-consuming) microbes was affected in patients with IBD. This imbalance was confirmed by the decreased abundance of SCFA species in the feces of patients with IBD and the change in anaerobic index, which mirrors the redox status of the intestine.

Conclusions

Our analyses highlighted how IBD-related dysbiotic microbiota-which are generally mainly linked to SCFA imbalance-may affect other important metabolic pathways, such as H2 metabolism, that are critical for host physiology and disease development.

SUBMITTER: Lo Sasso G

PROVIDER: S-EPMC7885336 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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Publications

Inflammatory Bowel Disease-Associated Changes in the Gut: Focus on Kazan Patients.

Lo Sasso Giuseppe G Khachatryan Lusine L Kondylis Athanasios A Battey James N D JND Sierro Nicolas N Danilova Natalia A NA Grigoryeva Tatiana V TV Markelova Maria I MI Khusnutdinova Dilyara R DR Laikov Alexander V AV Salafutdinov Ilnur I II Romanova Yulia D YD Siniagina Mariia N MN Vasiliev Ilya Yu IY Boulygina Eugenia A EA Solovyeva Valeriya V VV Garanina Ekaterina E EE Kitaeva Kristina V KV Ivanov Konstantin Y KY Chulpanova Darja S DS Kletenkov Konstantin S KS Valeeva Alina R AR Odintsova Alfiya Kh AK Ardatskaya Maria D MD Abdulkhakov Rustam A RA Ivanov Nikolai V NV Peitsch Manuel C MC Hoeng Julia J Abdulkhakov Sayar R SR

Inflammatory bowel diseases 20210201 3

<h4>Background</h4>Several studies have highlighted the role of host-microbiome interactions in the pathogenesis of inflammatory bowel disease (IBD), resulting in an increasing amount of data mainly focusing on Western patients. Because of the increasing prevalence of IBD in newly industrialized countries such as those in Asia, the Middle East, and South America, there is mounting interest in elucidating the gut microbiota of these populations. We present a comprehensive analysis of several IBD- ...[more]

PMID: 32766755

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Project description:Extracellular matrix (ECM) remodeling has emerged as a key feature of inflammatory bowel disease (IBD), and ECM fragments have been proposed as markers of clinical disease severity. Recent studies report increased protease activity in the gut microbiota of IBD patients. Nonetheless, the relationship between gut microbiota and ECM remodeling has remained unexplored. We hypothesized that members of the human gut microbiome could degrade the host ECM and that bacteria-driven remodeling, in turn, could enhance colonic inflammation. Through a variety of in vitro assays, we first confirmed that multiple bacterial species found in the human gut are capable of degrading specific ECM components. Clinical stool samples obtained from ulcerative colitis patients also exhibited higher levels of proteolytic activity in vitro, compared to those of their healthy counterparts. Furthermore, culture supernatants from bacteria species that are capable of degrading human ECM accelerated inflammation in dextran sodium sulfate (DSS)-induced colitis. Finally, we identified several of the bacterial proteases and carbohydrate degrading enzymes (CAZymes) that are potentially responsible for ECM degradation in vitro. Some of these protease families and CAZymes were also found in increased abundance in a metagenomic cohort of IBD. These results demonstrate that some commensal bacteria in the gut are indeed capable of degrading components of human ECM in vitro and suggest that this proteolytic activity may be involved in the progression of IBD. A better understanding of the relationship between nonpathogenic gut microbes, host ECM, and inflammation could be crucial to elucidating some of the mechanisms underlying host-bacteria interactions in IBD and beyond. IMPORTANCE Healthy gut epithelial cells form a barrier that keeps bacteria and other substances from entering the blood or tissues of the body. Those cells sit on scaffolding that maintains the structure of the gut and informs our immune system about the integrity of this barrier. In patients with inflammatory bowel disease (IBD), breaks are formed in this cellular barrier, and bacteria gain access to the underlying tissue and scaffolding. In our study, we discovered that bacteria that normally reside in the gut can modify and disassemble the underlying scaffolding. Additionally, we discovered that changes to this scaffolding affect the onset of IBD in mouse models of colitis as well as the abilities of these mice to recover. We propose that this new information will reveal how breaks in the gut wall lead to IBD and will open up new avenues by which to treat patients with IBD.

Dataset Information

Inflammatory Bowel Disease-Associated Changes in the Gut: Focus on Kazan Patients.

Background

Methods

Results

Conclusions

Publications

Inflammatory Bowel Disease-Associated Changes in the Gut: Focus on Kazan Patients.

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