Immune-Mediated Aggravation of the Campylobacter concisus-Induced Epithelial Barrier Dysfunction

Nattramilarasu, Praveen Kumar; Sá, Fábia Daniela Lobo de; Schulzke, Jörg–Dieter; Bücker, Roland

doi:10.3390/ijms22042043

Cited by 5 publications

(5 citation statements)

References 75 publications

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“… 52 Colonic epithelial barrier dysfunction is exacerbated by C. concisus activating M1-macrophage by reducing the expression of occludin and tricellsulin in the tricellular proteins of three-cell TJs. 53 Helicobacter hepaticus downregulates ZO-1 and Claudin-1, decreases numbers of lysozyme-positive immune cells in the colonic submucosa, and damages the intestinal barrier in Il-17a -/- mice. 54 Salmonella serovar virulence relies on Salmonella plasmid virulence (Spv) genes.…”

Section: Mechanisms Of Bacterial Translocationmentioning

confidence: 98%

Direct and indirect effects of pathogenic bacteria on the integrity of intestinal barrier

Li-sha

Yuan

Qin

et al. 2023

Therap Adv Gastroenterol

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Bacterial translocation is a pathological process involving migration of pathogenic bacteria across the intestinal barrier to enter the systemic circulation and gain access to distant organs. This phenomenon has been linked to a diverse range of diseases including inflammatory bowel disease, pancreatitis, and cancer. The intestinal barrier is an innate structure that maintains intestinal homeostasis. Pathogenic infections and dysbiosis can disrupt the integrity of the intestinal barrier, increasing its permeability, and thereby facilitating pathogen translocation. As translocation represents an essential step in pathogenesis, a clear understanding of how barrier integrity is disrupted and how this disruption facilitates bacterial translocation could identify new routes to effective prophylaxis and therapy. In this comprehensive review, we provide an in-depth analysis of bacterial translocation and intestinal barrier function. We discuss currently understood mechanisms of bacterial–enterocyte interactions, with a focus on tight junctions and endocytosis. We also discuss the emerging concept of bidirectional communication between the intestinal microbiota and other body systems. The intestinal tract has established ‘axes’ with various organs. Among our regulatory systems, the nervous, immune, and endocrine systems have been shown to play pivotal roles in barrier regulation. A mechanistic understanding of intestinal barrier regulation is crucial for the development of personalized management strategies for patients with bacterial translocation-related disorders. Advancing our knowledge of barrier regulation will pave the way for future research in this field and novel clinical intervention strategies.

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Section: Mechanisms Of Bacterial Translocationmentioning

confidence: 98%

Direct and indirect effects of pathogenic bacteria on the integrity of intestinal barrier

Li-sha

Yuan

Qin

et al. 2023

Therap Adv Gastroenterol

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“…To investigate the effect of oral microorganisms on intestinal epithelial barrier dysfunction, Nattramilarasu et al cultured colonic epithelial cell monolayers (HT-29/B6-GR/MR) and M1-macrophage-like THP-1 cells together in vitro. After infection with Campylobacter concisus, THP-1 cells promoted the release of cytokines (TNF-α, IL-1β, and IL-6) and consequently increased the permeability of the intestinal epithelium [ 105 ]. Oral pathobionts such as Klebsiella and Enterobacter derived from ligature-induced periodontitis and DSS-treated mice stimulated inflammasome production in colonic mononuclear phagocytes, followed by increased inflammation in the colonic mucosa.…”

Section: Introductionmentioning

confidence: 99%

“…nucleatum enhances the expression of TNF-α, IFN-gamma, IL-1β, IL-6, and IL-17, which further exacerbates IBD [ 127 ]. In addition, C. concisus promotes the secretion of proinflammatory cytokines from THP-1 cells, such as TNF-α, IL-1β, and IL-6, which increase the antigen permeability of the colonic epithelial barrier [ 105 ]. It should be pointed out that periodontitis fosters a proinflammatory microenvironment, and the levels of IL-1β, IL-4, IL-10, and IL-17A were significantly higher in diseased sites than healthy sites in the same oral cavity from periodontitis patients [ 128 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The oral microbiome in autoimmune diseases: friend or foe?

Huang

et al. 2023

J Transl Med

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The human body is colonized by abundant and diverse microorganisms, collectively known as the microbiome. The oral cavity has more than 700 species of bacteria and consists of unique microbiome niches on mucosal surfaces, on tooth hard tissue, and in saliva. The homeostatic balance between the oral microbiota and the immune system plays an indispensable role in maintaining the well-being and health status of the human host. Growing evidence has demonstrated that oral microbiota dysbiosis is actively involved in regulating the initiation and progression of an array of autoimmune diseases.Oral microbiota dysbiosis is driven by multiple factors, such as host genetic factors, dietary habits, stress, smoking, administration of antibiotics, tissue injury and infection. The dysregulation in the oral microbiome plays a crucial role in triggering and promoting autoimmune diseases via several mechanisms, including microbial translocation, molecular mimicry, autoantigen overproduction, and amplification of autoimmune responses by cytokines. Good oral hygiene behaviors, low carbohydrate diets, healthy lifestyles, usage of prebiotics, probiotics or synbiotics, oral microbiota transplantation and nanomedicine-based therapeutics are promising avenues for maintaining a balanced oral microbiome and treating oral microbiota-mediated autoimmune diseases. Thus, a comprehensive understanding of the relationship between oral microbiota dysbiosis and autoimmune diseases is critical for providing novel insights into the development of oral microbiota-based therapeutic approaches for combating these refractory diseases.

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“…Different mycobacterial pathogens [ 12 , 13 ], Corynebacterium species [ 14 , 15 ], Helicobacter pylori [ 16 ], Mycoplasma fermentans [ 17 ], rickettsiae [ 18 ] and S. enterica [ 19 ] were studied in respect to their interaction with human cell lines. In addition to other human pathogens [ 20 , 21 , 22 , 23 , 24 ], animal- [ 25 , 26 ] and plant-pathogenic bacteria [ 27 , 28 , 29 , 30 ] were investigated.…”

mentioning

confidence: 99%