Antibiotics in inflammatory bowel diseases: do we know what we’re doing?

Ledder, Oren

doi:10.21037/tp.2018.11.02

Cited by 32 publications

(25 citation statements)

References 143 publications

(172 reference statements)

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“…Exposure to antibiotics during pregnancy or early childhood can cause severe disruption to the developing microbiome and an increased risk of dysbiosis and IBD, particularly CD [ 65 , 66 , 67 , 68 ]. However, some studies suggest that antibiotics given antepartum or postpartum do not alter IBD risk in offspring [ 36 , 69 ].…”

Section: Influences On Colonizationmentioning

confidence: 99%

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

2020

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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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Section: Influences On Colonizationmentioning

confidence: 99%

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

2020

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“…An increase in IBD incidence in individuals who moved from the low incidence regions to high incidence regions again underscores the role of environmental factors[ 17 , 19 , 30 ]. Everyday life factors like less physical work demanding stressful living style, usage of antibiotics to fend off bacteria[ 31 ] are further suspected to be additional variables contributing to IBD development. Nicotine appears to induce IBD which is a very potent contributory factor in individuals of early age groups[ 20 , 32 ].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory bowel disease: Therapeutic limitations and prospective of the stem cell therapy

Mishra¹,

Dhawan

Srivastava³

et al. 2020

WJSC

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Inflammatory bowel disease (IBD), consisting primarily of ulcerative colitis and Crohn’s disease, is a group of debilitating auto-immune disorders, which also increases the risk of colitis-associated cancer. However, due to the chronic nature of the disease and inconsistent treatment outcomes of current anti-IBD drugs ( e.g. , approximately 30% non-responders to anti-TNFα agents), and related serious side effects, about half of all IBD patients (in millions) turn to alternative treatment options. In this regard, mucosal healing is gaining acceptance as a measure of disease activity in IBD patients as recent studies have correlated the success of mucosal healing with improved prognosis. However, despite the increasing clinical realization of the significance of the concept of mucosal healing, its regulation and means of therapeutic targeting remain largely unclear. Here, stem-cell therapy, which uses hematopoietic stem cells or mesenchymal stem cells, remains a promising option. Stem cells are the pluripotent cells with ability to differentiate into the epithelial and/or immune-modulatory cells. The over-reaching concept is that the stem cells can migrate to the damaged areas of the intestine to provide curative help in the mucosal healing process. Moreover, by differentiating into the mature intestinal epithelial cells, the stem cells also help in restoring the barrier integrity of the intestinal lining and hence prevent the immunomodulatory induction, the root cause of the IBD. In this article, we elaborate upon the current status of the clinical management of IBD and potential role of the stem cell therapy in improving IBD therapy and patient’s quality of life.

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“…Antibiotics decrease the number of luminal bacteria and change the composition of intestinal ora [8].…”

Section: Introductionmentioning

confidence: 99%

Enterobacter Ludwigii Protects Experimental Colitis Through CD103+DC and Treg Cells

Li¹,

Sun²,

Kobayashi³

et al. 2020

Preprint

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Background: Intestinal bacteria are closely related with inflammatory bowel disease (IBD), and regulatory cell-mediated immune tolerance is important to inhibit IBD. Commensal intestinal bacteria play key roles in regulating immune tolerance cell, however, bacterial strains directly involved in this regulation remain to be identified.Results: In the present study, metronidazole, among nine antibiotics, was found to have the best effect on protecting mice against DSS-induced colitis. Enterobacter ludwigi, abundant in mouse feces after metronidazole treatment, was identified to decrease mice susceptibility to DSS-induced colitis with or without the presence of complex intestinal bacteria. E. ludwigii gavage increased CD103+DCs and Foxp3+Treg cells in intestinal microenvironment, and effects of E. ludwigii on diminishing colitis were lost in DC or Treg depletion mice. CD103+DCs isolated from E. ludwigii-treated mice showed enhanced ability to promote the Treg differentiation from naive T cells. DCs, directly stimulated by live E. ludwigii strain or its culture supernatant, had increased immune tolerance ability for Treg differentiation in vitro. Conclusions: Overall, our findings identify a facultative anaerobe bacterial strain E. ludwigii, which directly enhances CD103+DC and Treg-mediated immune tolerance, resulting in protecting mice against DSS-induced colitis.

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Antibiotics in inflammatory bowel diseases: do we know what we’re doing?

Cited by 32 publications

References 143 publications

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

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

Inflammatory bowel disease: Therapeutic limitations and prospective of the stem cell therapy

Enterobacter Ludwigii Protects Experimental Colitis Through CD103+DC and Treg Cells

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