Dysbiosis in intestinal inflammation: Cause or consequence

Buttó, Ludovica F.; Haller, Dirk

doi:10.1016/j.ijmm.2016.02.010

Cited by 129 publications

(91 citation statements)

References 118 publications

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“…However, there is debate whether dysbiosis precedes or follows IBD pathology (Buttó & Haller, 2016). With the limited available knowledge, the association of antibiotic exposure and dysbiosis, along with the increased incidence of CD, suggests that microbial dysbiosis is likely present prior to the initiation of inflammation and subsequent disease development.…”

Section: Antimicrobial Therapymentioning

confidence: 99%

An overview of the bacterial contribution to Crohn disease pathogenesis

Alhagamhmad

Day

Lemberg

et al. 2016

Journal of Medical Microbiology

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Section: Antimicrobial Therapymentioning

confidence: 99%

An overview of the bacterial contribution to Crohn disease pathogenesis

Alhagamhmad

Day

Lemberg

et al. 2016

Journal of Medical Microbiology

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“…For example, Proteobacteria species are rapidly induced by inflammation and many Proteobacteria species express high levels of pro-inflammatory molecules such as flagellin and LPS [10,11]. In any case, a range of inflammatory phenotypes can be transferred upon microbiota transfer, indicating that the altered microbiota community is not purely a consequence of inflammation but rather plays a role in driving inflammation and associated phenotypes.…”

Section: Introduction: Characteristics Of a “Bad” (Ie Disease-promomentioning

confidence: 99%

How diet can impact gut microbiota to promote or endanger health

Chassaing

Vijay‐Kumar

Gewirtz

2017

Current Opinion in Gastroenterology

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Purpose of review Disturbances of the intestinal microbiota have been increasingly implicated in driving various diseases associated with a broad range of chronic inflammatory state. Such diseases have increased in incidence since the mid 20th century, and have roughly correlated with societal changes in food production during this period. Purpose of review Consider how changes in diet may have impacted gut microbiota and exploring whether targeted modulated of diet might be a means of optimizing microbiota composition to promote health. Summary Recent literature demonstrates that modulation of diet has potential to both beneficially and detrimentally impact microbiota composition and how it interacts with its host. Herein, we discuss recent studies by ourselves and others that demonstrate the potential for changes in diet to have profound impacts on the gut microbiota in ways that can have beneficial or detrimental effects on host health.

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“…Since cage and litter effects were excluded, our current hypothesis rests on the assumption that morphological modifications of the epithelial interface, previously described as focal lesions, 2 occur stochastically in the gut and may alter the local milieu affecting bacterial abundance and fitness 3,4 . Actually, while a healthy host is able to seal off the damage, the susceptible individual lacks the ability to restore mucosal integrity, resulting in an altered gut milieu leading to barrier dysfunction and expansion of focal lesions 2-4 (Fig.…”

Section: Gut Epithelial Stochastic Injuries Generate Focal Inflammatimentioning

confidence: 99%

Dysbiosis in Crohn's disease - Joint action of stochastic injuries and focal inflammation in the gut

Buttó

Haller

2017

Gut Microbes

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Gut homeostasis involves interrelated biological networks that include the immune system, specialized cells of the epithelium, such as Paneth and goblet cells, as well as triggers derived from the microbiota. Disruption of these homeostatic interactions may lead to the pathogenesis of inflammatory bowel diseases (IBD). To develop more targeted and individual treatments in Crohn's disease and ulcerative colitis, it becomes more and more important to link key mechanisms of the disease pathogenesis to distinct IBD subsets. For the first time, our laboratory demonstrated a causal role of the microbiota for the development of Crohn's disease (CD)-like ileitis, supporting the hypothesis that a non-infectious, dysbiotic microbial ecosystem harbors aggressive traits relevant for the induction of chronic inflammation in the disease-susceptible host (i.e. TNFΔARE mouse model). Despite a growing body of evidence claiming a primary role for Paneth cells in the pathogenesis of ileal CD, we showed in the TNFΔARE mouse model that Paneth cell failure or exhaustion is a secondary event to inflammation. Therefore, additional mechanisms may act synergistically to initialize the development of CD-like pathology. Hereby, we propose a novel hypothesis suggesting that individual development of dysbiotic communities is based on stochastic injury and focal inflammation of the epithelial lining that propagate radially, finally leading to an aggressive microbial milieu.

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Dysbiosis in intestinal inflammation: Cause or consequence

Cited by 129 publications

References 118 publications

An overview of the bacterial contribution to Crohn disease pathogenesis

An overview of the bacterial contribution to Crohn disease pathogenesis

How diet can impact gut microbiota to promote or endanger health

Dysbiosis in Crohn's disease - Joint action of stochastic injuries and focal inflammation in the gut

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