Microbiota in mesenteric adipose tissue from Crohn’s disease promote colitis in mice

He, Zhen; Wu, Jinjie; Ke, Jia; Ding, Tao; Zhao, Wenjing; Cheng, Wai Ming; Luo, Zhanhao; He, Qilang; Zeng, Wanyi; Yu, Jing; Jiao, Na; Liu, Yanmin; Zheng, Bin; Dai, Lei; Mao, Zhi; Wu, Xiaojian; Jobin, Christian; Lan, Ping

doi:10.1186/s40168-021-01178-8

Cited by 28 publications

(28 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…He et al (2021) demonstrated the ability of A . pulmonis to exacerbate colitis was associated with its ability to impair the colonic mucus layer and to colonize mesenteric fat [ 66 ]. Therefore, the mechanisms by which a member of the intestinal microbiota function as a pathobiont are varied and likely contextual.…”

Section: Discussionmentioning

confidence: 99%

Vertical transmission of attaching and invasive E. coli from the dam to neonatal mice predisposes to more severe colitis following exposure to a colitic insult later in life

et al. 2022

View full text Add to dashboard Cite

The gastrointestinal microbiota begins to be acquired at birth and continually matures through early adolescence. Despite the relevance for gut health, few studies have evaluated the impact of pathobiont colonization of neonates on the severity of colitis later in life. LF82 is an adherent invasive E. coli strain associated with ileal Crohn’s disease. The aim of this study was to evaluate the severity of dextran sodium sulfate (DSS)-induced colitis in mice following E. coli LF82 colonization. Gnotobiotic mice harboring the altered Schaedler flora (ASF) were used as the model. While E. coli LF82 is neither adherent nor invasive, it was been demonstrated that adult ASF mice colonized with E. coli LF82 develop more severe DSS-induced colitis compared to control ASF mice treated with DSS. Therefore, we hypothesized that E. coli LF82 colonization of neonatal ASF mice would reduce the severity of DSS-induced inflammation compared to adult ASF mice colonized with E. coli LF82. To test this hypothesis, adult ASF mice were colonized with E. coli LF82 and bred to produce offspring (LF82N) that were vertically colonized with LF82. LF82N and adult-colonized (LF82A) mice were given 2.0% DSS in drinking water for seven days to trigger colitis. More severe inflammatory lesions were observed in the LF82N + DSS mice when compared to LF82A + DSS mice, and were characterized as transmural in most of the LF82N + DSS mice. Colitis was accompanied by secretion of proinflammatory cytokines (IFNγ, IL-17) and specific mRNA transcripts within the colonic mucosa. Using 16S rRNA gene amplicon sequencing, LF82 colonization did not induce significant changes in the ASF community; however, minimal changes in spatial redistribution by fluorescent in situ hybridization were observed. These results suggest that the age at which mice were colonized with E. coli LF82 pathobiont differentially impacted severity of subsequent colitic events.

show abstract

Section: Discussionmentioning

confidence: 99%

Vertical transmission of attaching and invasive E. coli from the dam to neonatal mice predisposes to more severe colitis following exposure to a colitic insult later in life

et al. 2022

View full text Add to dashboard Cite

show abstract

“…This is further supported by a recent study demonstrating that bacteria isolated from creeping fat in patients with CD were able to translocate to mesenteric adipose tissue. Additionally, these bacteria were able to exacerbate colitis upon transfer to antibiotic-treated mice [ 152 ], thus lending credence to the hypothesis of creeping fat being a defense mechanism confining invading bacteria, thereby limiting systemic dissemination.…”

Section: Hdps and Barrier Dysfunction In Gastrointestinal Inflammationmentioning

confidence: 99%

Rewiring host–microbe interactions and barrier function during gastrointestinal inflammation

Jensen

Pærregaard

Brandum

et al. 2022

Gastroenterology Report

View full text Add to dashboard Cite

Organismal survival depends on a well-balanced immune system and maintenance of host–microbe mutualism. The fine-tuned relationship between the gut microbiota and host immunity is constantly challenged by opportunistic bacteria testing the integrity of gastrointestinal (GI) barrier defenses. Barrier dysfunction reduces immunological tolerance towards otherwise innocuous microbes; it is a process that may instigate chronic inflammation. Paradoxically, sustained inflammation further diminishes barrier function, enabling bacterial translocation to extra-intestinal tissues. Once translocated, these bacteria stimulate systemic inflammation, thereby compromising organ function. While genetic risk alleles associate with barrier dysfunction, environmental stressors are key triggers of GI inflammation and associated breakdown in immune tolerance towards resident gut microbes. As dietary components dictate substrate availability, they also orchestrate microbiota composition and function, including migratory and pro-inflammatory potential, thus holding the capacity to fuel both GI and extra-intestinal inflammation. Additionally, Western diet consumption may weaken barrier defenses via curbed Paneth cell function and diminished host-defense peptide secretion. This review focuses on intervenable niches of host–microbe interactions and mucosal immunity with the ambition to provide a framework of plausible strategies to improve barrier function and regain tolerance in the inflamed mucosa via nutritional intervention.

show abstract

“…He et al showed that presence of MAT microbiota was associated with the development of CD and translocation of Achromobacter pulmonis into the MAT exacerbates colitis symptoms [202]. Gummesson et al showed that visceral adiposity measured by waist circumference is positively correlated with increased permeability [203].…”

Section: Creeping Fat (Cf)mentioning

confidence: 99%

The Role of Gut Microbiota and Metabolites in Obesity-Associated Chronic Gastrointestinal Disorders

et al. 2022

View full text Add to dashboard Cite

The gut microbiota is a complex community of microorganisms that has become a new focus of attention due to its association with numerous human diseases. Research over the last few decades has shown that the gut microbiota plays a considerable role in regulating intestinal homeostasis, and disruption to the microbial community has been linked to chronic disease conditions such as inflammatory bowel disease (IBD), colorectal cancer (CRC), and obesity. Obesity has become a global pandemic, and its prevalence is increasing worldwide mostly in Western countries due to a sedentary lifestyle and consumption of high-fat/high-sugar diets. Obesity-mediated gut microbiota alterations have been associated with the development of IBD and IBD-induced CRC. This review highlights how obesity-associated dysbiosis can lead to the pathogenesis of IBD and CRC with a special focus on mechanisms of altered absorption of short-chain fatty acids (SCFAs)

show abstract

Microbiota in mesenteric adipose tissue from Crohn’s disease promote colitis in mice

Cited by 28 publications

References 51 publications

Vertical transmission of attaching and invasive E. coli from the dam to neonatal mice predisposes to more severe colitis following exposure to a colitic insult later in life

Vertical transmission of attaching and invasive E. coli from the dam to neonatal mice predisposes to more severe colitis following exposure to a colitic insult later in life

Rewiring host–microbe interactions and barrier function during gastrointestinal inflammation

The Role of Gut Microbiota and Metabolites in Obesity-Associated Chronic Gastrointestinal Disorders

Contact Info

Product

Resources

About