Degree of colitis correlates with microbial composition and cytokine responses in colon and caecum of Gαi2-deficient mice

Rangel, Ignacio; Mall, John Peter Ganda; Wïllén, Roger; Sjöberg, Fei; Hultgren-Hörnquist, Elisabeth

doi:10.1093/femsec/fiw098

Cited by 12 publications

(11 citation statements)

References 38 publications

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“…Disturbed gut microbiota, in either diversity or abundance, has been found to play an important role in the pathological development of inflammatory bowel diseases (Juste et al, 2014 ; Rangel et al, 2016 ). At genus level, 5-Fu treatment has been shown to decrease Clostridium, Lactobacillus, Streptococcus and Enterococcus and increase Escherichia in rat jejunum or colon (Stringer et al, 2007 , 2009b ).…”

Section: Discussionmentioning

confidence: 99%

Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis

Liu

Wang

et al. 2017

Front. Cell. Infect. Microbiol.

134

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Disturbed homeostasis of gut microbiota has been suggested to be closely associated with 5-fluorouracil (5-Fu) induced mucositis. However, current knowledge of the overall profiles of 5-Fu-disturbed gut microbiota is limited, and so far there is no direct convincing evidence proving the causality between 5-Fu-disturbed microbiota and colonic mucositis. In mice, in agreement with previous reports, 5-Fu resulted in severe colonic mucositis indicated by weight loss, diarrhea, bloody stool, shortened colon, and infiltration of inflammatory cells. It significantly changed the profiles of inflammatory cytokines/chemokines in serum and colon. Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and VE-Cadherin were increased. While tight junction protein occludin was reduced, however, zonula occludens-1 (ZO-1) and junctional adhesion molecule-A (JAM-A) were increased in colonic tissues of 5-Fu treated mice. Meanwhile, inflammation related signaling pathways including NF-κB and mitogen activated protein kinase (MAPKs) in the colon were activated. Further study disclosed that 5-Fu diminished bacterial community richness and diversity, leading to the relative lower abundance of Firmicutes and decreased Firmicutes/Bacteroidetes (F/B) ratio in feces and cecum contents. 5-Fu also reduced the proportion of Proteobacteria, Tenericutes, Cyanobacteria, and Candidate division TM7, but increased that of Verrucomicrobia and Actinobacteria in feces and/or cecum contents. The fecal transplant from healthy mice prevented body weight loss and colon shortening of 5-Fu treated mice. In addition, the fecal transplant from 5-Fu treated mice reduced body weight and colon length of vancomycin-pretreated mice. Taken together, our study demonstrated that gut microbiota was actively involved in the pathological process of 5-Fu induced intestinal mucositis, suggesting potential attenuation of 5-Fu induced intestinal mucositis by manipulating gut microbiota homeostasis.

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Section: Discussionmentioning

confidence: 99%

Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis

Liu

Wang

et al. 2017

Front. Cell. Infect. Microbiol.

134

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“…Absolute quantifications of the BCoAT gene copy numbers were measured from a standard curve as previously described [13]. F. prausnitzii and the C. leptum group were measured in relation to the total bacterial abundance using the DD-method [25,26].…”

Section: Qpcrmentioning

confidence: 99%

“…To assess the relative abundance of F. prausnitzii and the C. leptum group, the fold change for each respective target sequence was calculated in relation to the total presence of bacteria, as previously described [25]. Absolute quantification of the BCoAT gene was performed from a standard curve according to the procedure of Louis et al [13].…”

Section: Statisticsmentioning

confidence: 99%

Alterations in the relative abundance of Faecalibacterium prausnitzii correlate with changes in fecal calprotectin in patients with ileal Crohn’s disease: a longitudinal study

Björkqvist

Repsilber

Seifert

et al. 2019

Scandinavian Journal of Gastroenterology

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Objectives: Crohn's disease is characterized by a gut dysbiosis with decreased abundance of butyrate producers such as Faecalibacterium prausnitzii. Although F. prausnitzii secretes anti-inflammatory molecules, few studies have addressed the importance of F. prausnitzii in a longitudinal setting. We aimed to examine the relationship between temporal profiles of F. prausnitzii, the C. leptum group, overall butyrate production, and inflammatory activity. Material and methods: Fecal samples (n ¼ 59) were collected every third month from nine patients with ileal Crohn's disease. The abundance of F. prausnitzii and C. leptum was quantified relative to the total amount of bacteria using quantitative-PCR. To assess butyrate production of gut microbiota, gene copy numbers of the butyryl-CoA:acetate-CoA transferase (BCoAT) gene were quantified by qPCR. The inflammatory activity was defined by fecal (f)-calprotectin. Results: No correlation between the relative abundance of F. prausnitzii, the C. leptum group, or copy numbers of the BCoAT gene, and f-calprotectin was observed in the total sample set. By analyzing alterations between consecutive samples, a negative correlation between changes in the relative abundance of F. prausnitzii and f-calprotectin was observed (R ¼ À0.39; p ¼ .009). Changes in C. leptum (R ¼ À0.18, p ¼ .23) and number of copies of the BCoAT gene (R ¼ À0.12; p ¼ .42) did not correlate with f-calprotectin. Conclusions: There was an inverse correlation between temporal changes in the relative abundance of F. prausnitzii, but not overall butyrate producing capacity, and changes in inflammatory activity in ileal Crohn's disease. These findings indicate that F. prausnitzii may play a role in gut homeostasis, even though causality is still to be demonstrated.

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“…Similarly, Bacteroides [80], Prevotella [80, 81], and Clostridium [82] were closely correlated with cognitive abilities in prior studies. Moreover, the relative abundance of Bacteroides [83, 84], Prevotella [95], and Ruminococcus [85] were correlated with levels of inflammatory cytokines. Inversely, microbial infection and prebiotics may regulate levels of circulating cytokines, which have an obvious effect on brain function [86–88].…”

Section: Discussionmentioning

confidence: 99%

CA-30, an oligosaccharide fraction derived from Liuwei Dihuang decoction, ameliorates cognitive deterioration via the intestinal microbiome in the senescence-accelerated mouse prone 8 strain

Wang¹,

Xi²,

Xie³

et al. 2019

Aging

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Mounting evidence points to alterations in the gut microbiota-neuroendocrine immunomodulation (NIM) network that might drive Alzheimer’s Disease (AD) pathology. In previous studies, we found that Liuwei Dihuang decoction (LW) had beneficial effects on the cognitive impairments and gastrointestinal microbiota dysbiosis in an AD mouse model. In particular, CA-30 is an oligosaccharide fraction derived from LW. We sought to determine the effects of CA-30 on the composition and function of the intestinal microbiome in the senescence-accelerated mouse prone 8 (SAMP8) mouse strain, an AD mouse model. Treatment with CA-30 delayed aging processes, ameliorated cognition in SAMP8 mice. Moreover, CA-30 ameliorated abnormal NIM network in SAMP8 mice. In addition, we found that CA-30 mainly altered the abundance of four genera and 10 newborn genera. Advantageous changes in carbohydrate-active enzymes of SAMP8 mice following CA-30 treatment, especially GH85, were also noted. We further found that seven genera were significantly correlated with the NIM network and cognitive performance. CA-30 influenced the relative abundance of these intestinal microbiomes in SAMP8 mice and restored them to SAMR1 mouse levels. CA-30 ameliorated the intestinal microbiome, rebalanced the NIM network, improved the AD-like cognitive impairments in SAMP8 mice, and can thus be a potential therapeutic agent for AD.

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Degree of colitis correlates with microbial composition and cytokine responses in colon and caecum of Gαi2-deficient mice

Cited by 12 publications

References 38 publications

Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis

Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis

Alterations in the relative abundance of Faecalibacterium prausnitzii correlate with changes in fecal calprotectin in patients with ileal Crohn’s disease: a longitudinal study

CA-30, an oligosaccharide fraction derived from Liuwei Dihuang decoction, ameliorates cognitive deterioration via the intestinal microbiome in the senescence-accelerated mouse prone 8 strain

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