The Role of<i>Klebsiella</i>in Crohn’s Disease with a Potential for the Use of Antimicrobial Measures

Rashid, Taha; Ebringer, Alan; Wilson, Clyde

doi:10.1155/2013/610393

Cited by 40 publications

(21 citation statements)

References 71 publications

(72 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3B , are Klebsiella pneumonia , Campylobacter hominis , and two species of Bifidobacter. Klebsiella pneumonia and Campylobacter hominis are potent pro-inflammatory agents: Klebsiella has been show to play a major role in the initiation of inflammation in IBD 43 , and Campylobacter is a common cause of severe gastroenteritis. The two species of Bifidobacter may serve to protect the gut mucosa through inhibition of NF κ B 44 , and upregulation of these anti-inflammatory species in IBD is consistent with data from patient fecal samples showing increased populations of probiotics such as Bifidobacterium and Lactobacillus 45 .…”

Section: Resultsmentioning

confidence: 99%

Topological distortion and reorganized modular structure of gut microbial co-occurrence networks in inflammatory bowel disease

Baldassano

Bassett

2016

Sci Rep

View full text Add to dashboard Cite

The gut microbiome plays a key role in human health, and alterations of the normal gut flora are associated with a variety of distinct disease states. Yet, the natural dependencies between microbes in healthy and diseased individuals remain far from understood. Here we use a network-based approach to characterize microbial co-occurrence in individuals with inflammatory bowel disease (IBD) and healthy (non-IBD control) individuals. We find that microbial networks in patients with IBD differ in both global structure and local connectivity patterns. While a “core” microbiome is preserved, network topology of other densely interconnected microbe modules is distorted, with potent inflammation-mediating organisms assuming roles as integrative and highly connected inter-modular hubs. We show that while both networks display a rich-club organization, in which a small set of microbes commonly co-occur, the healthy network is more easily disrupted by elimination of a small number of key species. Further investigation of network alterations in disease might offer mechanistic insights into the specific pathogens responsible for microbiome-mediated inflammation in IBD.

show abstract

Section: Resultsmentioning

confidence: 99%

Topological distortion and reorganized modular structure of gut microbial co-occurrence networks in inflammatory bowel disease

Baldassano

Bassett

2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…In our study, the dominance of Klebsiella following ampicillin exposure is noteworthy because, in humans, Klebsiella oxytoca has been identified as the causative organism for antibiotic-associated hemorrhagic colitis ( Högenauer et al, 2006 ). Klebsiella also has a key role in the initiation of pathological damage in patients with Crohn’s disease ( Rashid et al, 2013 ). Various studies have suggested that commensal organisms, such as Enterococcus and Klebsiella species, drive the pathogenesis of experimental intestinal inflammation and human IBD ( Sartor, 2006 , 2008 ).…”

Section: Discussionmentioning

confidence: 99%

Structural and Functional Alterations in the Microbial Community and Immunological Consequences in a Mouse Model of Antibiotic-Induced Dysbiosis

et al. 2018

View full text Add to dashboard Cite

The aim of this study was to establish continuous therapeutic-dose ampicillin (CTDA)-induced dysbiosis in a mouse model, mimicking typical adult exposure, with a view to using this to assess its impact on gut microbiota, intestinal metabolites and host immune responses. Mice were exposed to ampicillin for 14 days and antibiotic-induced dysbiosis was evaluated by alteration of microbiota and gut permeability. The cecal index was increased in the CTDA group, and the gut permeability indicated by fluorescent dextran, endotoxin and D-Lactate in the serum was significantly increased after antibiotic use. The tight-junction proteins ZO-1 and occludin in the colon were reduced to half the control level in CTDA. We found that alpha-diversity was significantly decreased in mice receiving CTDA, and microbial community structure was altered compared with the control. Key taxa were identified as CTDA-specific, and the relative abundance of Enterococcus and Klebsiella was particularly enriched while Lachnospiraceae, Coprobacillus and Dorea were depleted after antibiotic treatment. In particular, a significant increase in succinate and a reduction in butyrate was detected in CTDA mice, and the triggering of NF-κB enhancement reflected that the host immune response was influenced by ampicillin use. The observed perturbation of the microbiota was accompanied by modulation of inflammatory state; this included increase in interferon-γ and RegIIIγ, and a decrease in secretory IgA in the colon mucosa. This study allowed us to identify the key taxa associated with an ampicillin-induced state of dysbiosis in mice and to characterize the microbial communities via molecular profiling. Thus, this work describes the bacterial ecology of antibiotic exposure model in combination with host physiological characteristics at a detailed level of microbial taxa.

show abstract

“…Strain-specific genes associated with Th1 cell induction are predicted to encode hemolysin-coregulated protein and enzymes involved in fructose-, galactitol-, mannose-, and long-chain fatty acidrelated uptake and metabolic pathways. Furthermore, the ability of pathobionts to outgrow other bacteria in the inflamed gut is supported by sequencing data, in which Klebsiella species and other bacteria associated with the oral cavity are more abundant in the guts of IBD patients compared to controls 28,88,89 . Klebsiella species are also more abundant in mouse models and human cohort studies of other gut diseases 90,91 .…”

Section: Microbial Strains Implicated In Ibdmentioning

confidence: 95%

Microbial genes and pathways in inflammatory bowel disease

et al. 2019

View full text Add to dashboard Cite

Perturbations in the intestinal microbiome are implicated in inflammatory bowel disease (IBD). Studies of treatment-naive patients have identified microbial taxa associated with disease course and treatment efficacy. In order to gain a mechanistic understanding of how the microbiome impacts gastrointestinal health, we need to move from census to function. Bacteria including those that adhere to epithelial cells as well as several Clostridium species can alter differentiation of T helper 17 cells and regulatory T cells. Similarly, microbial products such as short-chain fatty acids and sphingolipids also influence immune responses. Metagenomics and culturomics have identified strains of Ruminococcus gnavus and adherent invasive Escherichia coli that are linked to IBD and gut inflammation. Integrated analysis of multi-omics data, including metagenomics, metatranscriptomics, and metabolomics, with measurements of host response and culturomics have great potential in understanding the role of the microbiome in IBD. In this Review, we highlight current knowledge of gut microbial factors linked to IBD pathogenesis and discuss how multi-omics data from large-scale population studies in health and disease have been used to identify specific microbial strains, transcriptional changes, and metabolic alterations associated with IBD.

show abstract

The Role ofKlebsiellain Crohn’s Disease with a Potential for the Use of Antimicrobial Measures

Cited by 40 publications

References 71 publications

Topological distortion and reorganized modular structure of gut microbial co-occurrence networks in inflammatory bowel disease

Topological distortion and reorganized modular structure of gut microbial co-occurrence networks in inflammatory bowel disease

Structural and Functional Alterations in the Microbial Community and Immunological Consequences in a Mouse Model of Antibiotic-Induced Dysbiosis

Microbial genes and pathways in inflammatory bowel disease

Contact Info

Product

Resources

About