scholarly journals Colonization of C57BL/6 Mice by a Potential Probiotic Bifidobacterium bifidum Strain under Germ-Free and Specific Pathogen-Free Conditions and during Experimental Colitis

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0139935 ◽  
Author(s):  
Verena Grimm ◽  
Katarina Radulovic ◽  
Christian U. Riedel
Keyword(s):  
Experimental Colitis ◽  
Bifidobacterium Bifidum ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Specific Pathogen

Comparative analysis of microRNA expression profiles in the colons of specific pathogen-free mice and germ-free mice

2021 ◽  
Author(s):  
Ayako Aoki ◽  
Reiji Aoki ◽  
Madoka Yatagai ◽  
Toshiyuki Kawasumi
Keyword(s):  
Gene Ontology ◽  
Comparative Analysis ◽  
Expression Profiles ◽  
Microrna Expression ◽  
Gene Ontology Analysis ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Mrna Targets ◽  
Significant Gene ◽  
Specific Pathogen

ABSTRACT MicroRNAs play an important role in microbiota–host crosstalk. In this study, we compared microRNA expression in whole colons of specific pathogen-free mice and germ-free mice. Forty-eight microRNAs were differentially expressed by more than 2-fold. Gene ontology analysis of the predicted mRNA targets revealed that the majority of the most significant gene ontology terms were related to GTPases and nerves.

scholarly journals Microbiota Facilitates the Formation of the Aminated Metabolite of Tea Polyphenols Which Trap Deleterious Reactive Endogenous Metabolites (P06-022-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Shuwei Zhang ◽  
Yantao Zhao ◽  
Christina Ohland ◽  
Christian Jobin ◽  
Shengmin Sang
Keyword(s):  
Gut Microbiota ◽  
Chronic Diseases ◽  
Green Tea ◽  
Tea Polyphenols ◽  
Specific Pathogen Free ◽  
Tea Polyphenol ◽  
Germ Free ◽  
Specific Pathogen ◽  
Conjugated Metabolites

Abstract Objectives The in vivo mechanism of tea polyphenol-mediated prevention of many chronic diseases is still largely unknown. Studies have shown that accumulation of toxic reactive cellular metabolites, such as ammonia and reactive carbonyl species (RCS), is one of the causing factors to the development of many chronic diseases. The objective of this study is to investigated the in vivo interaction between tea polyphenols and ammonia and RCS. Methods In mice, we gave 200 mg/kg tea polyphenol ((-)-epigallocatechin-3-gallate (EGCG) or theaflavin) to CD-1 mice, 129/SvEv specific-pathogen-free (SPF) mice, or germ-free (GF) mice. Urinary and fecal samples were collected in metabolic cages for 24 h. In humans, two healthy volunteers drank 4 cups of Lipton green tea every day for four days. On the fourth day, 24 h urinary and fecal samples were collected after consuming the first cup of tea. Using LC tandem mass, we searched the formation of the aminated and RCS conjugated metabolites of tea polyphenols. Chemical standards were synthesized to confirm the structures of these metabolites. In order to study the impact of gut microbiota on the formation of these metabolites, we also quantified the concentrations of these metabolites in SPF and GF mice. Results We found that both EGCG and theaflavin could rapidly react with ammonia to generate the aminated metabolites. Both tea polyphenols and their aminated metabolites could further scavenge RCS, such as methylglyoxal (MGO), malondialdehyde (MDA), and trans-4-hydroxy-2-nonenal (4-HNE), to produce the RCS conjugates of tea polyphenols and the aminated tea polyphenols. Both the aminated and the RCS conjugated metabolites of EGCG were detected in human after drinking four cups of green tea per day. By comparing the levels of the aminated and the RCS conjugated metabolites in EGCG or theaflavin exposed germ-free (GF) mice and specific-pathogen-free (SPF) mice, we demonstrated that gut microbiota facilitate the formation of the aminated metabolites of tea polyphenols, the RCS conjugates of tea polyphenols, and the RCS conjugates of the aminated tea polyphenols. Conclusions Altogether, this study provides in vivo evidences that tea polyphenols have the capacity to scavenge toxic reactive metabolic wastes. This finding opens a new window to understand the underlying mechanisms by which drinking tea could prevent the development of chronic diseases. Funding Sources We gratefully acknowledge financial support from NIH R01 grant AT008623 to this work.

scholarly journals Effects of Breeding Environments on Generation and Activation of Autoreactive B-1 Cells in Anti-red Blood Cell Autoantibody Transgenic Mice

1997 ◽  
Vol 185 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Masao Murakami ◽  
Kazuo Nakajima ◽  
Ken-ichi Yamazaki ◽  
Takehiko Muraguchi ◽  
Tadao Serikawa ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Transgenic Mice ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Bacterial Infections ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Conventional Condition ◽  
Specific Pathogen ◽  
Almost All

In anti-red blood cell autoantibody transgenic (autoAb Tg) mice almost all B cells are deleted except for B-1 cells in the peritoneal cavity and the gut. About one-half of the auto Ab Tg mice suffer from autoimmune hemolytic anemia (AIHA) in the conventional condition. Oral administration of lipopolysaccharides activates B-1 cells and induces autoimmune symptoms in the Tg mice, suggesting that the autoimmune disease in anti-RBC autoAb Tg mice is triggered by infections. To examine the association of bacterial infections with the generation of B-1 cells and the occurrence of the autoimmune disease, we analyzed anti-RBC autoAb Tg mice bred in germ-free and specific pathogen-free conditions. In germ-free conditions, few peritoneal B-1 cells were detected, while a significant number of peritoneal B-1 cells existed in specific pathogen-free conditions. In both conditions, no mice suffered from AIHA. However, when these Tg mice were transferred to the conventional condition or injected with lipopolysaccharide, peritoneal B-1 cells expanded and some of these mice suffered from AIHA. These results clearly showed that bacterial infections are responsible for both the expansion of B-1 cells and the onset of the autoimmune disease in these Tg mice.

scholarly journals Mice, Models, Microbiota: How Can We More Accurately Reflect Human Disease?

2021 ◽  
Vol 15 (1) ◽  
pp. 8
Author(s):  
Rahman Ladak ◽  
Dana Philpott
Keyword(s):  
Gut Microbiota ◽  
Translational Research ◽  
Mouse Models ◽  
Human Disease ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Stage Of Development ◽  
Specific Pathogen

With growing evidence that human disease is affected by the microbiota, many researchers have sought to modulate the microbiomes of mice to improve translational research. Altering their microbiomes, which are usually germ-free or specific pathogen-free, might allow mice to more accurately model human disease and hence produce more applicable findings. However, this has been difficult to apply to individual projects due to the disparity of explained methods and results. In this review, we first describe the immunological functions of the gut microbiota and the methods of altering mice microbiota, from transplantation route to age of transplantation to microbiota source. We then present an approach for how the gut microbiota might be considered when modelling human disease in mice. By organizing findings by type of disease - neurological, immunological, chronic inflammatory, and cancer - we propose that mouse models can be improved by considering the source of the microbiota, the presence or absence of certain microbial phyla, and by timing the transplantation during a physiologically relevant stage of development, such as the first five weeks of life.

scholarly journals Deciphering the combinatorial influence of diet and the microbiota on experimental colitis

2017 ◽  
Author(s):  
Sean R. Llewellyn ◽  
Graham J. Britton ◽  
Eduardo J. Contijoch ◽  
Arthur Mortha ◽  
Jean-Frederic Colombel ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Intestinal Inflammation ◽  
High Protein Diet ◽  
Experimental Colitis ◽  
Mucosal Inflammation ◽  
Germ Free ◽  
Dss Colitis ◽  
Microbial Density ◽  
Specific Pathogen ◽  
Host Physiology

AbstractBackground & AimsThe complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis.MethodsTo examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or colitis models (dextran sodium sulfate (DSS) and T cell transfer).ResultsDiet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other.ConclusionsOur results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation.

Microbial regulation of a lincRNA–miRNA–mRNA network in the mouse hippocampus

Epigenomics ◽  
2020 ◽  
Vol 12 (16) ◽  
pp. 1377-1387
Author(s):  
Lanxiang Liu ◽  
Haiyang Wang ◽  
Ying Yu ◽  
Benhua Zeng ◽  
Xuechen Rao ◽  
...  
Keyword(s):  
Regulatory Network ◽  
Molecular Basis ◽  
Mapk Signaling ◽  
Specific Pathogen Free ◽  
Rna Transcription ◽  
Germ Free ◽  
Mouse Hippocampus ◽  
Specific Pathogen ◽  
Post Transcriptional Regulation ◽  
Mapk Signaling Pathways

Aim: To comprehensively understand microbiota-regulated lincRNA–miRNA–mRNA networks in psychiatric disorders. Materials & methods: Integrated analyses of lincRNAs, mRNAs and miRNAs, obtained by microarray analysis of hippocampus from specific pathogen-free, germ-free and colonized germ-free mice, were performed. Results: Expression of 139 mRNAs, seven miRNAs and one lincRNA was restored following colonization. The restored transcripts were mainly involved in CREB and Ras/MAPK signaling pathways. RNA transcription and post-transcriptional regulation were the primary perturbed functions. Finally, 12 lincRNAs, six miRNAs and 47 mRNAs were included in a lincRNA–miRNA–mRNA network, and lincRNA0926-miR-190a-5p-Celf4 interactions may play a pivotal role in this regulatory network. Conclusion: This study provides clues for understanding the molecular basis of gut microbiota–brain interactions in depressive- and anxiety-like behaviors.

scholarly journals Enterococcus Faecium is a Risk Factor for The Outbreak of Anxiety and Depression in Patients With Inflammatory Bowel Disease

2020 ◽  
Author(s):  
Hyo-Min Jang ◽  
Jeon-Kyung Kim ◽  
Min-Kyung Joo ◽  
Yun-Jung Shin ◽  
Kyung-Eon Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Cell Population ◽  
Enterococcus Faecium ◽  
Fecal Microbiota ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Specific Pathogen ◽  
Inflammatory Bowel ◽  
Anxiety Depression

Abstract BackgroundThe gut microbiota closely communicate with the brain through the microbiota-gut-brain axis. The interaction between gut microbiota may regulate the occurrence of neuropsychiatric disorders, including depression. Therefore, we transplanted the fecal microbiota of patients with inflammatory bowel disease (IBD) or their overpopulated gut bacteria into specific-pathogen-free or germ-free mice and examined their effects regarding the occurrence of colitis and anxiety/depression. ResultsFecal microbiota transplantations (FMTs) from patients with IBD with (/D+) or without depression (/D-) caused IBD-like colitis in the transplanted mice: they increased myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon. FMTs from patients with IBD/D+ caused anxiety-/depression-like behaviors and NF-κB+/Iba1+ and lipopolysaccharide (LPS)+/Iba1+ cell population and decreased the BDNF+/NeuN+ cell population in the hippocampus. FMTs from patients with IBD/D- caused anxiety-like, but not depression-like, behaviors. α-/β-diversities and composition of microbiota in the feces of patients with IBD (IBD-F) were different from those of healthy-control feces (HC-F). The Enterobacteriaceae and Enterococcaceae populations and fecal lipopolysaccharide levels were higher in IBD-F vs. HC-F. Moreover, the Enterococcaceae population was higher in IBD/D+-F vs. IBD/D--F, while the Bifidobacteria population was lower in IBD/D+-F. FMT from HC alleviated the IBD/D+-F-induced anxiety-/depression-like behaviors and colitis in the transplanted mice. Furthermore, it suppressed IBD/D+-F-induced Enterococcus sp. population in the feces. Enterobacteriaceae Klebsiella oxytoca, Klebsiella pneumoniae, Escherichia coli, and Cronobacter sakazakii abundant in IBD-F, singly or together, caused depression with colitis in germ-free and specific-pathogen-free mice, while Enterococcus faecium abundant in IBD/D+-F did not cause not anxiety/depression and colitis. However, the combination of Enterobacteriaceae with Enterococcus faecium synergistically deteriorated depression and colitis, while its combination with Bifidobacterium longum attenuated them. ConclusionThe interaction between gut microbiota Enterobacteriaceae, Enterococci, and Bifidobacteria may regulate the outbreak of anxiety/depression and IBD through the modulation of NF-κB-involved BDNF expression and gut microbiota. Enterococcus faecium, a probiotic strain, is a risk factor for the outbreak of anxiety/depression in patients with IBD.

scholarly journals Presence or absence of microbiome modulates the response of mice organism to administered drug nabumetone

2020 ◽  
pp. 583-594
Author(s):  
L Jourová ◽  
B Lišková ◽  
K Lněničková ◽  
N Zemanová ◽  
P Anzenbacher ◽  
...  
Keyword(s):  
Small Intestine ◽  
Molecular Mechanisms ◽  
Cytochromes P450 ◽  
Active Form ◽  
Drug Metabolizing Enzymes ◽  
Specific Pathogen Free ◽  
Metabolizing Enzymes ◽  
Germ Free ◽  
Wide Range ◽  
Specific Pathogen

The gut microbiota provides a wide range of beneficial functions for the host, and has an immense effect on the host’s health status. The presence of microbiome in the gut may often influence the effect of an orally administered drug. Molecular mechanisms of this process are however mostly unclear. We investigated how the effect of a nonsteroidal drug nabumetone on expression of drug metabolizing enzymes (DMEs) in mice intestine and liver is changed by the presence of microbiota, here, using the germ free (GF) and specific pathogen free (SPF) BALB/c mice. First, we have found in a preliminary experiment that in the GF mice there is a tendency to increase bioavailability of the active form of nabumetone, which we have found now to be possibly influenced by differences in expression of DMEs in the GF and SPF mice. Indeed, we have observed that the expression of the most of selected cytochromes P450 (CYPs) was significantly changed in the small intestine of GF mice compared to the SPF ones. Moreover, orally administered nabumetone itself altered the expression of some CYPs and above all, in different ways in the GF and SPF mice. In the GF mice, the expression of the DMEs (CYP1A) responsible for the formation of active form of the drug are significantly increased in the small intestine and liver after nabumetone application. These results highlight the importance of gut microbiome in processes involved in drug metabolism in the both gastrointestinal tract and in the liver with possible clinical relevance.

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