scholarly journals Fecal Microbiota Transplantation Eliminates Clostridium difficile in a Murine Model of Relapsing Disease

2015 ◽  
Vol 83 (10) ◽  
pp. 3838-3846 ◽  
Author(s):  
Anna M. Seekatz ◽  
Casey M. Theriot ◽  
Caitlyn T. Molloy ◽  
Katherine L. Wozniak ◽  
Ingrid L. Bergin ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Gut Microbiota ◽  
Murine Model ◽  
Fecal Microbiota Transplantation ◽  
Clinical Signs ◽  
Fecal Microbiota ◽  
Content Type ◽  
Health Care Associated Infections ◽  
Specific Community

RecurrentClostridium difficileinfection (CDI) is of particular concern among health care-associated infections. The role of the microbiota in disease recovery is apparent given the success of fecal microbiota transplantation (FMT) for recurrent CDI. Here, we present a murine model of CDI relapse to further define the microbiota recovery following FMT. Cefoperazone-treated mice were infected withC. difficile630 spores and treated with vancomycin after development of clinical disease. Vancomycin treatment suppressed bothC. difficilecolonization and cytotoxin titers. However,C. difficilecounts increased within 7 days of completing treatment, accompanied by relapse of clinical signs. The administration of FMT immediately after vancomycin clearedC. difficileand decreased cytotoxicity within 1 week. The effects of FMT on the gut microbiota community were detectable in recipients 1-day posttransplant. Conversely, mice not treated with FMT remained persistently colonized with high levels ofC. difficile, and the gut microbiota in these mice persisted at low diversity. These results suggest that full recovery of colonization resistance againstC. difficilerequires the restoration of a specific community structure.

scholarly journals Crosstalk between Gut and Brain in Alzheimer’s Disease: The Role of Gut Microbiota Modulation Strategies

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 690
Author(s):  
Umair Shabbir ◽  
Muhammad Sajid Arshad ◽  
Aysha Sameen ◽  
Deog-Hwan Oh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gut Microbiota ◽  
Dietary Habits ◽  
Inflammatory Responses ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Gut Dysbiosis ◽  
Dynamic Population

The gut microbiota (GM) represents a diverse and dynamic population of microorganisms and about 100 trillion symbiotic microbial cells that dwell in the gastrointestinal tract. Studies suggest that the GM can influence the health of the host, and several factors can modify the GM composition, such as diet, drug intake, lifestyle, and geographical locations. Gut dysbiosis can affect brain immune homeostasis through the microbiota–gut–brain axis and can play a key role in the pathogenesis of neurodegenerative diseases, including dementia and Alzheimer’s disease (AD). The relationship between gut dysbiosis and AD is still elusive, but emerging evidence suggests that it can enhance the secretion of lipopolysaccharides and amyloids that may disturb intestinal permeability and the blood–brain barrier. In addition, it can promote the hallmarks of AD, such as oxidative stress, neuroinflammation, amyloid-beta formation, insulin resistance, and ultimately the causation of neural death. Poor dietary habits and aging, along with inflammatory responses due to dysbiosis, may contribute to the pathogenesis of AD. Thus, GM modulation through diet, probiotics, or fecal microbiota transplantation could represent potential therapeutics in AD. In this review, we discuss the role of GM dysbiosis in AD and potential therapeutic strategies to modulate GM in AD.

scholarly journals Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 145
Author(s):  
Julio Plaza-Díaz ◽  
Patricio Solis-Urra ◽  
Jerónimo Aragón-Vela ◽  
Fernando Rodríguez-Rodríguez ◽  
Jorge Olivares-Arancibia ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Liver Steatosis ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
Current Treatment ◽  
Immune Defense ◽  
Alcoholic Fatty Liver ◽  
The Impact

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

scholarly journals Lupus Gut Microbiota Transplants Cause Autoimmunity and Inflammation

2021 ◽  
Author(s):  
Yiyangzi Ma ◽  
Ruru Guo ◽  
Yiduo Sun ◽  
Xin Li ◽  
Lun He ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lupus Erythematosus ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Healthy Controls ◽  
Germ Free ◽  
Autoimmune Antibodies ◽  
Expression Of Genes ◽  
Rdna Sequencing

Background: The etiology of systemic lupus erythematosus (SLE) is multifactorial. Recently, growing evidence suggests that the microbiota plays a role in SLE, yet whether gut microbiota participates in the development of SLE remains largely unknown. To investigate this issue, we carried out 16s rDNA sequencing analyses in a cohort of 18 female un-treated active SLE patients and 7 female healthy controls, and performed fecal microbiota transplantation from patients and healthy controls to germ-free mice. Results: Compared to the healthy controls, we found no significant different microbial diversity but some significantly different species in SLE patients including Turicibacter genus and other 5 species. Fecal transfer from SLE patients to germ free (GF) C57BL/6 mice caused GF mice to develop a series of lupus-like phenotyptic features, which including an increased serum autoimmune antibodies, and imbalanced cytokines, altered distribution of immune cells in mucosal and peripheral immune response, and upregulated expression of genes related to SLE in recipient mice that received SLE fecal microbiota transplantation (FMT). Moreover, the metabolism of histidine was significantly altered in GF mice treated with SLE patient feces, as compared to those which received healthy fecal transplants. Conclusions: Overall, our results describe a causal role of aberrant gut microbiota in contributing to the pathogenesis of SLE. The interplay of gut microbial and histidine metabolism may be one of the mechanisms intertwined with autoimmune activation in SLE.

scholarly journals Intestinal Microbiota: A Novel Target to Improve Anti-Tumor Treatment?

2019 ◽  
Vol 20 (18) ◽  
pp. 4584 ◽  
Author(s):  
Romain Villéger ◽  
Amélie Lopès ◽  
Guillaume Carrier ◽  
Julie Veziant ◽  
Elisabeth Billard ◽  
...  
Keyword(s):  
Side Effects ◽  
Gut Microbiota ◽  
Host Response ◽  
Fecal Microbiota Transplantation ◽  
Direct Interaction ◽  
Fecal Microbiota ◽  
Intestinal Microbiome ◽  
Wide Range ◽  
Novel Target

Recently, preclinical and clinical studies targeting several types of cancer strongly supported the key role of the gut microbiota in the modulation of host response to anti-tumoral therapies such as chemotherapy, immunotherapy, radiotherapy and even surgery. Intestinal microbiome has been shown to participate in the resistance to a wide range of anticancer treatments by direct interaction with the treatment or by indirectly stimulating host response through immunomodulation. Interestingly, these effects were described on colorectal cancer but also in other types of malignancies. In addition to their role in therapy efficacy, gut microbiota could also impact side effects induced by anticancer treatments. In the first part of this review, we summarized the role of the gut microbiome on the efficacy and side effects of various anticancer treatments and underlying mechanisms. In the second part, we described the new microbiota-targeting strategies, such as probiotics and prebiotics, antibiotics, fecal microbiota transplantation and physical activity, which could be effective adjuvant therapies developed in order to improve anticancer therapeutic efficiency.

scholarly journals The Gut Microbiota in Multiple Sclerosis: An Overview of Clinical Trials

2019 ◽  
Vol 28 (12) ◽  
pp. 1507-1527 ◽  
Author(s):  
Giovanni Schepici ◽  
Serena Silvestro ◽  
Placido Bramanti ◽  
Emanuela Mazzon
Keyword(s):  
Multiple Sclerosis ◽  
Immune System ◽  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
System A ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Review Reports

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating, and degenerative disease that affects the central nervous system. A recent study showed that interaction between the immune system and the gut microbiota plays a crucial role in the development of MS. This review reports the clinical studies carried out in recent years that aimed to evaluate the composition of the microbiota in patients with relapsing–remitting MS (RR-MS). We also report what is available in the literature regarding the effectiveness of fecal microbiota transplantation and the role of the diet in restoring the intestinal bacterial population. Studies report that patients with RR-MS have a microbiota that, compared with healthy controls, has higher amounts of Pedobacteria, Flavobacterium, Pseudomonas, Mycoplana, Acinetobacter, Eggerthella, Dorea, Blautia, Streptococcus and Akkermansia. In contrast, MS patients have a microbiota with impoverished microbial populations of Prevotella, Bacteroides, Parabacteroides, Haemophilus, Sutterella, Adlercreutzia, Coprobacillus, Lactobacillus, Clostridium, Anaerostipes and Faecalibacterium. In conclusion, the restoration of the microbial population in patients with RR-MS appears to reduce inflammatory events and the reactivation of the immune system.

scholarly journals Role of Leptin-Mediated Colonic Inflammation in Defense against Clostridium difficile Colitis

2013 ◽  
Vol 82 (1) ◽  
pp. 341-349 ◽  
Author(s):  
Rajat Madan ◽  
Xiaoti Guo ◽  
Caitlin Naylor ◽  
Erica L. Buonomo ◽  
Donald Mackay ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Murine Model ◽  
Leptin Receptor ◽  
Mucosal Immune Response ◽  
Infectious Colitis ◽  
Content Type ◽  
Bacterial Peritonitis ◽  
Stat3 Signaling ◽  
Increased Risk

ABSTRACTThe role of leptin in the mucosal immune response toClostridium difficilecolitis, a leading cause of nosocomial infection, was studied in humans and in a murine model. Previously, a mutation in the receptor for leptin (LEPR) was shown to be associated with susceptibility to infectious colitis and liver abscess due toEntamoeba histolyticaas well as to bacterial peritonitis. Here we discovered that European Americans homozygous for the sameLEPRQ223R mutation (rs1137101), known to result in decreased STAT3 signaling, were at increased risk ofC. difficileinfection (odds ratio, 3.03;P= 0.015). The mechanism of increased susceptibility was studied in a murine model. Mice lacking a functional leptin receptor (db/db) had decreased clearance ofC. difficilefrom the gut lumen and diminished inflammation. Mutation of tyrosine 1138 in the intracellular domain of LepRb that mediates signaling through the STAT3/SOCS3 pathway also resulted in decreased mucosal chemokine and cell recruitment. Collectively, these data support a protective mucosal immune function for leptin inC. difficilecolitis partially mediated by a leptin-STAT3 inflammatory pathway that is defective in theLEPRQ223R mutation. Identification of the role of leptin in protection fromC. difficileoffers the potential for host-directed therapy and demonstrates a connection between metabolism and immunity.

scholarly journals Environmental Contamination in Households of Patients with Recurrent Clostridium difficile Infection

2016 ◽  
Vol 82 (9) ◽  
pp. 2686-2692 ◽  
Author(s):  
Megan K. Shaughnessy ◽  
Aleh Bobr ◽  
Michael A. Kuskowski ◽  
Brian D. Johnston ◽  
Michael J. Sadowsky ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Hospital Environment ◽  
Molecular Characteristics ◽  
Species Identity ◽  
Fecal Samples ◽  
Content Type ◽  
Environmental Surfaces ◽  
Household Environment

ABSTRACTRecurrentClostridium difficileinfection (R-CDI) is common and difficult to treat, potentially necessitating fecal microbiota transplantation (FMT). AlthoughC. difficilespores persist in the hospital environment and cause infection, little is known about their potential presence or importance in the household environment. Households of R-CDI subjects in the peri-FMT period and of geographically matched and age-matched controls were analyzed for the presence ofC. difficile. Household environmental surfaces and fecal samples from humans and pets in the household were examined. Households of post-FMT subjects were also examined (environmental surfaces only). Participants were surveyed regarding their personal history and household cleaning habits. Species identity and molecular characteristics of presumptiveC. difficileisolates from environmental and fecal samples were determined by using the Pro kit (Remel, USA), Gram staining, PCR, toxinotyping,tcdCgene sequencing, and pulsed-field gel electrophoresis (PFGE). Environmental cultures detectedC. difficileon ≥1 surface in 8/8 (100%) peri-FMT households, versus 3/8 (38%) post-FMT households and 3/8 (38%) control households (P= 0.025). The most commonC. difficile-positive sites were the vacuum (11/27; 41%), toilet (8/30; 27%), and bathroom sink (5/29; 17%).C. difficilewas detected in 3/36 (8%) fecal samples (two R-CDI subjects and one household member). Nine (90%) of 10 households with multipleC. difficile-positive samples had a single genotype present each. In conclusion,C. difficilewas found in the household environment of R-CDI patients, but whether it was found as a cause or consequence of R-CDI is unknown. If household contamination leads to R-CDI, effective decontamination may be protective.

scholarly journals Recovery of the Gut Microbiome following Fecal Microbiota Transplantation

mBio ◽  
2014 ◽  
Vol 5 (3) ◽  
Author(s):  
Anna M. Seekatz ◽  
Johannes Aas ◽  
Charles E. Gessert ◽  
Timothy A. Rubin ◽  
Daniel M. Saman ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Antibiotic Therapy ◽  
Bacterial Infections ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Transport Systems ◽  
Colonization Resistance ◽  
Treatment Methods ◽  
Content Type ◽  
Functional Changes

ABSTRACT Clostridium difficile infection is one of the most common health care-associated infections, and up to 40% of patients suffer from recurrence of disease following standard antibiotic therapy. Recently, fecal microbiota transplantation (FMT) has been successfully used to treat recurrent C. difficile infection. It is hypothesized that FMT aids in recovery of a microbiota capable of colonization resistance to C. difficile. However, it is not fully understood how this occurs. Here we investigated changes in the fecal microbiota structure following FMT in patients with recurrent C. difficile infection, and imputed a hypothetical functional profile based on the 16S rRNA profile using a predictive metagenomic tool. Increased relative abundance of Bacteroidetes and decreased abundance of Proteobacteria were observed following FMT. The fecal microbiota of recipients following transplantation was more diverse and more similar to the donor profile than the microbiota prior to transplantation. Additionally, we observed differences in the imputed metagenomic profile. In particular, amino acid transport systems were overrepresented in samples collected prior to transplantation. These results suggest that functional changes accompany microbial structural changes following this therapy. Further identification of the specific community members and functions that promote colonization resistance may aid in the development of improved treatment methods for C. difficile infection. IMPORTANCE Within the last decade, Clostridium difficile infection has surpassed other bacterial infections to become the leading cause of nosocomial infections. Antibiotic use, which disrupts the gut microbiota and its capability in providing colonization resistance against C. difficile, is a known risk factor in C. difficile infection. In particular, recurrent C. difficile remains difficult to treat with standard antibiotic therapy. Fecal microbiota transplantation (FMT) has provided a successful treatment method for some patients with recurrent C. difficile infection, but its mechanism and long-term effects remain unknown. Our results provide insight into the structural and potential metabolic changes that occur following FMT, which may aid in the development of new treatment methods for C. difficile infection.

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