Faculty Opinions recommendation of Bacterial colonization factors control specificity and stability of the gut microbiota.

Foodborne pathogens are a public health threat globally. Shiga toxin-producing Escherichia coli (STEC), particularly O26, O111, and O157 STEC, are often associated with foodborne illness in humans. To create effective preharvest interventions, it is critical to understand which factors STEC strains use to colonize the gastrointestinal tract of cattle, which serves as the reservoir for these pathogens. Several colonization factors are known, but little is understood about initial STEC colonization factors. Our objective was to identify these factors via contrasting gene expression between nonpathogenic E. coli and STEC. Colonic explants were inoculated with nonpathogenic E. coli strain MG1655 or STEC strains (O26, O111, or O157), bacterial colonization levels were determined, and RNA was isolated and sequenced. STEC strains adhered to colonic explants at numerically but not significantly higher levels compared to MG1655. After incubation with colonic explants, flagellin (fliC) was upregulated (log2 fold-change = 4.0, p < 0.0001) in O157 STEC, and collectively, Lon protease (lon) was upregulated (log2 fold-change = 3.6, p = 0.0009) in STEC strains compared to MG1655. These results demonstrate that H7 flagellum and Lon protease may play roles in early colonization and could be potential targets to reduce colonization in cattle.

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Multiple in vivo passages enhance the ability of a clinical Helicobacter pylori isolate to colonize the stomach of Mongolian gerbils and to induce gastritis

Laboratory Animals ◽

10.1258/0023677053739800 ◽

2005 ◽

Vol 39 (2) ◽

pp. 221-229 ◽

Cited By ~ 10

Author(s):

A Bleich ◽

I Köhn ◽

S Glage ◽

W Beil ◽

S Wagner ◽

...

Keyword(s):

Helicobacter Pylori ◽

Bacterial Colonization ◽

Underlying Mechanism ◽

Mongolian Gerbils ◽

Histopathological Changes ◽

Genetic Changes ◽

Colonization Ability ◽

Colonization Factors ◽

H Pylori

The Mongolian gerbil is an excellent animal model for Helicobacter pylori-induced gastritis in humans. In this study, initially low colonization rates of the H. pylori strains ATCC 43504, SS1, or HP87 inoculated into gerbils caused difficulties in establishing this model. In order to increase the colonization ability and pathogenicity, the clinical HP87 isolate was selected for adaptation to the gerbil stomach by multiple in vivo passages through gerbils. Development of gastritis was examined histologically at 4–52 weeks after infection. The proportion of gerbils which tested positive for H. pylori by culture at four weeks after inoculation gradually increased from 11.1% of gerbils inoculated with HP87 without prior in vivo passage (P0) to 100% of gerbils inoculated with HP87 with seven in vivo passages (P7). In addition, adaptation of HP87 resulted in more severe histopathological changes. Gerbils infected with adapted HP87 (P7) exhibited severe infiltration by monomorphonuclear and polymorphonuclear leukocytes in the mucosa, submucosa, and subserosa of the gastric antrum, as well as epithelial changes consisting of hyperplasia, erosion, and ulceration. Histopathological changes increased in severity from four to 52 weeks after infection. Adaptation of HP87 during its passages through gerbils could be due to genetic changes in bacterial colonization factors. Identification of these changes might be useful to understand the underlying mechanism of gastric adaptation and pathogenesis of H. pylori.

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The Bacterium Frischella perrara Causes Scab Formation in the Gut of its Honeybee Host

mBio ◽

10.1128/mbio.00193-15 ◽

2015 ◽

Vol 6 (3) ◽

Cited By ~ 49

Author(s):

Philipp Engel ◽

Kelsey D. Bartlett ◽

Nancy A. Moran

Keyword(s):

Immune Response ◽

Immune System ◽

Gut Microbiota ◽

Bacterial Colonization ◽

Bacterial Species ◽

Host Immune System ◽

Natural Ecosystems ◽

Epithelial Surface ◽

Host Interactions ◽

Key Species

ABSTRACT Honeybees harbor well-defined bacterial communities in their guts. The major members of these communities appear to benefit the host, but little is known about how they interact with the host and specifically how they interface with the host immune system. In the pylorus, a short region between the midgut and hindgut, honeybees frequently exhibit scab-like structures on the epithelial gut surface. These structures are reminiscent of a melanization response of the insect immune system. Despite the wide distribution of this phenotype in honeybee populations, its cause has remained elusive. Here, we show that the presence of a common member of the bee gut microbiota, the gammaproteobacterium Frischella perrara, correlates with the appearance of the scab phenotype. Bacterial colonization precedes scab formation, and F. perrara specifically localizes to the melanized regions of the host epithelium. Under controlled laboratory conditions, we demonstrate that exposure of microbiota-free bees to F. perrara but not to other bacteria results in scab formation. This shows that F. perrara can become established in a spatially restricted niche in the gut and triggers a morphological change of the epithelial surface, potentially due to a host immune response. As an intermittent colonizer, this bacterium holds promise for addressing questions of community invasion in a simple yet relevant model system. Moreover, our results show that gut symbionts of bees engage in differential host interactions that are likely to affect gut homeostasis. Future studies should focus on how these different gut bacteria impact honeybee health. IMPORTANCE As pollinators, honeybees are key species for agricultural and natural ecosystems. Their guts harbor simple communities composed of characteristic bacterial species. Because of these features, bees are ideal systems for studying fundamental aspects of gut microbiota-host interactions. However, little is known about how these bacteria interact with their host. Here, we show that a common member of the bee gut microbiota causes the formation of a scab-like structure on the gut epithelium of its host. This phenotype was first described in 1946, but since then it has not been much further characterized, despite being found in bee populations worldwide. The scab phenotype is reminiscent of melanization, a conserved innate immune response of insects. Our results show that high abundance of one member of the bee gut microbiota triggers this specific phenotype, suggesting that the gut microbiota composition can affect the immune status of this key pollinator species.

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Understanding Microbiome Data: A Primer for Clinicians

Digestive Diseases ◽

10.1159/000437034 ◽

2015 ◽

Vol 33 (Suppl. 1) ◽

pp. 11-16 ◽

Cited By ~ 13

Author(s):

Philippe Seksik ◽

Cécilia Landman

Keyword(s):

Gut Microbiota ◽

Bacterial Colonization ◽

Data Sets ◽

Human Gut ◽

Microbial Composition ◽

Host Determinants ◽

Host Interaction ◽

Bacterial Genes ◽

Micro Organisms ◽

Microbiome Data

The human gut contains 1014 bacteria and many other micro-organisms such as Archaea, viruses and fungi. This gut microbiota has co-evolved with host determinants through symbiotic and co-dependent relationships. Bacteria, which represent 10 times the number of human cells, form the most depicted part of this black box owing to new tools. Re-evaluating the gut microbiota showed how this entity participates in gut physiology and beyond this in human health. Studying and handling this real ‘hidden organ' remains a challenge for clinicians. In this review, we aimed to bring information about gut microbiota, its structure, its roles and the way to capture and measure it. After bacterial colonization in infant, intestinal microbial composition is unique for each individual although more than 95% can be assigned to 4 major phyla. Besides its biodiversity, the major characteristics of gut microbiota are stability over time and resilience after perturbation. In pathological situations, dysbiosis (i.e. imbalance in gut microbiota composition) is observed with a loss in overall diversity. Dysbiosis associated with inflammatory bowel disease was specified with the reduction in biodiversity, the decreased representation of different taxa in the Firmicutes phylum and an increase in Gammaproteobacteria. Beyond depicting gut microbial composition, metagenomics allows the description of the combined genomes of the microorganisms present in the gut, giving access to their potential functions. In fact, each individual overall microbial metagenome outnumbers the size of human genome by a factor of 150. Besides a functional core in which there is redundancy for mandatory functions assuring the robustness of the ecosystem, human gut contains an important diversity and high number of non-redundant bacterial genes. Clinical data, treatment and all the factors able to influence microbiome should enter integrated big data sets to put in light pathways of interplay within the supra organism composed of gut microbiome and host. A better understanding of dynamics within human gut microbiota and microbes-host interaction will allow new insight into gut pathophysiology especially regarding resilience mechanisms and dysbiosis onset and maintenance. This will lead to description of biomarkers of diseases, development of new probiotics/prebiotics and new therapies.

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Fecal microbiota transplantation brings about bacterial strain displacement in patients with inflammatory bowel diseases

10.1101/439687 ◽

2018 ◽

Cited By ~ 1

Author(s):

Manli Zou ◽

Zhuye Jie ◽

Bota Cui ◽

Honggang Wang ◽

Qiang Feng ◽

...

Keyword(s):

Gut Microbiota ◽

Fecal Microbiota Transplantation ◽

Bacterial Colonization ◽

Fecal Microbiota ◽

Classification Model ◽

Metagenomic Data ◽

Metagenomic Sequencing ◽

Fecal Samples ◽

Inflammatory Bowel

ABSTRACTFecal microbiota transplantation (FMT), which is thought to have the potential to correct dysbiosis of gut microbiota, has recently been used to treat inflammatory bowel disease (IBD). To elucidate the extent and principles of microbiota engraftment in IBD patients after FMT treatment, we conducted an interventional prospective cohort study. The cohort included two categories of patients: (1) patients with moderate to severe Crohn’s disease (CD) (Harvey-Bradshaw Index ≥ 7, n = 11, and (2) patients with ulcerative colitis (UC) (Montreal classification, S2 and S3, n = 4). All patients were treated with a single FMT (via mid-gut, from healthy donors) and follow-up visits were performed at baseline, 3 days, one week, and one month after FMT (missing time points included). At each follow-up time point, fecal samples of the participants were collected along with their clinical metadata. For comparative analysis, 10 fecal samples from 10 healthy people were included to represent the diversity level of normal gut microbiota. Additionally, the metagenomic data of 25 fecal samples from 5 individuals with metabolic syndrome who underwent autologous FMT treatment were downloaded from a previous published paper to represent natural microbiota shifts during FMT. All fecal samples underwent shotgun metagenomic sequencing.We found that 3 days after FMT, 11 out of 15 recipients were in remission (3 out of 4 UC recipients; 8 out of 11 CD recipients). Generally, bacterial colonization was observed to be lower in CD recipients than in UC recipients at both species and strain levels. Furthermore, across species, different strains displayed disease-specific displacement advantages under two-disease status. Finally, most post-FMT species (> 80%) could be properly predicted (AUC > 85%) using a random forest classification model, with the gut microbiota composition and clinical parameters of pre-FMT recipients acting as the most contributive factors for prediction accuracy.

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Caesarean section and gut microbiota in children

World Nutrition Journal ◽

10.25220/wnj.v04.s2.0002 ◽

2020 ◽

Vol 4 (1-2) ◽

pp. 8

Author(s):

Ariani Dewi Widodo ◽

Mohammad Juffrie

Keyword(s):

Gut Microbiota ◽

Intestinal Microbiota ◽

Bacterial Colonization ◽

Composition Studies ◽

Mode Of Delivery ◽

Immune Disorders ◽

Immune Development ◽

Gut Dysbiosis ◽

Colonization Patterns ◽

Regulation Changes

Over the last two decades, the C-section rate has increased worldwide. It is understood that colonization patterns of intestinal microbiota in infant delivery in C-section vary from those that were delivered vaginally. These different microbial pattern and diversity will impact and respond to immune and dysbiosis-related diseases. This article examined the effect of C-section on gut microbiota in children.Recent Findings: Newborns are influenced by various factors, including mode of delivery, feeding, nutrition, hospitalization, antibiotic and host gene. Several studies have shown that infants with C-section have lower Bifidobacterium while others have shown lower abundance of Enterobactericeae and Bacteroides in infants with C-section compared to infants born vaginally. Although the mode of delivery is only one factor that influences infant microbiota composition, studies conclude that reduced microbial exposure during the C-section is important because it can affect dysbiosis several years after birth. Good microbiota is a key source of microbial-driven immune regulation, changes in normal patterns of bacterial colonization can alter the immune development outcome and may predispose to certain immune-related disorders later in life.Summary: The composition and concentrations of intestinal microbiota between vaginally and C-section born infants are significantly different. Among C-section infants, gut microbiota is associated with lower diversity and therefore induces dysbiosis, which can affect immune development and may predispose to some immune disorders, i.e. allergies in particular. Nutritional approach with pre-, probiotics, and/or synbiotics can have a promising effect early in life in preventing gut dysbiosis.

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Microbiota in Pancreatic Diseases: A Review of the Literature

Journal of Clinical Medicine ◽

10.3390/jcm10245920 ◽

2021 ◽

Vol 10 (24) ◽

pp. 5920

Author(s):

Tommaso Schepis ◽

Sara S. De Lucia ◽

Enrico C. Nista ◽

Vittoria Manilla ◽

Giulia Pignataro ◽

...

Keyword(s):

Gut Microbiota ◽

Small Molecules ◽

Bacterial Colonization ◽

Bacterial Flora ◽

Critical Element ◽

High Morbidity ◽

Pancreatic Diseases ◽

Therapeutic Implications ◽

Health And Disease

The gut microbiota is a critical element in the balance between human health and disease. Its impairment, defined as dysbiosis, is associated with gastroenterological and systemic diseases. Pancreatic secretions are involved in the composition and changes of the gut microbiota, and the gut microbiota may colonize the pancreatic parenchyma and be associated with the occurrence of diseases. The gut microbiota and the pancreas influence each other, resulting in a “gut microbiota-pancreas axis”. Moreover, the gut microbiota may be involved in pancreatic diseases, both through direct bacterial colonization and an indirect effect of small molecules and toxins derived from dysbiosis. Pancreatic diseases such as acute pancreatitis, chronic pancreatitis, autoimmune pancreatitis, and pancreatic cancer are common gastroenterological diseases associated with high morbidity and mortality. The involvement of the microbiota in pancreatic diseases is increasingly recognized. Therefore, modifying the intestinal bacterial flora could have important therapeutic implications on these pathologies. The aim of this study is to review the literature to evaluate the alterations of the gut microbiota in pancreatic diseases, and the role of the microbiota in the treatment of these diseases.

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Zeaxanthin Drives Dynamic Changes in the Mouse Metabolome Through Gut Microbiome Shift

Current Developments in Nutrition ◽

10.1093/cdn/nzab054_025 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 1170-1170

Author(s):

Peiran Lu ◽

Siau Yen Wong ◽

Jianmin Chai ◽

Paniz Jasbi ◽

Lei Wu ◽

...

Keyword(s):

Fatty Acid ◽

Gut Microbiota ◽

Gut Microbiome ◽

Fatty Acid Biosynthesis ◽

Bacterial Colonization ◽

Antioxidant Properties ◽

Beta Carotene ◽

Acid Oxidation ◽

Funding Sources ◽

Tyrosine Metabolism

Abstract Objectives Zeaxanthin, an oxygenized carotenoid, exerts antioxidant properties in human nutrition and metabolism. Likely other carotenoids, zeaxanthin is poorly absorbed in the small intestine. The large portion of zeaxanthin reaches the colon and is not fully recovered in the colon. In this study, we aimed to investigate the association of zeaxanthin intake with the gut microbiome homeostasis and metabolomic responses in mice. Methods Six-week-old male and female C57BL/6J wild type (WT), beta-carotene oxygenase 2 (BCO2) knockout mice were fed with AIN93M chow diets supplemented with or without zeaxanthin (0.02% w/w) for 10 weeks. At the termination of the study, mice were fasted for 3 hrs prior to euthanization. Cecal contents, colon, serum, feces, and other tissues were collected for laboratory assessments.16S rRNA sequencing and LC-MS/MS were performed for gut microbiota profiling and serum and fecal metabolomics analysis, respectively. Results Significant zeaxanthin accumulation occurred in BCO2 KO, but not WT mice. Zeaxanthin accumulation was associated with the alteration of colonic gut microbiota composition, for example, zeaxanthin-increased abundance in Lachnospiraceae, Proteobacteria, and Parabacteroides, indicating enhanced short-chain production, improved intestinal integrity, and anaerobic bacterial colonization. The results of fecal and serum metabolomics revealed that zeaxanthin significantly altered tyrosine metabolism, branched-chain fatty acid oxidation, fatty acid biosynthesis, and phospholipid biosynthesis, and suppressed levels of kynurenine and trimethylamine N-oxide (TMAO). Conclusions The results suggested that zeaxanthin accumulation promotes gut microbiome homeostasis and alters the gut microbial metabolites as signals in stimulating the host-gut microbe interplay. Funding Sources USDA/NIFA 2021-67018-34023 and 2020-67017-30842.

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