Special Issue "Gut Microbiome"

Quicklinks

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (1 March 2014)

Special Issue Editors

Guest Editor
Prof. Dr. Jean E. Crabtree (Website)

Molecular Gastroenterology Section, Leeds Institute of Biomedical and Clinical Sciences, Wellcome Trust Brenner Building, St. James's University Hospital, Leeds LS9 7TF, UK
Interests: Helicobacter pylori; host-pathogen interactions in gastrointestinal tract; infection and gastrointestinal cancer; mucosal immunology
Co-Guest Editor
Prof. Dr. Lars Engstrand (Website)

Department of Microbiology, Tumor and Cell Biology for Life Laboratory, Karolinska Institute, Stockholm, Sweden
Phone: +46 70 678 0318
Interests: role of Gut microbiota in health and disease; Helicobacter pylori associated diseases; Population-based epidemiological studies of the gut system

Special Issue Information

Dear Colleagues,

Advances in metagenomics and bioinformatics are pioneering our understanding of the gut microbiota in health and disease. Phylum level differences in gut microbiota occur in many clinical conditions bringing the opportunity that manipulation of the gut microbiome may be a way to impact on multiple diseases. The gut microbiome can modify human physiology influencing nutrient extraction from dietary intake and effect gut mucosal immune responses contributing to both the maturation of the gut immune system as well as autoimmune diseases. The Human Microbiome Project has identified the normal gut microbiome in individuals in developed countries. There is little data on the normal human gut microbiome in developing countries and the impact of global dietary variations.  Exciting recent data indicate that the gut microbiome can contribute to both malnutrition and obesity and that exposure to antibiotics early in life can lead to increased adiposity. Also, antibiotic overuse will kill beneficial bacteria. Diet impacts on the composition of the gut microbiome opening the opportunity for therapeutic dietary manipulation of gut microbiota. We look forward to your contributions and to a valuable edition that will promote further developments in this exciting field.

Thank you for your collaboration.

Prof. Dr. Jean E. Crabtree
Prof. Dr. Lars Engstrand
Guest Editors

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 600 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Published Papers (14 papers)

View options order results:
result details:
Displaying articles 1-14
Export citation of selected articles as:

Research

Jump to: Review, Other

Open AccessArticle Pyrosequencing Reveals the Predominance of Pseudomonadaceae in Gut Microbiome of a Gall Midge
Pathogens 2014, 3(2), 459-472; doi:10.3390/pathogens3020459
Received: 1 April 2014 / Revised: 13 May 2014 / Accepted: 3 June 2014 / Published: 11 June 2014
Cited by 4 | PDF Full-text (670 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Gut microbes are known to play various roles in insects such as digestion of inaccessible nutrients, synthesis of deficient amino acids, and interaction with ecological environments, including host plants. Here, we analyzed the gut microbiome in Hessian fly, a serious pest of [...] Read more.
Gut microbes are known to play various roles in insects such as digestion of inaccessible nutrients, synthesis of deficient amino acids, and interaction with ecological environments, including host plants. Here, we analyzed the gut microbiome in Hessian fly, a serious pest of wheat. A total of 3,654 high quality sequences of the V3 hypervariable region of the 16S rRNA gene were obtained through 454-pyrosequencing. From these sequences, 311 operational taxonomic units (OTUs) were obtained at the >97% similarity cutoff. In the gut of 1st instar, otu01, a member of Pseudomonas, was predominant, representing 90.2% of total sequences. otu13, an unidentified genus in the Pseudomonadaceae family, represented 1.9% of total sequences. The remaining OTUs were each less than 1%. In the gut of the 2nd instar, otu01 and otu13 decreased to 85.5% and 1.5%, respectively. otu04, a member of Buttiauxella, represented 9.7% of total sequences. The remaining OTUs were each less than 1%. In the gut of the 3rd instar, otu01 and otu13 further decreased to 29.0% and 0%, respectively. otu06, otu08, and otu16, also three members of the Pseudomonadaceae family were 13.2%, 8.6%, and 2.3%, respectively. In addition, otu04 and otu14, two members of the Enterobacteriaceae family, were 4.7% and 2.5%; otu18 and otu20, two members of the Xanthomonadaceae family, were 1.3% and 1.2%, respectively; otu12, a member of Achromobacter, was 4.2%; otu19, a member of Undibacterium, was 1.4%; and otu9, otu10, and otu15, members of various families, were 6.1%, 6.3%, and 1.9%, respectively. The investigation into dynamics of Pseudomonas, the most abundant genera, revealed that its population level was at peak in freshly hatched or 1 day larvae as well as in later developmental stages, thus suggesting a prominent role for this bacterium in Hessian fly development and in its interaction with host plants. This study is the first comprehensive survey on bacteria associated with the gut of a gall midge, and provides a foundation for future studies to elucidate the roles of gut microbes in Hessian fly virulence and biology. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessArticle Secretory IgA is Concentrated in the Outer Layer of Colonic Mucus along with Gut Bacteria
Pathogens 2014, 3(2), 390-403; doi:10.3390/pathogens3020390
Received: 29 December 2013 / Revised: 22 April 2014 / Accepted: 24 April 2014 / Published: 29 April 2014
Cited by 13 | PDF Full-text (6307 KB) | HTML Full-text | XML Full-text
Abstract
Antibodies of the secretory IgA (SIgA) class comprise the first line of antigen-specific immune defense, preventing access of commensal and pathogenic microorganisms and their secreted products into the body proper. In addition to preventing infection, SIgA shapes the composition of the gut [...] Read more.
Antibodies of the secretory IgA (SIgA) class comprise the first line of antigen-specific immune defense, preventing access of commensal and pathogenic microorganisms and their secreted products into the body proper. In addition to preventing infection, SIgA shapes the composition of the gut microbiome. SIgA is transported across intestinal epithelial cells into gut secretions by the polymeric immunoglobulin receptor (pIgR). The epithelial surface is protected by a thick network of mucus, which is composed of a dense, sterile inner layer and a loose outer layer that is colonized by commensal bacteria. Immunofluorescence microscopy of mouse and human colon tissues demonstrated that the SIgA co-localizes with gut bacteria in the outer mucus layer. Using mice genetically deficient for pIgR and/or mucin-2 (Muc2, the major glycoprotein of intestinal mucus), we found that Muc2 but not SIgA was necessary for excluding gut bacteria from the inner mucus layer in the colon. Our findings support a model whereby SIgA is anchored in the outer layer of colonic mucus through combined interactions with mucin proteins and gut bacteria, thus providing immune protection against pathogens while maintaining a mutually beneficial relationship with commensals. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessArticle Morphine Attenuates Apically-Directed Cytokine Secretion from Intestinal Epithelial Cells in Response to Enteric Pathogens
Pathogens 2014, 3(2), 249-257; doi:10.3390/pathogens3020249
Received: 26 November 2013 / Revised: 17 March 2014 / Accepted: 20 March 2014 / Published: 2 April 2014
Cited by 2 | PDF Full-text (256 KB) | HTML Full-text | XML Full-text
Abstract
Epithelial cells represent the first line of host immune defense at mucosal surfaces. Although opioids appear to increase host susceptibility to infection, no studies have examined opioid effects on epithelial immune functions. We tested the hypothesis that morphine alters vectorial cytokine secretion [...] Read more.
Epithelial cells represent the first line of host immune defense at mucosal surfaces. Although opioids appear to increase host susceptibility to infection, no studies have examined opioid effects on epithelial immune functions. We tested the hypothesis that morphine alters vectorial cytokine secretion from intestinal epithelial cell (IPEC-J2) monolayers in response to enteropathogens. Both entero-adherent Escherichia coli O157:H7 and entero-invasive Salmonella enterica serovar Typhimurium increased apically-directed IL-6 secretion and bi-directional IL-8 secretion from epithelial monolayers, but only IL-6 secretion evoked by E. coli was reduced by morphine acting through a naloxone-sensitive mechanism. Moreover, the respective type 4 and 5 Toll-like receptor agonists, lipopolysaccharide and flagellin, increased IL-8 secretion from monolayers, which was also attenuated by morphine pretreatment. These results suggest that morphine decreases cytokine secretion and potentially phagocyte migration and activation directed towards the mucosal surface; actions that could increase host susceptibility to some enteric infections. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessArticle Evaluation of Automated Ribosomal Intergenic Spacer Analysis for Bacterial Fingerprinting of Rumen Microbiome Compared to Pyrosequencing Technology
Pathogens 2014, 3(1), 109-120; doi:10.3390/pathogens3010109
Received: 24 November 2013 / Revised: 18 December 2013 / Accepted: 9 January 2014 / Published: 22 January 2014
Cited by 2 | PDF Full-text (321 KB) | HTML Full-text | XML Full-text
Abstract
The mammalian gut houses a complex microbial community which is believed to play a significant role in host physiology. In recent years, several microbial community analysis methods have been implemented to study the whole gut microbial environment, in contrast to classical microbiological [...] Read more.
The mammalian gut houses a complex microbial community which is believed to play a significant role in host physiology. In recent years, several microbial community analysis methods have been implemented to study the whole gut microbial environment, in contrast to classical microbiological methods focusing on bacteria which can be cultivated. One of these is automated ribosomal intergenic spacer analysis (ARISA), an inexpensive and popular way of analyzing bacterial diversity and community fingerprinting in ecological samples. ARISA uses the natural variability in length of the DNA fragment found between the 16S and 23S genes in different bacterial lineages to infer diversity. This method is now being supplanted by affordable next-generation sequencing technologies that can also simultaneously annotate operational taxonomic units for taxonomic identification. We compared ARISA and pyrosequencing of samples from the rumen microbiome of cows, previously sampled at different stages of development and varying in microbial complexity using several ecological parameters. We revealed close agreement between ARISA and pyrosequencing outputs, especially in their ability to discriminate samples from different ecological niches. In contrast, the ARISA method seemed to underestimate sample richness. The good performance of the relatively inexpensive ARISA makes it relevant for straightforward use in bacterial fingerprinting analysis as well as for quick cross-validation of pyrosequencing data. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessArticle Metabolism of Cholesterol and Bile Acids by the Gut Microbiota
Pathogens 2014, 3(1), 14-24; doi:10.3390/pathogens3010014
Received: 21 November 2013 / Revised: 18 December 2013 / Accepted: 19 December 2013 / Published: 30 December 2013
Cited by 22 | PDF Full-text (514 KB) | HTML Full-text | XML Full-text
Abstract
The human gastro-intestinal tract hosts a complex and diverse microbial community, whose collective genetic coding capacity vastly exceeds that of the human genome. As a consequence, the gut microbiota produces metabolites from a large range of molecules that host’s enzymes are not [...] Read more.
The human gastro-intestinal tract hosts a complex and diverse microbial community, whose collective genetic coding capacity vastly exceeds that of the human genome. As a consequence, the gut microbiota produces metabolites from a large range of molecules that host’s enzymes are not able to convert. Among these molecules, two main classes of steroids, cholesterol and bile acids, denote two different examples of bacterial metabolism in the gut. Therefore, cholesterol is mainly converted into coprostanol, a non absorbable sterol which is excreted in the feces. Moreover, this conversion occurs in a part of the human population only. Conversely, the primary bile acids (cholic and chenodeoxycholic acids) are converted to over twenty different secondary bile acid metabolites by the gut microbiota. The main bile salt conversions, which appear in the gut of the whole human population, include deconjugation, oxidation and epimerization of hydroxyl groups at C3, C7 and C12, 7-dehydroxylation, esterification and desulfatation. If the metabolisms of cholesterol and bile acids by the gut microbiota are known for decades, their consequences on human health and disease are poorly understood and only start to be considered. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessArticle Healthcare Workers’ Hand Microbiome May Mediate Carriage of Hospital Pathogens
Pathogens 2014, 3(1), 1-13; doi:10.3390/pathogens3010001
Received: 11 October 2013 / Revised: 26 November 2013 / Accepted: 19 December 2013 / Published: 27 December 2013
Cited by 3 | PDF Full-text (687 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
One function of skin microbiota is to resist colonization and infection by external microorganisms. We sought to detect whether the structure of the hand microbiota of 34 healthcare workers (HCW) in a surgical intensive care unit mediates or modifies the relationship between [...] Read more.
One function of skin microbiota is to resist colonization and infection by external microorganisms. We sought to detect whether the structure of the hand microbiota of 34 healthcare workers (HCW) in a surgical intensive care unit mediates or modifies the relationship between demographic and behavioral factors and potential pathogen carriage on hands after accounting for pathogen exposure. We used a taxonomic screen (16S rRNA) to characterize the bacterial community, and qPCR to detect presence of Staphylococcus aureus, Enterococcus spp., methicillin-resistant Staphylococcus aureus (MRSA), and Candida albicans on their dominant hands. Hands were sampled weekly over a 3-week period. Age, hand hygiene, and work shift were significantly associated with potential pathogen carriage and the associations were pathogen dependent. Additionally, the overall hand microbiota structure was associated with the carriage of potential pathogens. Hand microbiota community structure may act as a biomarker of pathogen carriage, and modifying that structure may potentially limit pathogen carriage among HCW. Full article
(This article belongs to the Special Issue Gut Microbiome)
Figures

Open AccessArticle Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo
Pathogens 2013, 2(4), 571-590; doi:10.3390/pathogens2040571
Received: 13 August 2013 / Revised: 16 September 2013 / Accepted: 26 September 2013 / Published: 14 October 2013
Cited by 1 | PDF Full-text (1655 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Helicobacter pylori transactivates the Epidermal Growth Factor Receptor (EGFR) and predisposes to gastric cancer development in humans and animal models. To examine the importance of EGFR signalling to gastric pathology, this study investigated whether treatment of Mongolian gerbils with a selective EGFR [...] Read more.
Helicobacter pylori transactivates the Epidermal Growth Factor Receptor (EGFR) and predisposes to gastric cancer development in humans and animal models. To examine the importance of EGFR signalling to gastric pathology, this study investigated whether treatment of Mongolian gerbils with a selective EGFR tyrosine kinase inhibitor, EKB-569, altered gastric pathology in chronic H. pylori infection. Gerbils were infected with H. pylori and six weeks later received either EKB-569-supplemented, or control diet, for 32 weeks prior to sacrifice. EKB-569-treated H. pylori-infected gerbils had no difference in H. pylori colonisation or inflammation scores compared to infected animals on control diet, but showed significantly less corpus atrophy, mucous metaplasia and submucosal glandular herniations along with markedly reduced antral and corpus epithelial proliferation to apoptosis ratios. EKB-569-treated infected gerbils had significantly decreased abundance of Cox-2, Adam17 and Egfr gastric transcripts relative to infected animals on control diet. EGFR inhibition by EKB-569 therefore reduced the severity of pre-neoplastic gastric pathology in chronically H. pylori-infected gerbils. EKB-569 increased gastric epithelial apoptosis in H. pylori-infected gerbils which counteracted some of the consequences of increased gastric epithelial cell proliferation. Similar chemopreventative strategies may be useful in humans who are at high risk of developing H.pylori-induced gastric adenocarcinoma. Full article
(This article belongs to the Special Issue Gut Microbiome)

Review

Jump to: Research, Other

Open AccessReview Early Development of the Gut Microbiota and Immune Health
Pathogens 2014, 3(3), 769-790; doi:10.3390/pathogens3030769
Received: 18 December 2013 / Revised: 29 August 2014 / Accepted: 19 September 2014 / Published: 24 September 2014
Cited by 8 | PDF Full-text (241 KB) | HTML Full-text | XML Full-text
Abstract
In recent years, the increase in human microbiome research brought about by the rapidly evolving “omic” technologies has established that the balance among the microbial groups present in the human gut, and their multipronged interactions with the host, are crucial for health. [...] Read more.
In recent years, the increase in human microbiome research brought about by the rapidly evolving “omic” technologies has established that the balance among the microbial groups present in the human gut, and their multipronged interactions with the host, are crucial for health. On the other hand, epidemiological and experimental support has also grown for the ‘early programming hypothesis’, according to which factors that act in utero and early in life program the risks for adverse health outcomes later on. The microbiota of the gut develops during infancy, in close interaction with immune development, and with extensive variability across individuals. It follows that the specific process of gut colonization and the microbe-host interactions established in an individual during this period have the potential to represent main determinants of life-long propensity to immune disease. Although much remains to be learnt on the progression of events by which the gut microbiota becomes established and initiates its intimate relationships with the host, and on the long-term repercussions of this process, recent works have advanced significatively in this direction. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessReview Perturbation of the Human Microbiome as a Contributor to Inflammatory Bowel Disease
Pathogens 2014, 3(3), 510-527; doi:10.3390/pathogens3030510
Received: 26 March 2014 / Revised: 6 June 2014 / Accepted: 9 June 2014 / Published: 30 June 2014
Cited by 9 | PDF Full-text (223 KB) | HTML Full-text | XML Full-text
Abstract
The human microbiome consist of the composite genome of native flora that have evolved with humanity over millennia and which contains 150-fold more genes than the human genome. A “healthy” microbiome plays an important role in the maintenance of health and prevention [...] Read more.
The human microbiome consist of the composite genome of native flora that have evolved with humanity over millennia and which contains 150-fold more genes than the human genome. A “healthy” microbiome plays an important role in the maintenance of health and prevention of illness, inclusive of autoimmune disease such as inflammatory bowel disease (IBD). IBD is a prevalent spectrum of disorders, most notably defined by Crohn’s disease (CD) and ulcerative colitis (UC), which are associated with considerable suffering, morbidity, and cost. This review presents an outline of the loss of a normal microbiome as an etiology of immune dysregulation and IBD pathogenesis initiation. We, furthermore, summarize the knowledge on the role of a healthy microbiome in terms of its diversity and important functional elements and, lastly, conclude with some of the therapeutic interventions and modalities that are now being explored as potential applications of microbiome-host interactions. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessReview Integrons in the Intestinal Microbiota as Reservoirs for Transmission of Antibiotic Resistance Genes
Pathogens 2014, 3(2), 238-248; doi:10.3390/pathogens3020238
Received: 24 December 2013 / Revised: 13 March 2014 / Accepted: 13 March 2014 / Published: 31 March 2014
Cited by 5 | PDF Full-text (265 KB) | HTML Full-text | XML Full-text
Abstract
The human intestinal microbiota plays a major beneficial role in immune development and resistance to pathogens. The use of antibiotics, however, can cause the spread of antibiotic resistance genes within the resident intestinal microbiota. Important vectors for this are integrons. This review [...] Read more.
The human intestinal microbiota plays a major beneficial role in immune development and resistance to pathogens. The use of antibiotics, however, can cause the spread of antibiotic resistance genes within the resident intestinal microbiota. Important vectors for this are integrons. This review therefore focuses on the integrons in non-pathogenic bacteria as a potential source for the development and persistence of multidrug resistance. Integrons are a group of genetic elements which are assembly platforms that can capture specific gene cassettes and express them. Integrons in pathogenic bacteria have been extensively investigated, while integrons in the intestinal microbiota have not yet gained much attention. Knowledge of the integrons residing in the microbiota, however, can potentially aid in controlling the spread of antibiotic resistance genes to pathogens. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessReview Heat Shock Proteins: Intestinal Gatekeepers that Are Influenced by Dietary Components and the Gut Microbiota
Pathogens 2014, 3(1), 187-210; doi:10.3390/pathogens3010187
Received: 21 December 2013 / Revised: 6 February 2014 / Accepted: 18 February 2014 / Published: 28 February 2014
Cited by 4 | PDF Full-text (686 KB) | HTML Full-text | XML Full-text
Abstract
Trillions of microorganisms that inhabit the intestinal tract form a diverse and intricate ecosystem with a deeply embedded symbiotic relationship with their hosts. As more detailed information on gut microbiota complexity and functional diversity accumulates, we are learning more about how diet-microbiota [...] Read more.
Trillions of microorganisms that inhabit the intestinal tract form a diverse and intricate ecosystem with a deeply embedded symbiotic relationship with their hosts. As more detailed information on gut microbiota complexity and functional diversity accumulates, we are learning more about how diet-microbiota interactions can influence the immune system within and outside the gut and host health in general. Heat shock proteins are a set of highly conserved proteins that are present in all types of cells, from microbes to mammals. These proteins carry out crucial intracellular housekeeping functions and unexpected extracellular immuno-regulatory features in order to maintain the mucosal barrier integrity and gut homeostasis. It is becoming evident that the enteric microbiota is one of the major determinants of heat shock protein production in intestinal epithelial cells. This review will focus on the interactions between diet, gut microbiota and their role for regulating heat shock protein production and, furthermore, how these interactions influence the immune system and the integrity of the mucosal barrier. Full article
(This article belongs to the Special Issue Gut Microbiome)
Figures

Open AccessReview The Natural Antimicrobial Enzyme Lysozyme is Up-Regulated in Gastrointestinal Inflammatory Conditions
Pathogens 2014, 3(1), 73-92; doi:10.3390/pathogens3010073
Received: 24 October 2013 / Revised: 3 January 2014 / Accepted: 7 January 2014 / Published: 16 January 2014
Cited by 8 | PDF Full-text (6792 KB) | HTML Full-text | XML Full-text
Abstract
The cells that line the mucosa of the human gastrointestinal tract (GI, that is, oral cavity, oesophagus, stomach, small intestine, large intestine, and rectum) are constantly challenged by adverse micro-environmental factors, such as different pH, enzymes, and bacterial flora. With exception of [...] Read more.
The cells that line the mucosa of the human gastrointestinal tract (GI, that is, oral cavity, oesophagus, stomach, small intestine, large intestine, and rectum) are constantly challenged by adverse micro-environmental factors, such as different pH, enzymes, and bacterial flora. With exception of the oral cavity, these microenvironments also contain remnant cocktails of secreted enzymes and bacteria from upper organs along the tract. The density of the GI bacteria varies, from 103/mL near the gastric outlet, to 1010/mL at the ileocecal valve, to 1011 to 1012/mL in the colon. The total microbial population (ca. 1014) exceeds the total number of cells in the tract. It is, therefore, remarkable that despite the prima facie inauspicious mixture of harmful secretions and bacteria, the normal GI mucosa retains a healthy state of cell renewal. To counteract the hostile microenvironment, the GI epithelia react by speeding cell exfoliation (the GI mucosa has a turnover time of two to three days), by increasing peristalsis, by eliminating bacteria through secretion of plasma cell-immunoglobulins and by increasing production of natural antibacterial compounds, such as defensin-5 and lysozyme. Only recently, lysozyme was found up-regulated in Barrett’s oesophagitis, chronic gastritis, gluten-induced atrophic duodenitis (coeliac disease), collagenous colitis, lymphocytic colitis, and Crohn’s colitis. This up-regulation is a response directed to the special types of bacteria recently detected in these diseases. The aim of lysozyme up-regulation is to protect individual mucosal segments to chronic inflammation. The molecular mechanisms connected to the crosstalk between the intraluminal bacterial flora and the production of lysozyme released by the GI mucosae, are discussed. Bacterial resistance continues to exhaust our supply of commercial antibiotics. The potential use of lysozyme to treat infectious diseases is receiving much attention. Full article
(This article belongs to the Special Issue Gut Microbiome)
Open AccessReview The Metabolic and Ecological Interactions of Oxalate-Degrading Bacteria in the Mammalian Gut
Pathogens 2013, 2(4), 636-652; doi:10.3390/pathogens2040636
Received: 10 October 2013 / Revised: 26 November 2013 / Accepted: 27 November 2013 / Published: 6 December 2013
Cited by 7 | PDF Full-text (257 KB) | HTML Full-text | XML Full-text
Abstract
Oxalate-degrading bacteria comprise a functional group of microorganisms, commonly found in the gastrointestinal tract of mammals. Oxalate is a plant secondary compound (PSC) widely produced by all major taxa of plants and as a terminal metabolite by the mammalian liver. As a [...] Read more.
Oxalate-degrading bacteria comprise a functional group of microorganisms, commonly found in the gastrointestinal tract of mammals. Oxalate is a plant secondary compound (PSC) widely produced by all major taxa of plants and as a terminal metabolite by the mammalian liver. As a toxin, oxalate can have a significant impact on the health of mammals, including humans. Mammals do not have the enzymes required to metabolize oxalate and rely on their gut microbiota for this function. Thus, significant metabolic interactions between the mammalian host and a complex gut microbiota maintain the balance of oxalate in the body. Over a dozen species of gut bacteria are now known to degrade oxalate. This review focuses on the host-microbe and microbe-microbe interactions that regulate the degradation of oxalate by the gut microbiota. We discuss the pathways of oxalate throughout the body and the mammalian gut as a series of differentiated ecosystems that facilitate oxalate degradation. We also explore the mechanisms and functions of microbial oxalate degradation along with the implications for the ecological and evolutionary interactions within the microbiota and for mammalian hosts. Throughout, we consider questions that remain, as well as recent technological advances that can be employed to answer them. Full article
(This article belongs to the Special Issue Gut Microbiome)

Other

Jump to: Research, Review

Open AccessCommentary The Gastrointestinal Microbiome and Musculoskeletal Diseases: A Beneficial Role for Probiotics and Prebiotics
Pathogens 2013, 2(4), 606-626; doi:10.3390/pathogens2040606
Received: 29 September 2013 / Revised: 4 November 2013 / Accepted: 7 November 2013 / Published: 14 November 2013
Cited by 4 | PDF Full-text (478 KB) | HTML Full-text | XML Full-text
Abstract
Natural medicines are an attractive option for patients diagnosed with common and debilitating musculoskeletal diseases such as Osteoarthritis (OA) or Rheumatoid Arthritis (RA). The high rate of self-medication with natural products is due to (1) lack of an available cure and (2) [...] Read more.
Natural medicines are an attractive option for patients diagnosed with common and debilitating musculoskeletal diseases such as Osteoarthritis (OA) or Rheumatoid Arthritis (RA). The high rate of self-medication with natural products is due to (1) lack of an available cure and (2) serious adverse events associated with chronic use of pharmaceutical medications in particular non-steroidal anti-inflammatory drugs (NSAIDs) and high dose paracetamol. Pharmaceuticals to treat pain may disrupt gastrointestinal (GIT) barrier integrity inducing GIT inflammation and a state of and hyper-permeability. Probiotics and prebiotics may comprise plausible therapeutic options that can restore GIT barrier functionality and down regulate pro-inflammatory mediators by modulating the activity of, for example, Clostridia species known to induce pro-inflammatory mediators. The effect may comprise the rescue of gut barrier physiological function. A postulated requirement has been the abrogation of free radical formation by numerous natural antioxidant molecules in order to improve musculoskeletal health outcomes, this notion in our view, is in error. The production of reactive oxygen species (ROS) in different anatomical environments including the GIT by the epithelial lining and the commensal microbe cohort is a regulated process, leading to the formation of hydrogen peroxide which is now well recognized as an essential second messenger required for normal cellular homeostasis and physiological function. The GIT commensal profile that tolerates the host does so by regulating pro-inflammatory and anti-inflammatory GIT mucosal actions through the activity of ROS signaling thereby controlling the activity of pathogenic bacterial species. Full article
(This article belongs to the Special Issue Gut Microbiome)

Journal Contact

MDPI AG
Pathogens Editorial Office
St. Alban-Anlage 66, 4052 Basel, Switzerland
pathogens@mdpi.com
Tel. +41 61 683 77 34
Fax: +41 61 302 89 18
Editorial Board
Contact Details Submit to Pathogens
Back to Top