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Antibiotics and the gut microbiota
Sheetal R. Modi, … , James J. Collins, David A. Relman
Sheetal R. Modi, … , James J. Collins, David A. Relman
Published October 1, 2014
Citation Information: J Clin Invest. 2014;124(10):4212-4218. https://doi.org/10.1172/JCI72333.
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Antibiotics and the gut microbiota

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Abstract

Antibiotics have been a cornerstone of innovation in the fields of public health, agriculture, and medicine. However, recent studies have shed new light on the collateral damage they impart on the indigenous host-associated communities. These drugs have been found to alter the taxonomic, genomic, and functional capacity of the human gut microbiota, with effects that are rapid and sometimes persistent. Broad-spectrum antibiotics reduce bacterial diversity while expanding and collapsing membership of specific indigenous taxa. Furthermore, antibiotic treatment selects for resistant bacteria, increases opportunities for horizontal gene transfer, and enables intrusion of pathogenic organisms through depletion of occupied natural niches, with profound implications for the emergence of resistance. Because these pervasive alterations can be viewed as an uncoupling of mutualistic host-microbe relationships, it is valuable to reconsider antimicrobial therapies in the context of an ecological framework. Understanding the biology of competitive exclusion, interspecies protection, and gene flow of adaptive functions in the gut environment may inform the design of new strategies that treat infections while preserving the ecology of our beneficial constituents.

Authors

Sheetal R. Modi, James J. Collins, David A. Relman

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Bacteroides fragilis subverts mucosal biology: from symbiont to colon carcinogenesis
Cynthia L. Sears, … , Abby L. Geis, Franck Housseau
Cynthia L. Sears, … , Abby L. Geis, Franck Housseau
Published August 8, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72334.
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Bacteroides fragilis subverts mucosal biology: from symbiont to colon carcinogenesis

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Abstract

The human body comprises fewer host cells than bacterial cells, most of which are obligate anaerobes residing in the gut. The symbiont Bacteroides fragilis constitutes a relatively small proportion (up to 1%–2%) of cultured fecal bacteria, but colonizes most humans. There are 2 classes of B. fragilis distinguished by their ability to secrete a zinc-dependent metalloprotease toxin, B. fragilis toxin (BFT). Strains that do not secrete BFT are nontoxigenic B. fragilis (NTBF), and those that do are called enterotoxigenic B. fragilis (ETBF). ETBF can induce clinical pathology, including inflammatory diarrhea, although asymptomatic colonization may be common. Intestinal inflammation is mediated by BFT, as yet the only known virulence factor of ETBF. Recent experimental evidence demonstrating that ETBF-driven colitis promotes colon tumorigenesis has generated interest in the potential contribution of ETBF to human colon carcinogenesis. Critical questions about the epidemiology of chronic, subclinical human colonization with ETBF and its impact on the biology of the colon need to be addressed.

Authors

Cynthia L. Sears, Abby L. Geis, Franck Housseau

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Host-microbial interactions in the metabolism of therapeutic and diet-derived xenobiotics
Rachel N. Carmody, Peter J. Turnbaugh
Rachel N. Carmody, Peter J. Turnbaugh
Published August 8, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72335.
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Host-microbial interactions in the metabolism of therapeutic and diet-derived xenobiotics

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Abstract

Our associated microbial communities play a critical role in human health and predisposition to disease, but the degree to which they also shape therapeutic interventions is not well understood. Here, we integrate results from classic and current studies of the direct and indirect impacts of the gut microbiome on the metabolism of therapeutic drugs and diet-derived bioactive compounds. We pay particular attention to microbial influences on host responses to xenobiotics, adding to the growing consensus that treatment outcomes reflect our intimate partnership with the microbial world, and providing an initial framework from which to consider a more comprehensive view of pharmacology and nutrition.

Authors

Rachel N. Carmody, Peter J. Turnbaugh

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The microbial basis of inflammatory bowel diseases
Sushila R. Dalal, Eugene B. Chang
Sushila R. Dalal, Eugene B. Chang
Published August 1, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72330.
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The microbial basis of inflammatory bowel diseases

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Abstract

Inflammatory bowel diseases (IBD) are chronic, progressive diseases characterized by aberrant immune responses to environmental and gut microbial triggers in genetically susceptible hosts. Clinical, genetic, and experimental data support the role of gut microbes in causing and sustaining these diseases. Our understanding of IBD has changed dramatically as the result of advances in cultivation-independent approaches and computational platforms for the analysis of large data sets. However, investigations relevant to clinical observations and the natural history of the diseases will be essential for the development of microbial, genetic, and biological metrics that may be used to individualize assessment of risk and improve clinical outcomes in IBD.

Authors

Sushila R. Dalal, Eugene B. Chang

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Clostridium difficile and the microbiota
Anna M. Seekatz, Vincent B. Young
Anna M. Seekatz, Vincent B. Young
Published July 18, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72336.
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Clostridium difficile and the microbiota

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Abstract

Clostridium difficile infection (CDI) is the leading health care–associated illness. Both human and animal models have demonstrated the importance of the gut microbiota’s capability of providing colonization resistance against C. difficile. Risk factors for disease development include antibiotic use, which disrupts the gut microbiota, leading to the loss of colonization resistance and subsequent CDI. Identification of the specific microbes capable of restoring this function remains elusive. Future studies directed at how microbial communities influence the metabolic environment may help elucidate the role of the microbiota in disease development. These findings will improve current biotherapeutics for patients with CDI, particularly those with recurrent disease.

Authors

Anna M. Seekatz, Vincent B. Young

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Deciphering the tête-à-tête between the microbiota and the immune system
Neeraj K. Surana, Dennis L. Kasper
Neeraj K. Surana, Dennis L. Kasper
Published July 18, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72332.
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Deciphering the tête-à-tête between the microbiota and the immune system

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Abstract

The past decade has witnessed an explosion in studies — both clinical and basic science — examining the relationship between the microbiota and human health, and it is now clear that the effects of commensal organisms are much broader than previously believed. Among the microbiota’s major contributions to host physiology is regulation of the development and maintenance of the immune system. There are now a handful of examples of intestinal commensal bacteria with defined immunomodulatory properties, but our mechanistic understanding of how microbes influence the immune system is still in its infancy. Nevertheless, several themes have emerged that provide a framework for appreciating microbe-induced immunoregulation. In this Review, we discuss the current state of knowledge regarding the role of the intestinal microbiota in immunologic development, highlighting mechanistic principles that can guide future work.

Authors

Neeraj K. Surana, Dennis L. Kasper

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Mechanisms of vancomycin resistance in Staphylococcus aureus
Susana Gardete, Alexander Tomasz
Susana Gardete, Alexander Tomasz
Published July 1, 2014
Citation Information: J Clin Invest. 2014;124(7):2836-2840. https://doi.org/10.1172/JCI68834.
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Mechanisms of vancomycin resistance in Staphylococcus aureus

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Abstract

Vancomycin is a glycopeptide antibiotic used for the treatment of Gram-positive bacterial infections. Traditionally, it has been used as a drug of last resort; however, clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) strains with decreased susceptibility to vancomycin (vancomycin intermediate-resistant S. aureus [VISA]) and more recently with high-level vancomycin resistance (vancomycin-resistant S. aureus [VRSA]) have been described in the clinical literature. The rare VRSA strains carry transposon Tn1546, acquired from vancomycin-resistant Enterococcus faecalis, which is known to alter cell wall structure and metabolism, but the resistance mechanisms in VISA isolates are less well defined. Herein, we review selected mechanistic aspects of resistance in VISA and summarize biochemical studies on cell wall synthesis in a VRSA strain. Finally, we recapitulate a model that integrates common mechanistic features of VRSA and VISA strains and is consistent with the mode of action of vancomycin.

Authors

Susana Gardete, Alexander Tomasz

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Uterine NK cells: active regulators at the maternal-fetal interface
Ashley Moffett, Francesco Colucci
Ashley Moffett, Francesco Colucci
Published May 1, 2014
Citation Information: J Clin Invest. 2014;124(5):1872-1879. https://doi.org/10.1172/JCI68107.
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Uterine NK cells: active regulators at the maternal-fetal interface

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Abstract

Pregnancy presents an immunological conundrum because two genetically different individuals coexist. The maternal lymphocytes at the uterine maternal-fetal interface that can recognize mismatched placental cells are T cells and abundant distinctive uterine NK (uNK) cells. Multiple mechanisms exist that avoid damaging T cell responses to the fetus, whereas activation of uNK cells is probably physiological. Indeed, genetic epidemiological data suggest that the variability of NK cell receptors and their MHC ligands define pregnancy success; however, exactly how uNK cells function in normal and pathological pregnancy is still unclear, and any therapies aimed at suppressing NK cells must be viewed with caution. Allorecognition of fetal placental cells by uNK cells is emerging as the key maternal-fetal immune mechanism that regulates placentation.

Authors

Ashley Moffett, Francesco Colucci

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Emerging therapies for food allergy
Corinne A. Keet, Robert A. Wood
Corinne A. Keet, Robert A. Wood
Published May 1, 2014
Citation Information: J Clin Invest. 2014;124(5):1880-1886. https://doi.org/10.1172/JCI72061.
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Emerging therapies for food allergy

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Abstract

Food allergy is a common condition for which there are currently no approved treatments except avoidance of the allergenic food and treatment of accidental reactions. There are several potential treatments that are under active investigation in animal and human studies, but it is not yet clear what the best approach may be. Here, we review approaches that are currently in clinical trials, including oral, sublingual, and epicutaneous immunotherapy, immunotherapy combined with anti-IgE, and Chinese herbal medicine as well as approaches that are in preclinical or early clinical investigation, including modified protein immunotherapy, adjuvants, DNA vaccines, and helminth administration. We discuss the importance of fully exploring the risks and benefits of any treatment before it is taken to general clinical practice and the need for clarity about the goals of treatment.

Authors

Corinne A. Keet, Robert A. Wood

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Harnessing FOXP3+ regulatory T cells for transplantation tolerance
Herman Waldmann, … , Duncan Howie, Stephen Cobbold
Herman Waldmann, … , Duncan Howie, Stephen Cobbold
Published April 1, 2014
Citation Information: J Clin Invest. 2014;124(4):1439-1445. https://doi.org/10.1172/JCI67226.
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Harnessing FOXP3+ regulatory T cells for transplantation tolerance

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Abstract

Early demonstrations that mice could be tolerized to transplanted tissues with short courses of immunosuppressive therapy and that with regard to tolerance to self, CD4+FOXP3+ regulatory T cells (Tregs) appeared to play a critical role, have catalyzed strategies to harness FOXP3-dependent processes to control rejection in human transplantation. This review seeks to examine the scientific underpinning for this new approach to finesse immunosuppression.

Authors

Herman Waldmann, Robert Hilbrands, Duncan Howie, Stephen Cobbold

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