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Results: 21 to 29 of 29

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Toward primary prevention of asthma. Reviewing the evidence for early-life respiratory viral infections as modifiable risk factors to prevent childhood asthma.
Feldman AS, He Y, Moore ML, Hershenson MB, Hartert TV
(2015) Am J Respir Crit Care Med 191: 34-44
MeSH Terms: Antibodies, Monoclonal, Humanized, Antiviral Agents, Asthma, Child, Preschool, Diet, Environmental Exposure, Epigenesis, Genetic, Genetic Predisposition to Disease, Humans, Infant, Microbiota, Palivizumab, Primary Prevention, Respiratory Syncytial Virus Infections, Respiratory Syncytial Viruses, Respiratory Tract Infections, Rhinovirus, Risk Factors, Severity of Illness Index, Tobacco Smoke Pollution
Show Abstract · Added January 20, 2015
A first step in primary disease prevention is identifying common, modifiable risk factors that contribute to a significant proportion of disease development. Infant respiratory viral infection and childhood asthma are the most common acute and chronic diseases of childhood, respectively. Common clinical features and links between these diseases have long been recognized, with early-life respiratory syncytial virus (RSV) and rhinovirus (RV) lower respiratory tract infections (LRTIs) being strongly associated with increased asthma risk. However, there has long been debate over the role of these respiratory viruses in asthma inception. In this article, we systematically review the evidence linking early-life RSV and RV LRTIs with asthma inception and whether they could therefore be targets for primary prevention efforts.
0 Communities
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20 MeSH Terms
Maternal influences on fetal microbial colonization and immune development.
Romano-Keeler J, Weitkamp JH
(2015) Pediatr Res 77: 189-95
MeSH Terms: Female, Fetus, Humans, Immune System, Maternal-Fetal Exchange, Microbiota, Models, Immunological, Placenta, Pregnancy
Show Abstract · Added February 12, 2015
While critical for normal development, the exact timing of establishment of the intestinal microbiome is unknown. For example, although preterm labor and birth have been associated with bacterial colonization of the amniotic cavity and fetal membranes for many years, the prevailing dogma of a sterile intrauterine environment during normal term pregnancies has been challenged more recently. While found to be a key contributor of evolution in the animal kingdom, maternal transmission of commensal bacteria may also constitute a critical process during healthy pregnancies in humans with yet unclear developmental importance. Metagenomic sequencing has elucidated a rich placental microbiome in normal term pregnancies likely providing important metabolic and immune contributions to the growing fetus. Conversely, an altered microbial composition during pregnancy may produce aberrant metabolites impairing fetal brain development and life-long neurological outcomes. Here we review the current understanding of microbial colonization at the feto-maternal interface and explain how normal gut colonization drives a balanced neonatal mucosal immune system, while dysbiosis contributes to aberrant immune function early in life and beyond. We discuss how maternal genetics, diet, medications, and probiotics inform the fetal microbiome in preparation for perinatal and postnatal bacterial colonization.
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9 MeSH Terms
TLR sorting by Rab11 endosomes maintains intestinal epithelial-microbial homeostasis.
Yu S, Nie Y, Knowles B, Sakamori R, Stypulkowski E, Patel C, Das S, Douard V, Ferraris RP, Bonder EM, Goldenring JR, Ip YT, Gao N
(2014) EMBO J 33: 1882-95
MeSH Terms: Animals, Drosophila, Drosophila Proteins, Endosomes, Enterocytes, Gene Deletion, Homeostasis, Intestinal Mucosa, Mice, Microbiota, Receptors, Immunologic, Toll-Like Receptor 9, rab GTP-Binding Proteins
Show Abstract · Added March 28, 2016
Compartmentalization of Toll-like receptors (TLRs) in intestinal epithelial cells (IECs) regulates distinct immune responses to microbes; however, the specific cellular machinery that controls this mechanism has not been fully identified. Here we provide genetic evidences that the recycling endosomal compartment in enterocytes maintains a homeostatic TLR9 intracellular distribution, supporting mucosal tolerance to normal microbiota. Genetic ablation of a recycling endosome resident small GTPase, Rab11a, a gene adjacent to a Crohn's disease risk locus, in mouse IECs and in Drosophila midgut caused epithelial cell-intrinsic cytokine production, inflammatory bowel phenotype, and early mortality. Unlike wild-type controls, germ-free Rab11a-deficient mouse intestines failed to tolerate the intraluminal stimulation of microbial agonists. Thus, Rab11a endosome controls intestinal host-microbial homeostasis at least partially via sorting TLRs.
© 2014 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
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13 MeSH Terms
Incorporation of therapeutically modified bacteria into gut microbiota inhibits obesity.
Chen Z, Guo L, Zhang Y, Walzem RL, Pendergast JS, Printz RL, Morris LC, Matafonova E, Stien X, Kang L, Coulon D, McGuinness OP, Niswender KD, Davies SS
(2014) J Clin Invest 124: 3391-406
MeSH Terms: Acyltransferases, Animals, Arabidopsis Proteins, DNA-Binding Proteins, Diet, High-Fat, Digestive System, Disease Models, Animal, Eating, Escherichia coli, Female, Humans, Liver, Male, Mice, Mice, Inbred C57BL, Microbiota, Obesity, Phosphatidylethanolamines, Recombinant Proteins, Weight Gain
Show Abstract · Added July 21, 2014
Metabolic disorders, including obesity, diabetes, and cardiovascular disease, are widespread in Westernized nations. Gut microbiota composition is a contributing factor to the susceptibility of an individual to the development of these disorders; therefore, altering a person's microbiota may ameliorate disease. One potential microbiome-altering strategy is the incorporation of modified bacteria that express therapeutic factors into the gut microbiota. For example, N-acylphosphatidylethanolamines (NAPEs) are precursors to the N-acylethanolamide (NAE) family of lipids, which are synthesized in the small intestine in response to feeding and reduce food intake and obesity. Here, we demonstrated that administration of engineered NAPE-expressing E. coli Nissle 1917 bacteria in drinking water for 8 weeks reduced the levels of obesity in mice fed a high-fat diet. Mice that received modified bacteria had dramatically lower food intake, adiposity, insulin resistance, and hepatosteatosis compared with mice receiving standard water or control bacteria. The protective effects conferred by NAPE-expressing bacteria persisted for at least 4 weeks after their removal from the drinking water. Moreover, administration of NAPE-expressing bacteria to TallyHo mice, a polygenic mouse model of obesity, inhibited weight gain. Our results demonstrate that incorporation of appropriately modified bacteria into the gut microbiota has potential as an effective strategy to inhibit the development of metabolic disorders.
2 Communities
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20 MeSH Terms
Helminth co-infection in Helicobacter pylori infected INS-GAS mice attenuates gastric premalignant lesions of epithelial dysplasia and glandular atrophy and preserves colonization resistance of the stomach to lower bowel microbiota.
Whary MT, Muthupalani S, Ge Z, Feng Y, Lofgren J, Shi HN, Taylor NS, Correa P, Versalovic J, Wang TC, Fox JG
(2014) Microbes Infect 16: 345-55
MeSH Terms: Animals, Atrophy, Coinfection, Disease Models, Animal, Drug Resistance, Bacterial, Gastric Mucosa, Helicobacter Infections, Helminthiasis, Male, Mice, Mice, Transgenic, Microbiota
Show Abstract · Added May 28, 2014
Higher prevalence of helminth infections in Helicobacter pylori infected children was suggested to potentially lower the life-time risk for gastric adenocarcinoma. In rodent models, helminth co-infection does not reduce Helicobacter-induced inflammation but delays progression of pre-malignant gastric lesions. Because gastric cancer in INS-GAS mice is promoted by intestinal microflora, the impact of Heligmosomoides polygyrus co-infection on H. pylori-associated gastric lesions and microflora were evaluated. Male INS-GAS mice co-infected with H. pylori and H. polygyrus for 5 months were assessed for gastrointestinal lesions, inflammation-related mRNA expression, FoxP3(+) cells, epithelial proliferation, and gastric colonization with H. pylori and Altered Schaedler Flora. Despite similar gastric inflammation and high levels of proinflammatory mRNA, helminth co-infection increased FoxP3(+) cells in the corpus and reduced H. pylori-associated gastric atrophy (p < 0.04), dysplasia (p < 0.02) and prevented H. pylori-induced changes in the gastric flora (p < 0.05). This is the first evidence of helminth infection reducing H. pylori-induced gastric lesions while inhibiting changes in gastric flora, consistent with prior observations that gastric colonization with enteric microbiota accelerated gastric lesions in INS-GAS mice. Identifying how helminths reduce gastric premalignant lesions and impact bacterial colonization of the H. pylori infected stomach could lead to new treatment strategies to inhibit progression from chronic gastritis to cancer in humans.
Copyright © 2014 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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12 MeSH Terms
Gastrointestinal malignancy and the microbiome.
Abreu MT, Peek RM
(2014) Gastroenterology 146: 1534-1546.e3
MeSH Terms: Animals, Bacteria, Cell Transformation, Neoplastic, Disease Models, Animal, Gastrointestinal Neoplasms, Gastrointestinal Tract, Humans, Microbiota, Probiotics, Risk Factors
Show Abstract · Added March 10, 2014
Microbial species participate in the genesis of a substantial number of malignancies-in conservative estimates, at least 15% of all cancer cases are attributable to infectious agents. Little is known about the contribution of the gastrointestinal microbiome to the development of malignancies. Resident microbes can promote carcinogenesis by inducing inflammation, increasing cell proliferation, altering stem cell dynamics, and producing metabolites such as butyrate, which affect DNA integrity and immune regulation. Studies in human beings and rodent models of cancer have identified effector species and relationships among members of the microbial community in the stomach and colon that increase the risk for malignancy. Strategies to manipulate the microbiome, or the immune response to such bacteria, could be developed to prevent or treat certain gastrointestinal cancers.
Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
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10 MeSH Terms
What is the value of a food and drug administration investigational new drug application for fecal microbiota transplantation to treat Clostridium difficile Infection?
Hecht GA, Blaser MJ, Gordon J, Kaplan LM, Knight R, Laine L, Peek R, Sanders ME, Sartor B, Wu GD, Yang VW
(2014) Clin Gastroenterol Hepatol 12: 289-91
MeSH Terms: Biological Therapy, Feces, Humans, Investigational New Drug Application, Microbiota
Added March 7, 2014
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5 MeSH Terms
The capacious hologenome.
Brucker RM, Bordenstein SR
(2013) Zoology (Jena) 116: 260-1
MeSH Terms: Animals, Genome, Microbiota, Symbiosis
Show Abstract · Added October 8, 2015
Blending disciplines can be transformative in science, yet interdisciplinary mergers should not escape healthy skepticism. Indeed, the history of biology shows us that debates about the relative importance of nuclear genetics vs. microbial symbiosis in eukaryotic biology are among the most engaging. Today's technology may help resolve this century old debate as it illuminates the interwoven genomics and functions of symbionts with their host genome. Thus, we can now assert that all subdisciplines of zoology require microbiology. Although controversial to some, the evidence from studies of host-associated microbial communities indicates that metazoans are hologenomes - interconnected compositions of animal and microbes.
Published by Elsevier GmbH.
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4 MeSH Terms
Mom knows best: the universality of maternal microbial transmission.
Funkhouser LJ, Bordenstein SR
(2013) PLoS Biol 11: e1001631
MeSH Terms: Animals, Breast Feeding, Female, Humans, Infant, Newborn, Infectious Disease Transmission, Vertical, Maternal Exposure, Microbiota, Pregnancy
Show Abstract · Added October 8, 2015
The sterile womb paradigm is an enduring premise in biology that human infants are born sterile. Recent studies suggest that infants incorporate an initial microbiome before birth and receive copious supplementation of maternal microbes through birth and breastfeeding. Moreover, evidence for microbial maternal transmission is increasingly widespread across animals. This collective knowledge compels a paradigm shift—one in which maternal transmission of microbes advances from a taxonomically specialized phenomenon to a universal one in animals. It also engenders fresh views on the assembly of the microbiome, its role in animal evolution, and applications to human health and disease.
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9 MeSH Terms