7 results on '"Aa, Amoyo"'
Search Results
2. Microbiome Influences Prenatal and Adult Microglia in a Sex-Specific Manner.
- Author
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Thion MS, Low D, Silvin A, Chen J, Grisel P, Schulte-Schrepping J, Blecher R, Ulas T, Squarzoni P, Hoeffel G, Coulpier F, Siopi E, David FS, Scholz C, Shihui F, Lum J, Amoyo AA, Larbi A, Poidinger M, Buttgereit A, Lledo PM, Greter M, Chan JKY, Amit I, Beyer M, Schultze JL, Schlitzer A, Pettersson S, Ginhoux F, and Garel S
- Subjects
- Animals, Brain cytology, Brain embryology, Brain metabolism, Cell Differentiation, Cells, Cultured, Chromatin Assembly and Disassembly, Female, Humans, Male, Mice, Mice, Inbred C57BL, Microglia metabolism, Pregnancy, Sex Factors, Germ-Free Life, Microbiota, Microglia cytology, Prenatal Exposure Delayed Effects microbiology, Transcriptome
- Abstract
Microglia are embryonically seeded macrophages that contribute to brain development, homeostasis, and pathologies. It is thus essential to decipher how microglial properties are temporally regulated by intrinsic and extrinsic factors, such as sexual identity and the microbiome. Here, we found that microglia undergo differentiation phases, discernable by transcriptomic signatures and chromatin accessibility landscapes, which can diverge in adult males and females. Remarkably, the absence of microbiome in germ-free mice had a time and sexually dimorphic impact both prenatally and postnatally: microglia were more profoundly perturbed in male embryos and female adults. Antibiotic treatment of adult mice triggered sexually biased microglial responses revealing both acute and long-term effects of microbiota depletion. Finally, human fetal microglia exhibited significant overlap with the murine transcriptomic signature. Our study shows that microglia respond to environmental challenges in a sex- and time-dependent manner from prenatal stages, with major implications for our understanding of microglial contributions to health and disease., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
3. Quantum changes in Helicobacter pylori gene expression accompany host-adaptation.
- Author
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Chua EG, Wise MJ, Khosravi Y, Seow SW, Amoyo AA, Pettersson S, Peters F, Tay CY, Perkins TT, Loke MF, Marshall BJ, and Vadivelu J
- Subjects
- Animals, Genome, Bacterial, Helicobacter pylori physiology, Lipopolysaccharides biosynthesis, Mice, Mutation, Recombination, Genetic, Adaptation, Physiological, Gene Expression, Helicobacter pylori genetics, Host-Pathogen Interactions, Quantum Theory
- Abstract
Helicobacter pylori is a highly successful gastric pathogen. High genomic plasticity allows its adaptation to changing host environments. Complete genomes of H. pylori clinical isolate UM032 and its mice-adapted serial derivatives 298 and 299, generated using both PacBio RS and Illumina MiSeq sequencing technologies, were compared to identify novel elements responsible for host-adaptation. The acquisition of a jhp0562-like allele, which encodes for a galactosyltransferase, was identified in the mice-adapted strains. Our analysis implies a new β-1,4-galactosyltransferase role for this enzyme, essential for Ley antigen expression. Intragenomic recombination between babA and babB genes was also observed. Further, we expanded on the list of candidate genes whose expression patterns have been mediated by upstream homopolymer-length alterations to facilitate host adaption. Importantly, greater than four-fold reduction of mRNA levels was demonstrated in five genes. Among the down-regulated genes, three encode for outer membrane proteins, including BabA, BabB and HopD. As expected, a substantial reduction in BabA protein abundance was detected in mice-adapted strains 298 and 299 via Western analysis. Our results suggest that the expression of Ley antigen and reduced outer membrane protein expressions may facilitate H. pylori colonisation of mouse gastric epithelium., (© The Author 2016. Published by Oxford University Press on behalf of Kazusa DNA Research Institute.)
- Published
- 2017
- Full Text
- View/download PDF
4. Helicobacter pylori and gut microbiota modulate energy homeostasis prior to inducing histopathological changes in mice.
- Author
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Khosravi Y, Bunte RM, Chiow KH, Tan TL, Wong WY, Poh QH, Doli Sentosa IM, Seow SW, Amoyo AA, Pettersson S, Loke MF, and Vadivelu J
- Subjects
- Animals, Gastric Mucosa microbiology, Ghrelin metabolism, Helicobacter Infections microbiology, Humans, Insulin metabolism, Leptin metabolism, Mice, Peptide YY metabolism, Energy Metabolism, Gastric Mucosa metabolism, Gastrointestinal Microbiome, Helicobacter pylori metabolism
- Abstract
Helicobacter pylori have been shown to influence physiological regulation of metabolic hormones involved in food intake, energy expenditure and body mass. It has been proposed that inducing H. pylori-induced gastric atrophy damages hormone-producing endocrine cells localized in gastric mucosal layers and therefore alter their concentrations. In a recent study, we provided additional proof in mice under controlled conditions that H. pylori and gut microbiota indeed affects circulating metabolic gut hormones and energy homeostasis. In this addendum, we presented data from follow-up investigations that demonstrated H. pylori and gut microbiota-associated modulation of metabolic gut hormones was independent and precedes H. pylori-induced histopathological changes in the gut of H. pylori-infected mice. Thus, H. pylori-associated argumentation of energy homeostasis is not caused by injury to endocrine cells in gastric mucosa.
- Published
- 2016
- Full Text
- View/download PDF
5. Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice.
- Author
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Khosravi Y, Seow SW, Amoyo AA, Chiow KH, Tan TL, Wong WY, Poh QH, Sentosa IM, Bunte RM, Pettersson S, Loke MF, and Vadivelu J
- Subjects
- Animals, Body Mass Index, Chemokine CCL11 metabolism, Ghrelin metabolism, Helicobacter Infections microbiology, Helicobacter pylori physiology, Host-Pathogen Interactions, Humans, Insulin metabolism, Intestine, Large microbiology, Leptin metabolism, Mice, Inbred C57BL, Microbiota physiology, Models, Biological, Peptide YY metabolism, Specific Pathogen-Free Organisms, Weight Gain physiology, Energy Metabolism, Helicobacter Infections metabolism, Intestine, Large metabolism, Peptide Hormones metabolism
- Abstract
Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.
- Published
- 2015
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6. Comparing the genomes of Helicobacter pylori clinical strain UM032 and Mice-adapted derivatives.
- Author
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Khosravi Y, Rehvathy V, Wee WY, Wang S, Baybayan P, Singh S, Ashby M, Ong J, Amoyo AA, Seow SW, Choo SW, Perkins T, Chua EG, Tay A, Marshall BJ, Loke MF, Goh KL, Pettersson S, and Vadivelu J
- Abstract
Background: Helicobacter pylori is a Gram-negative bacterium that persistently infects the human stomach inducing chronic inflammation. The exact mechanisms of pathogenesis are still not completely understood. Although not a natural host for H. pylori, mouse infection models play an important role in establishing the immunology and pathogenicity of H. pylori. In this study, for the first time, the genome sequences of clinical H. pylori strain UM032 and mice-adapted derivatives, 298 and 299, were sequenced using the PacBio Single Molecule, Real-Time (SMRT) technology., Result: Here, we described the single contig which was achieved for UM032 (1,599,441 bp), 298 (1,604,216 bp) and 299 (1,601,149 bp). Preliminary analysis suggested that methylation of H. pylori genome through its restriction modification system may be determinative of its host specificity and adaptation., Conclusion: Availability of these genomic sequences will aid in enhancing our current level of understanding the host specificity of H. pylori.
- Published
- 2013
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7. Lipocalin 2 performs contrasting, location-dependent roles in APCmin tumor initiation and progression.
- Author
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Reilly PT, Teo WL, Low MJ, Amoyo-Brion AA, Dominguez-Brauer C, Elia AJ, Berger T, Greicius G, Pettersson S, and Mak TW
- Subjects
- Acute-Phase Proteins deficiency, Acute-Phase Proteins genetics, Animals, Apoptosis physiology, Disease Progression, Female, Genes, APC, Intestinal Neoplasms genetics, Lipocalin-2, Lipocalins genetics, Male, Mice, Mice, Inbred C57BL, Oncogene Proteins deficiency, Oncogene Proteins genetics, Acute-Phase Proteins biosynthesis, Intestinal Neoplasms metabolism, Intestinal Neoplasms pathology, Lipocalins biosynthesis, Oncogene Proteins biosynthesis
- Abstract
Evidence that lipocalin 2 (LCN2) is oncogenic has grown in recent years and comes from both animal models and expression analysis from a variety of human cancers. In the intestine, LCN2 is overexpressed in colitis patients and its overexpression is a negative prognostic indicator in colorectal cancer. Functionally, LCN2 has a number of different activities that may contribute to its oncogenic potential, including increasing matrix metalloproteinase activity, control of iron availability and stimulating inflammation. In this report, we examined APCmin intestinal tumorigenesis in an LCN2-deficient background. We found that the loss of LCN2 increased tumor multiplicity specifically in the duodenum, suggesting a potential tumor-suppressive activity. Concurrently, however, LCN2 increased the average small intestinal tumor size particularly in the distal small intestine. We found that this increase was correlated to tumor iron(II) content, suggesting that an iron-scavenging role is important for LCN2 oncogenic activity in the intestine.
- Published
- 2013
- Full Text
- View/download PDF
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