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Search Results: 1 - 10 of 318268 matches for " Martin J Blaser "
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Control of intestinal bacterial proliferation in regulation of lifespan in Caenorhabditis elegans
Cynthia Portal-Celhay, Ellen R Bradley, Martin J Blaser
BMC Microbiology , 2012, DOI: 10.1186/1471-2180-12-49
Abstract: We show that as adult worms age, several C. elegans genotypes show diminished capacity to control intestinal bacterial accumulation. We provide evidence that intestinal bacterial load, regulated by gut immunity, is an important causative factor of lifespan determination; the effects are specified by bacterial strain, worm genotype, and biologic age, all acting in concert.In total, these studies focus attention on the worm intestine as a locus that influences longevity in the presence of an accumulating bacterial population. Further studies defining the interplay between bacterial species and host immunity in C. elegans may provide insights into the general mechanisms of aging and age-related diseases.Aging results in alterations in multiple physiologic processes [1]. The identification and measurement of markers of aging to predict lifespan is a major element of aging research [2]. Because the nematode Caenorhabditis elegans is genetically tractable, it has become a major model organism for studies of aging [3-5], neurobiology [6,7], cell cycle [8], chemosensation [9], microbial pathogenesis, and host defenses [10-12]. C. elegans is particularly suited to studies of aging, since numerous single-gene mutations have been identified that affect C. elegans lifespan (AGE genes) [3,4,13,14].C. elegans are free-living nematodes residing in the soil, where they feed on bacteria. In the laboratory, C. elegans are normally cultured on a lawn of Escherichia coli (strain OP50), on which they feed ad libitum. Although E. coli OP50 is considered non-pathogenic for the worms, as C. elegans age, the pharynx and the intestine are frequently distended and packed with bacterial cells [15]. This striking phenotype of bacterial proliferation exhibited by old animals, has been hypothesized to contribute to worm aging and demise [15,16]. C. elegans grown on bacteria that were unable to proliferate, including those killed by UV treatment or by antibiotics, had much lower rates of intestina
Correction: Early-Life Family Structure and Microbially Induced Cancer Risk
Martin J Blaser,Abraham Nomura,James Lee,Grant N Stemmerman,Guillermo I Perez-Perez
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040100
Abstract:
Early-Life Family Structure and Microbially Induced Cancer Risk
Martin J Blaser ,Abraham Nomura,James Lee,Grant N Stemmerman,Guillermo I Perez-Perez
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040007
Abstract: Background Cancer may follow exposure to an environmental agent after many decades. The bacterium Helicobacter pylori, known to be acquired early in life, increases risk for gastric adenocarcinoma, but other factors are also important. In this study, we considered whether early-life family structure affects the risk of later developing gastric cancer among H. pylori+ men. Methods and Findings We examined a long-term cohort of Japanese-American men followed for 28 y, and performed a nested case-control study among those carrying H. pylori or the subset carrying the most virulent cagA+ H. pylori strains to address whether family structure predicted cancer development. We found that among the men who were H. pylori+ and/or cagA+ (it is possible to be cagA+ and H. pylori? if the H. pylori test is falsely negative), belonging to a large sibship or higher birth order was associated with a significantly increased risk of developing gastric adenocarcinoma late in life. For those with cagA+ strains, the risk of developing gastric cancer was more than twice as high (odds ratio 2.2; 95% confidence interval 1.2–4.0) among those in a sibship of seven or more individuals than in a sibship of between one and three persons. Conclusions These results provide evidence that early-life social environment plays a significant role in risk of microbially induced malignancies expressing five to eight decades later, and these findings lead to new models to explain these interactions.
Substantial Alterations of the Cutaneous Bacterial Biota in Psoriatic Lesions
Zhan Gao, Chi-hong Tseng, Bruce E. Strober, Zhiheng Pei, Martin J. Blaser
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002719
Abstract: For psoriasis, an idiopathic inflammatory disorder of the skin, the microbial biota has not been defined using cultivation-independent methods. We used broad-range 16S rDNA PCR for archaea and bacteria to examine the microbiota of normal and psoriatic skin. From 6 patients, 19 cutaneous samples (13 from diseased skin and 6 from normal skin) were obtained. Extracted DNA was subjected to the broad range PCR, and 1,925 cloned products were compared with 2,038 products previously reported from healthy persons. Using 98% sequence identity as a species boundary, 1,841 (95.6%) clones were similar to known bacterial 16S rDNA, representing 6 phyla, 86 genera, or 189 species-level operational taxonomic unit (SLOTU); 84 (4.4%) clones with <98% identity probably represented novel species. The most abundant and diverse phylum populating the psoriatic lesions was Firmicutes (46.2%), significantly (P<0.001) overrepresented, compared to the samples from uninvolved skin of the patients (39.0%) and healthy persons (24.4%). In contrast, Actinobacteria, the most prevalent and diverse phylum in normal skin samples from both healthy persons (47.6%) and the patients (47.8%), was significantly (P<0.01) underrepresented in the psoriatic lesion samples (37.3%). Representation of Propionibacterium species were lower in the psoriatic lesions (2.9±5.5%) than from normal persons (21.1±18.2%; P<0.001), whereas normal skin from the psoriatic patients showed intermediate levels (12.3±21.6%). We conclude that psoriasis is associated with substantial alteration in the composition and representation of the cutaneous bacterial biota.
Evidence of host-virus co-evolution in tetranucleotide usage patterns of bacteriophages and eukaryotic viruses
David T Pride, Trudy M Wassenaar, Chandrabali Ghose, Martin J Blaser
BMC Genomics , 2006, DOI: 10.1186/1471-2164-7-8
Abstract: We found that bacteriophages have unique TUD patterns, representing genomic signatures that are relatively conserved among those with similar host range. Analysis of TUD-based phylogeny indicates that host influences are important in bacteriophage evolution, and phylogenies containing both phages and their hosts support their co-evolution. TUD-based phylogeny of eukaryotic viruses indicates that they cluster largely based on nucleic acid type and genome size. Similarities between eukaryotic virus phylogenies based on TUD and gene content substantiate the TUD methodology.Differences between phenotypic and TUD analysis may provide clues to virus ancestry not previously inferred. As such, TUD analysis provides a complementary approach to morphology-based systems in analysis of virus evolution.Eukaryotic viruses and bacteriophages exist in numerous forms and are capable of infecting disparate hosts. The taxonomy of viruses is based upon morphological features, including capsid and tail structures, specific type of genetic material, and mechanism of replication and assembly [1,2]. Genetic comparison across virus species has been complicated by generally different rates of gene evolution, thus, their overall classification rests on phenotypic and morphologic characteristics [3]. Horizontal gene transfer has been substantial in virus evolution [4-7], complicating reproduction of ontogeny based on the current presence of particular loci. Analysis of phylogenies based on phenotypic systems is limited by convergent evolution, in which like characteristics are evolved by unrelated organisms to suit particular niches or evolutionary requirements [8]. Taxonomy of bacteriophages also has been based on morphologic characteristics [9,10]. Tail morphology forms the basis for bacteriophage classification into 3 separate families: Myoviridae (contractile tails), Podoviridae (short tail stubs), and Siphoviridae (long tails) [1]. Studies examining phage tail assemblies [11] have not asc
Diversity of 23S rRNA Genes within Individual Prokaryotic Genomes
Anna Pei, Carlos W. Nossa, Pooja Chokshi, Martin J. Blaser, Liying Yang, David M. Rosmarin, Zhiheng Pei
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005437
Abstract: Background The concept of ribosomal constraints on rRNA genes is deduced primarily based on the comparison of consensus rRNA sequences between closely related species, but recent advances in whole-genome sequencing allow evaluation of this concept within organisms with multiple rRNA operons. Methodology/Principal Findings Using the 23S rRNA gene as an example, we analyzed the diversity among individual rRNA genes within a genome. Of 184 prokaryotic species containing multiple 23S rRNA genes, diversity was observed in 113 (61.4%) genomes (mean 0.40%, range 0.01%–4.04%). Significant (1.17%–4.04%) intragenomic variation was found in 8 species. In 5 of the 8 species, the diversity in the primary structure had only minimal effect on the secondary structure (stem versus loop transition). In the remaining 3 species, the diversity significantly altered local secondary structure, but the alteration appears minimized through complex rearrangement. Intervening sequences (IVS), ranging between 9 and 1471 nt in size, were found in 7 species. IVS in Deinococcus radiodurans and Nostoc sp. encode transposases. T. tengcongensis was the only species in which intragenomic diversity >3% was observed among 4 paralogous 23S rRNA genes. Conclusions/Significance These findings indicate tight ribosomal constraints on individual 23S rRNA genes within a genome. Although classification using primary 23S rRNA sequences could be erroneous, significant diversity among paralogous 23S rRNA genes was observed only once in the 184 species analyzed, indicating little overall impact on the mainstream of 23S rRNA gene-based prokaryotic taxonomy.
Natural Transformation of Helicobacter pylori Involves the Integration of Short DNA Fragments Interrupted by Gaps of Variable Size
Edward A. Lin ,Xue-Song Zhang,Steven M. Levine,Steven R. Gill,Daniel Falush,Martin J. Blaser
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000337
Abstract: Helicobacter pylori are gram-negative bacteria notable for their high level of genetic diversity and plasticity, features that may play a key role in the organism's ability to colonize the human stomach. Homeologous natural transformation, a key contributor to genomic diversification, has been well-described for H. pylori. To examine the mechanisms involved, we performed restriction analysis and sequencing of recombination products to characterize the length, fragmentation, and position of DNA imported via natural transformation. Our analysis revealed DNA imports of small size (1,300 bp, 95% confidence limits 950–1850 bp) with instances of substantial asymmetry in relation to selectable antibiotic-resistance markers. We also observed clustering of imported DNA endpoints, suggesting a possible role for restriction endonucleases in limiting recombination length. Additionally, we observed gaps in integrated DNA and found evidence suggesting that these gaps are the result of two or more separate strand invasions. Taken together, these observations support a system of highly efficient short-fragment recombination involving multiple recombination events within a single locus.
Sparse and Compositionally Robust Inference of Microbial Ecological Networks
Zachary D. Kurtz?,Christian L. Müller?,Emily R. Miraldi?,Dan R. Littman?,Martin J. Blaser,Richard A. Bonneau
PLOS Computational Biology , 2015, DOI: 10.1371/journal.pcbi.1004226
Abstract: 16S ribosomal RNA (rRNA) gene and other environmental sequencing techniques provide snapshots of microbial communities, revealing phylogeny and the abundances of microbial populations across diverse ecosystems. While changes in microbial community structure are demonstrably associated with certain environmental conditions (from metabolic and immunological health in mammals to ecological stability in soils and oceans), identification of underlying mechanisms requires new statistical tools, as these datasets present several technical challenges. First, the abundances of microbial operational taxonomic units (OTUs) from amplicon-based datasets are compositional. Counts are normalized to the total number of counts in the sample. Thus, microbial abundances are not independent, and traditional statistical metrics (e.g., correlation) for the detection of OTU-OTU relationships can lead to spurious results. Secondly, microbial sequencing-based studies typically measure hundreds of OTUs on only tens to hundreds of samples; thus, inference of OTU-OTU association networks is severely under-powered, and additional information (or assumptions) are required for accurate inference. Here, we present SPIEC-EASI (SParse InversE Covariance Estimation for Ecological Association Inference), a statistical method for the inference of microbial ecological networks from amplicon sequencing datasets that addresses both of these issues. SPIEC-EASI combines data transformations developed for compositional data analysis with a graphical model inference framework that assumes the underlying ecological association network is sparse. To reconstruct the network, SPIEC-EASI relies on algorithms for sparse neighborhood and inverse covariance selection. To provide a synthetic benchmark in the absence of an experimentally validated gold-standard network, SPIEC-EASI is accompanied by a set of computational tools to generate OTU count data from a set of diverse underlying network topologies. SPIEC-EASI outperforms state-of-the-art methods to recover edges and network properties on synthetic data under a variety of scenarios. SPIEC-EASI also reproducibly predicts previously unknown microbial associations using data from the American Gut project.
Sparse and compositionally robust inference of microbial ecological networks
Zachary D. Kurtz,Christian L. Mueller,Emily R. Miraldi,Dan R. Littman,Martin J. Blaser,Richard A. Bonneau
Quantitative Biology , 2014,
Abstract: 16S-ribosomal sequencing and other metagonomic techniques provide snapshots of microbial communities, revealing phylogeny and the abundances of microbial populations across diverse ecosystems. While changes in microbial community structure are demonstrably associated with certain environmental conditions, identification of underlying mechanisms requires new statistical tools, as these datasets present several technical challenges. First, the abundances of microbial operational taxonomic units (OTUs) from 16S datasets are compositional, and thus, microbial abundances are not independent. Secondly, microbial sequencing-based studies typically measure hundreds of OTUs on only tens to hundreds of samples; thus, inference of OTU-OTU interaction networks is severely under-powered, and additional assumptions are required for accurate inference. Here, we present SPIEC-EASI (SParse InversE Covariance Estimation for Ecological Association Inference), a statistical method for the inference of microbial ecological interactions from metagenomic datasets that addresses both of these issues. SPIEC-EASI combines data transformations developed for compositional data analysis with a graphical model inference framework that assumes the underlying ecological interaction network is sparse. To reconstruct the interaction network, SPIEC-EASI relies on algorithms for sparse neighborhood and inverse covariance selection. Because no large-scale microbial ecological networks have been experimentally validated, SPIEC-EASI comprises computational tools to generate realistic OTU count data from a set of diverse underlying network topologies. SPIEC-EASI outperforms state-of-the-art methods in terms of edge recovery and network properties on realistic synthetic data under a variety of scenarios. SPIEC-EASI also reproducibly predicts previously unknown microbial interactions using data from the American Gut project.
Helicobacter pylori Seropositivity and Risk of Lung Cancer
Jill Koshiol, Roberto Flores, Tram K. Lam, Philip R. Taylor, Stephanie J. Weinstein, Jarmo Virtamo, Demetrius Albanes, Guillermo Perez-Perez, Neil E. Caporaso, Martin J. Blaser
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032106
Abstract: Lung cancer is the leading cause of cancer mortality worldwide. Helicobacter pylori (H. pylori) is a risk factor for distal stomach cancer, and a few small studies have suggested that H. pylori may be a potential risk factor for lung cancer. To test this hypothesis, we conducted a study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 controls nested within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. Controls were one-to-one matched by age and date of baseline serum draw. Using enzyme-linked immunosorbent assays to detect immunoglobulin G antibodies against H. pylori whole-cell and cytotoxin-associated gene (CagA) antigens, we calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between H. pylori seropositivity and lung cancer risk using conditional logistic regression. H. pylori seropositivity was detected in 79.7% of cases and 78.5% of controls. After adjusting for pack-years and cigarettes smoked per day, H. pylori seropositivity was not associated with either adenocarcinoma (OR: 1.1, 95% CI: 0.75–1.6) or squamous cell carcinoma (OR: 1.1, 95% CI: 0.77–1.7). Results were similar for CagA-negative and CagA-positive H. pylori seropositivity. Despite earlier small studies suggesting that H. pylori may contribute to lung carcinogenesis, H. pylori seropositivity does not appear to be associated with lung cancer.
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