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      Fibrin is a critical regulator of neutrophil effector function at the oral mucosal barrier

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          Metagenomic biomarker discovery and explanation

          This study describes and validates a new method for metagenomic biomarker discovery by way of class comparison, tests of biological consistency and effect size estimation. This addresses the challenge of finding organisms, genes, or pathways that consistently explain the differences between two or more microbial communities, which is a central problem to the study of metagenomics. We extensively validate our method on several microbiomes and a convenient online interface for the method is provided at http://huttenhower.sph.harvard.edu/lefse/.
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            Neutrophil recruitment and function in health and inflammation.

            Neutrophils have traditionally been thought of as simple foot soldiers of the innate immune system with a restricted set of pro-inflammatory functions. More recently, it has become apparent that neutrophils are, in fact, complex cells capable of a vast array of specialized functions. Although neutrophils are undoubtedly major effectors of acute inflammation, several lines of evidence indicate that they also contribute to chronic inflammatory conditions and adaptive immune responses. Here, we discuss the key features of the life of a neutrophil, from its release from bone marrow to its death. We discuss the possible existence of different neutrophil subsets and their putative anti-inflammatory roles. We focus on how neutrophils are recruited to infected or injured tissues and describe differences in neutrophil recruitment between different tissues. Finally, we explain the mechanisms that are used by neutrophils to promote protective or pathological immune responses at different sites.
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              Periodontitis: from microbial immune subversion to systemic inflammation.

              Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities that can mediate inflammatory pathology at local as well as distant sites. This Review discusses the mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites.
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                Author and article information

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                Journal
                Science
                Science
                American Association for the Advancement of Science (AAAS)
                0036-8075
                1095-9203
                December 24 2021
                December 24 2021
                : 374
                : 6575
                Affiliations
                [1 ]Proteases and Tissue Remodeling Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
                [2 ]Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
                [3 ]NIDCR Imaging Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
                [4 ]Department of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.
                [5 ]Department of Pathology and Oral Medicine, Faculty of Dentistry, University of Chile, Santiago, Chile.
                [6 ]Michael Smith Laboratories and Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, BC, Canada.
                [7 ]Division of Oral and Craniofacial Health Sciences, Adams School of Dentistry, University of North Carolina, Chapel Hill, NC, USA.
                [8 ]Molecular Biology of Bones and Teeth Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
                [9 ]NIDCR Genomics and Computational Biology Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
                [10 ]Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
                [11 ]WM Keck Center for Transgene Research, University of Notre Dame, Notre Dame, IN, USA.
                [12 ]Blood Research Institute, Versiti, Milwaukee, WI, USA.
                [13 ]Departments of Surgery, Biochemistry, Biomedical Engineering, and Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA.
                [14 ]Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA.
                [15 ]Division of Pediatric and Public Health, Adams School of Dentistry, University of North Carolina, Chapel Hill, NC, USA.
                [16 ]Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
                Article
                10.1126/science.abl5450
                34941394
                8e8292eb-763b-43a2-be12-e2d85f0d7fac
                © 2021
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