The epipharynx-kidney axis triggers glomerular vasculitis in immunoglobulin A nephropathy
Macroscopic hematuria concomitant with acute pharyngitis is a characteristic feature of immunoglobulin A nephropathy (IgAN). Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is tho...
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Veröffentlicht in: | Immunologic research 2019-10, Vol.67 (4-5), p.304-309 |
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description | Macroscopic hematuria concomitant with acute pharyngitis is a characteristic feature of immunoglobulin A nephropathy (IgAN). Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is thought to play an important role. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. As latent but significant epipharyngitis presents in most IgAN patients, it is plausible that acute pharyngitis due to airway infection may contribute as a trigger of the epipharyngeal innate immune system, which is already upregulated in the chronically inflamed environment. The aim of this review was to discuss the mechanism of epipharynx-kidney axis involvement in glomerular vasculitis responsible for the worsening of hematuria in IgAN. |
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Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is thought to play an important role. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. As latent but significant epipharyngitis presents in most IgAN patients, it is plausible that acute pharyngitis due to airway infection may contribute as a trigger of the epipharyngeal innate immune system, which is already upregulated in the chronically inflamed environment. The aim of this review was to discuss the mechanism of epipharynx-kidney axis involvement in glomerular vasculitis responsible for the worsening of hematuria in IgAN.</description><identifier>ISSN: 0257-277X</identifier><identifier>EISSN: 1559-0755</identifier><identifier>DOI: 10.1007/s12026-019-09099-3</identifier><identifier>PMID: 31745821</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Activation ; Airborne infection ; Allergology ; Biomedical and Life Sciences ; Biomedicine ; Glomerulonephritis, IGA - etiology ; Glomerulonephritis, IGA - immunology ; Glomerulonephritis, IGA - pathology ; Hematuria ; Humans ; Immune system ; Immunity, Innate ; Immunoglobulin A ; Immunoglobulins ; Immunology ; Infections ; Innate immunity ; Internal Medicine ; Interpretive Synthesis Review Article ; Kidney Glomerulus - immunology ; Kidney Glomerulus - pathology ; Kidneys ; Medicine/Public Health ; Nasopharynx ; Nephropathy ; Pharyngitis - complications ; Pharyngitis - immunology ; Pharyngitis - pathology ; Pharynx - immunology ; Pharynx - pathology ; Vasculitis</subject><ispartof>Immunologic research, 2019-10, Vol.67 (4-5), p.304-309</ispartof><rights>The Author(s) 2019</rights><rights>Immunologic Research is a copyright of Springer, (2019). All Rights Reserved. © 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is thought to play an important role. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. As latent but significant epipharyngitis presents in most IgAN patients, it is plausible that acute pharyngitis due to airway infection may contribute as a trigger of the epipharyngeal innate immune system, which is already upregulated in the chronically inflamed environment. 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Oda, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-abcd18d2f1fb2286ca073d1e31f26cc4394358bac1ef98774e311456388e5bed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Activation</topic><topic>Airborne infection</topic><topic>Allergology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Glomerulonephritis, IGA - etiology</topic><topic>Glomerulonephritis, IGA - immunology</topic><topic>Glomerulonephritis, IGA - pathology</topic><topic>Hematuria</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunity, Innate</topic><topic>Immunoglobulin A</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Infections</topic><topic>Innate immunity</topic><topic>Internal Medicine</topic><topic>Interpretive Synthesis Review Article</topic><topic>Kidney Glomerulus - immunology</topic><topic>Kidney Glomerulus - pathology</topic><topic>Kidneys</topic><topic>Medicine/Public Health</topic><topic>Nasopharynx</topic><topic>Nephropathy</topic><topic>Pharyngitis - complications</topic><topic>Pharyngitis - immunology</topic><topic>Pharyngitis - pathology</topic><topic>Pharynx - immunology</topic><topic>Pharynx - pathology</topic><topic>Vasculitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hotta, Osamu</creatorcontrib><creatorcontrib>Oda, Takashi</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Immunologic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hotta, Osamu</au><au>Oda, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The epipharynx-kidney axis triggers glomerular vasculitis in immunoglobulin A nephropathy</atitle><jtitle>Immunologic research</jtitle><stitle>Immunol Res</stitle><addtitle>Immunol Res</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>67</volume><issue>4-5</issue><spage>304</spage><epage>309</epage><pages>304-309</pages><issn>0257-277X</issn><eissn>1559-0755</eissn><abstract>Macroscopic hematuria concomitant with acute pharyngitis is a characteristic feature of immunoglobulin A nephropathy (IgAN). Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is thought to play an important role. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. As latent but significant epipharyngitis presents in most IgAN patients, it is plausible that acute pharyngitis due to airway infection may contribute as a trigger of the epipharyngeal innate immune system, which is already upregulated in the chronically inflamed environment. 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subjects | Activation Airborne infection Allergology Biomedical and Life Sciences Biomedicine Glomerulonephritis, IGA - etiology Glomerulonephritis, IGA - immunology Glomerulonephritis, IGA - pathology Hematuria Humans Immune system Immunity, Innate Immunoglobulin A Immunoglobulins Immunology Infections Innate immunity Internal Medicine Interpretive Synthesis Review Article Kidney Glomerulus - immunology Kidney Glomerulus - pathology Kidneys Medicine/Public Health Nasopharynx Nephropathy Pharyngitis - complications Pharyngitis - immunology Pharyngitis - pathology Pharynx - immunology Pharynx - pathology Vasculitis |
title | The epipharynx-kidney axis triggers glomerular vasculitis in immunoglobulin A nephropathy |
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