Dipeptidyl Peptidase 4 Distribution in the Human Respiratory Tract
Identifieur interne : 000A46 ( Pmc/Curation ); précédent : 000A45; suivant : 000A47Dipeptidyl Peptidase 4 Distribution in the Human Respiratory Tract
Auteurs : David K. Meyerholz [États-Unis] ; Allyn M. Lambertz [États-Unis] ; Paul B. Mccray [États-Unis]Source :
- The American Journal of Pathology [ 0002-9440 ] ; 2015.
Abstract
Dipeptidyl peptidase 4 (DPP4, CD26), a type II transmembrane ectopeptidase, is the receptor for the Middle Eastern respiratory syndrome coronavirus (MERS-CoV). MERS emerged in 2012 and has a high mortality associated with severe lung disease. A lack of autopsy studies from MERS fatalities has hindered understanding of MERS-CoV pathogenesis. We investigated the spatial and cellular localization of DPP4 to evaluate an association MERS clinical disease. DPP4 was rarely detected in the surface epithelium from nasal cavity to conducting airways with a slightly increased incidence in distal airways. DPP4 was also found in a subset of mononuclear leukocytes and in serous cells of submucosal glands. In the parenchyma, DPP4 was found principally in type I and II cells and alveolar macrophages and was also detected in vascular endothelium (eg, lymphatics) and pleural mesothelia. Patients with chronic lung disease, such as chronic obstructive pulmonary disease and cystic fibrosis, exhibited increased DPP4 immunostaining in alveolar epithelia (type I and II cells) and alveolar macrophages with similar trends in reactive mesothelia. This finding suggests that preexisting pulmonary disease could increase MERS-CoV receptor abundance and predispose individuals to MERS morbidity and mortality, which is consistent with current clinical observations. We speculate that the preferential spatial localization of DPP4 in alveolar regions may explain why MERS is characterized by lower respiratory tract disease.
Url:
DOI: 10.1016/j.ajpath.2015.09.014
PubMed: 26597880
PubMed Central: 4715219
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<front><div type="abstract" xml:lang="en"><p>Dipeptidyl peptidase 4 (DPP4, CD26), a type II transmembrane ectopeptidase, is the receptor for the Middle Eastern respiratory syndrome coronavirus (MERS-CoV). MERS emerged in 2012 and has a high mortality associated with severe lung disease. A lack of autopsy studies from MERS fatalities has hindered understanding of MERS-CoV pathogenesis. We investigated the spatial and cellular localization of DPP4 to evaluate an association MERS clinical disease. DPP4 was rarely detected in the surface epithelium from nasal cavity to conducting airways with a slightly increased incidence in distal airways. DPP4 was also found in a subset of mononuclear leukocytes and in serous cells of submucosal glands. In the parenchyma, DPP4 was found principally in type I and II cells and alveolar macrophages and was also detected in vascular endothelium (eg, lymphatics) and pleural mesothelia. Patients with chronic lung disease, such as chronic obstructive pulmonary disease and cystic fibrosis, exhibited increased DPP4 immunostaining in alveolar epithelia (type I and II cells) and alveolar macrophages with similar trends in reactive mesothelia. This finding suggests that preexisting pulmonary disease could increase MERS-CoV receptor abundance and predispose individuals to MERS morbidity and mortality, which is consistent with current clinical observations. We speculate that the preferential spatial localization of DPP4 in alveolar regions may explain why MERS is characterized by lower respiratory tract disease.</p>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id>
<journal-id journal-id-type="iso-abbrev">Am. J. Pathol</journal-id>
<journal-title-group><journal-title>The American Journal of Pathology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0002-9440</issn>
<issn pub-type="epub">1525-2191</issn>
<publisher><publisher-name>American Society for Investigative Pathology. Published by Elsevier Inc.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26597880</article-id>
<article-id pub-id-type="pmc">4715219</article-id>
<article-id pub-id-type="publisher-id">S0002-9440(15)00576-3</article-id>
<article-id pub-id-type="doi">10.1016/j.ajpath.2015.09.014</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Dipeptidyl Peptidase 4 Distribution in the Human Respiratory Tract</article-title>
<subtitle>Implications for the Middle East Respiratory Syndrome</subtitle>
</title-group>
<contrib-group><contrib contrib-type="author" id="au1"><name><surname>Meyerholz</surname>
<given-names>David K.</given-names>
</name>
<xref rid="aff1" ref-type="aff">∗</xref>
</contrib>
<contrib contrib-type="author" id="au2"><name><surname>Lambertz</surname>
<given-names>Allyn M.</given-names>
</name>
<xref rid="aff1" ref-type="aff">∗</xref>
</contrib>
<contrib contrib-type="author" id="au3"><name><surname>McCray</surname>
<given-names>Paul B.</given-names>
<suffix>Jr.</suffix>
</name>
<email>paul-mccray@uiowa.edu</email>
<xref rid="aff2" ref-type="aff">†</xref>
<xref rid="cor1" ref-type="corresp">∗</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>∗</label>
Department of Pathology, Carver College of Medicine, University of Iowa, Iowa City, Iowa</aff>
<aff id="aff2"><label>†</label>
Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa</aff>
<author-notes><corresp id="cor1"><label>∗</label>
Address correspondence to Paul B. McCray, Jr., M.D., 6320 PBDB, Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242. <email>paul-mccray@uiowa.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release"><day>18</day>
<month>11</month>
<year>2015</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>1</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>18</day>
<month>11</month>
<year>2015</year>
</pub-date>
<volume>186</volume>
<issue>1</issue>
<fpage>78</fpage>
<lpage>86</lpage>
<history><date date-type="accepted"><day>4</day>
<month>9</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>American Society for Investigative Pathology</copyright-holder>
<license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<abstract id="abs0010"><p>Dipeptidyl peptidase 4 (DPP4, CD26), a type II transmembrane ectopeptidase, is the receptor for the Middle Eastern respiratory syndrome coronavirus (MERS-CoV). MERS emerged in 2012 and has a high mortality associated with severe lung disease. A lack of autopsy studies from MERS fatalities has hindered understanding of MERS-CoV pathogenesis. We investigated the spatial and cellular localization of DPP4 to evaluate an association MERS clinical disease. DPP4 was rarely detected in the surface epithelium from nasal cavity to conducting airways with a slightly increased incidence in distal airways. DPP4 was also found in a subset of mononuclear leukocytes and in serous cells of submucosal glands. In the parenchyma, DPP4 was found principally in type I and II cells and alveolar macrophages and was also detected in vascular endothelium (eg, lymphatics) and pleural mesothelia. Patients with chronic lung disease, such as chronic obstructive pulmonary disease and cystic fibrosis, exhibited increased DPP4 immunostaining in alveolar epithelia (type I and II cells) and alveolar macrophages with similar trends in reactive mesothelia. This finding suggests that preexisting pulmonary disease could increase MERS-CoV receptor abundance and predispose individuals to MERS morbidity and mortality, which is consistent with current clinical observations. We speculate that the preferential spatial localization of DPP4 in alveolar regions may explain why MERS is characterized by lower respiratory tract disease.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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