Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy
Identifieur interne : 000B04 ( Pmc/Curation ); précédent : 000B03; suivant : 000B05Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy
Auteurs : Kyung-Yil Lee [Corée du Sud]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2017.
Abstract
Acute respiratory distress syndrome (ARDS) is caused by infectious insults, such as pneumonia from various pathogens or related to other noninfectious events. Clinical and histopathologic characteristics are similar across severely affected patients, suggesting that a common mode of immune reaction may be involved in the immunopathogenesis of ARDS. There may be etiologic substances that have an affinity for respiratory cells and induce lung cell injury in cases of ARDS. These substances originate not only from pathogens, but also from injured host cells. At the molecular level, these substances have various sizes and biochemical characteristics, classifying them as protein substances and non-protein substances. Immune cells and immune proteins may recognize and act on these substances, including pathogenic proteins and peptides, depending upon the size and biochemical properties of the substances (this theory is known as the protein-homeostasis-system hypothesis). The severity or chronicity of ARDS depends on the amount of etiologic substances with corresponding immune reactions, the duration of the appearance of specific immune cells, or the repertoire of specific immune cells that control the substances. Therefore, treatment with early systemic immune modulators (corticosteroids and/or intravenous immunoglobulin) as soon as possible may reduce aberrant immune responses in the potential stage of ARDS.
Url:
DOI: 10.3390/ijms18020388
PubMed: 28208675
PubMed Central: 5343923
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy</title><author><name sortKey="Lee, Kyung Yil" sort="Lee, Kyung Yil" uniqKey="Lee K" first="Kyung-Yil" last="Lee">Kyung-Yil Lee</name><affiliation><nlm:aff id="af1-ijms-18-00388">Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea;<email>leekyungyil@catholic.ac.kr</email>; Tel.: +82-42-220-9540; Fax: +82-42-221-2925</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijms-18-00388">Department of Pediatrics, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Pediatrics, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">28208675</idno><idno type="pmc">5343923</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343923</idno><idno type="RBID">PMC:5343923</idno><idno type="doi">10.3390/ijms18020388</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">000B04</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B04</idno><idno type="wicri:Area/Pmc/Curation">000B04</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000B04</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy</title><author><name sortKey="Lee, Kyung Yil" sort="Lee, Kyung Yil" uniqKey="Lee K" first="Kyung-Yil" last="Lee">Kyung-Yil Lee</name><affiliation><nlm:aff id="af1-ijms-18-00388">Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea;<email>leekyungyil@catholic.ac.kr</email>; Tel.: +82-42-220-9540; Fax: +82-42-221-2925</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijms-18-00388">Department of Pediatrics, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Pediatrics, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943</wicri:regionArea></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Acute respiratory distress syndrome (ARDS) is caused by infectious insults, such as pneumonia from various pathogens or related to other noninfectious events. Clinical and histopathologic characteristics are similar across severely affected patients, suggesting that a common mode of immune reaction may be involved in the immunopathogenesis of ARDS. There may be etiologic substances that have an affinity for respiratory cells and induce lung cell injury in cases of ARDS. These substances originate not only from pathogens, but also from injured host cells. At the molecular level, these substances have various sizes and biochemical characteristics, classifying them as protein substances and non-protein substances. Immune cells and immune proteins may recognize and act on these substances, including pathogenic proteins and peptides, depending upon the size and biochemical properties of the substances (this theory is known as the protein-homeostasis-system hypothesis). The severity or chronicity of ARDS depends on the amount of etiologic substances with corresponding immune reactions, the duration of the appearance of specific immune cells, or the repertoire of specific immune cells that control the substances. Therefore, treatment with early systemic immune modulators (corticosteroids and/or intravenous immunoglobulin) as soon as possible may reduce aberrant immune responses in the potential stage of ARDS.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Sharma, S" uniqKey="Sharma S">S. Sharma</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ranieri, V M" uniqKey="Ranieri V">V.M. Ranieri</name></author><author><name sortKey="Rubenfeld, G D" uniqKey="Rubenfeld G">G.D. Rubenfeld</name></author><author><name sortKey="Thompson, B T" uniqKey="Thompson B">B.T. Thompson</name></author><author><name sortKey="Ferguson, N D" uniqKey="Ferguson N">N.D. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id><journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id><journal-id journal-id-type="publisher-id">ijms</journal-id><journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title></journal-title-group><issn pub-type="epub">1422-0067</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">28208675</article-id><article-id pub-id-type="pmc">5343923</article-id><article-id pub-id-type="doi">10.3390/ijms18020388</article-id><article-id pub-id-type="publisher-id">ijms-18-00388</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Kyung-Yil</given-names></name><xref ref-type="aff" rid="af1-ijms-18-00388">1</xref><xref ref-type="aff" rid="af2-ijms-18-00388">2</xref></contrib></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Esposito</surname><given-names>Susanna</given-names></name><role>Academic Editor</role></contrib></contrib-group><aff id="af1-ijms-18-00388"><label>1</label>Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea;<email>leekyungyil@catholic.ac.kr</email>; Tel.: +82-42-220-9540; Fax: +82-42-221-2925</aff><aff id="af2-ijms-18-00388"><label>2</label>Department of Pediatrics, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943, Korea</aff><pub-date pub-type="epub"><day>11</day><month>2</month><year>2017</year></pub-date><pub-date pub-type="collection"><month>2</month><year>2017</year></pub-date><volume>18</volume><issue>2</issue><elocation-id>388</elocation-id><history><date date-type="received"><day>18</day><month>11</month><year>2016</year></date><date date-type="accepted"><day>06</day><month>2</month><year>2017</year></date></history><permissions><copyright-statement>© 2017 by the author.</copyright-statement><copyright-year>2017</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Acute respiratory distress syndrome (ARDS) is caused by infectious insults, such as pneumonia from various pathogens or related to other noninfectious events. Clinical and histopathologic characteristics are similar across severely affected patients, suggesting that a common mode of immune reaction may be involved in the immunopathogenesis of ARDS. There may be etiologic substances that have an affinity for respiratory cells and induce lung cell injury in cases of ARDS. These substances originate not only from pathogens, but also from injured host cells. At the molecular level, these substances have various sizes and biochemical characteristics, classifying them as protein substances and non-protein substances. Immune cells and immune proteins may recognize and act on these substances, including pathogenic proteins and peptides, depending upon the size and biochemical properties of the substances (this theory is known as the protein-homeostasis-system hypothesis). The severity or chronicity of ARDS depends on the amount of etiologic substances with corresponding immune reactions, the duration of the appearance of specific immune cells, or the repertoire of specific immune cells that control the substances. Therefore, treatment with early systemic immune modulators (corticosteroids and/or intravenous immunoglobulin) as soon as possible may reduce aberrant immune responses in the potential stage of ARDS.</p></abstract><kwd-group><kwd>pneumonia</kwd><kwd>acute respiratory distress syndrome</kwd><kwd>pathogenesis</kwd><kwd>protein-homeostasis-system</kwd><kwd>corticosteroid</kwd><kwd>intravenous immunoglobulin</kwd></kwd-group></article-meta></front><floats-group><table-wrap id="ijms-18-00388-t001" position="float"><object-id pub-id-type="pii">ijms-18-00388-t001_Table 1</object-id><label>Table 1</label><caption><p>Causes of pneumonia and acute respiratory distress syndrome.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Infectious *</th><th align="left" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Noninfectious **</th></tr></thead><tbody><tr><td align="left" valign="middle" rowspan="1" colspan="1">Bacterial</td><td align="left" valign="middle" rowspan="1" colspan="1">Aspiration of gastric contents</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Streptococcus pneumoniae</italic></td><td align="left" valign="middle" rowspan="1" colspan="1">Near-drowning</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Group B streptococci</td><td align="left" valign="middle" rowspan="1" colspan="1">Pulmonary contusion</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Group A streptococci</td><td align="left" valign="middle" rowspan="1" colspan="1">Toxic inhalation injury</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Staphylococcus aureus</italic></td><td align="left" valign="middle" rowspan="1" colspan="1">Multiple transfusions Pancreatitis</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Hemophilus influenzae</italic></td><td align="left" valign="middle" rowspan="1" colspan="1">Burns</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"></td><td align="left" valign="middle" rowspan="1" colspan="1">Drug overdose</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Neisseria</italic> species<break></break> Mixed anaerobes<break></break> <italic>Enterococcus</italic> species<break></break> <italic>Mycoplasma pneumonia Chlamydia pneumonia</italic><break></break> Mycobacterial<break></break> <italic>Mycobacterium tuberculosis</italic><break></break> <italic>Mycobacterium avium</italic><break></break> Viral</td><td align="left" valign="middle" rowspan="1" colspan="1">Multiple bone fractures <break></break>Post cardio-pulmonary bypass <break></break>Traumatic brain injury</td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Influenza A,B</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Parainfluenza types 1–3</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Respiratory syncytial virus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Coronavirus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Adenovirus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Metapneumovirus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Measles virus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> Varicella zoster virus</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1">Fungal</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Aspergillus</italic> species</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Blastomyces</italic> species</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Cryptococcus</italic> species</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1">Parasitic</td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" rowspan="1" colspan="1"> <italic>Pneumocystis jiroveci</italic></td><td align="left" valign="middle" rowspan="1" colspan="1"></td></tr><tr><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"> Malaria</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td></tr></tbody></table><table-wrap-foot><fn><p>* References [<xref rid="B3-ijms-18-00388" ref-type="bibr">3</xref>,<xref rid="B4-ijms-18-00388" ref-type="bibr">4</xref>,<xref rid="B5-ijms-18-00388" ref-type="bibr">5</xref>,<xref rid="B6-ijms-18-00388" ref-type="bibr">6</xref>,<xref rid="B7-ijms-18-00388" ref-type="bibr">7</xref>,<xref rid="B8-ijms-18-00388" ref-type="bibr">8</xref>,<xref rid="B9-ijms-18-00388" ref-type="bibr">9</xref>,<xref rid="B10-ijms-18-00388" ref-type="bibr">10</xref>,<xref rid="B11-ijms-18-00388" ref-type="bibr">11</xref>,<xref rid="B12-ijms-18-00388" ref-type="bibr">12</xref>,<xref rid="B13-ijms-18-00388" ref-type="bibr">13</xref>,<xref rid="B14-ijms-18-00388" ref-type="bibr">14</xref>,<xref rid="B15-ijms-18-00388" ref-type="bibr">15</xref>,<xref rid="B16-ijms-18-00388" ref-type="bibr">16</xref>,<xref rid="B17-ijms-18-00388" ref-type="bibr">17</xref>,<xref rid="B18-ijms-18-00388" ref-type="bibr">18</xref>,<xref rid="B19-ijms-18-00388" ref-type="bibr">19</xref>,<xref rid="B20-ijms-18-00388" ref-type="bibr">20</xref>,<xref rid="B21-ijms-18-00388" ref-type="bibr">21</xref>,<xref rid="B22-ijms-18-00388" ref-type="bibr">22</xref>,<xref rid="B23-ijms-18-00388" ref-type="bibr">23</xref>], ** References [<xref rid="B24-ijms-18-00388" ref-type="bibr">24</xref>,<xref rid="B25-ijms-18-00388" ref-type="bibr">25</xref>,<xref rid="B26-ijms-18-00388" ref-type="bibr">26</xref>,<xref rid="B27-ijms-18-00388" ref-type="bibr">27</xref>,<xref rid="B28-ijms-18-00388" ref-type="bibr">28</xref>,<xref rid="B29-ijms-18-00388" ref-type="bibr">29</xref>,<xref rid="B30-ijms-18-00388" ref-type="bibr">30</xref>,<xref rid="B31-ijms-18-00388" ref-type="bibr">31</xref>,<xref rid="B32-ijms-18-00388" ref-type="bibr">32</xref>,<xref rid="B33-ijms-18-00388" ref-type="bibr">33</xref>,<xref rid="B34-ijms-18-00388" ref-type="bibr">34</xref>,<xref rid="B35-ijms-18-00388" ref-type="bibr">35</xref>].</p></fn></table-wrap-foot></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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| HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd \
| NlmPubMed2Wicri -a CovidV2
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