Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy
Identifieur interne : 000763 ( Main/Exploration ); précédent : 000762; suivant : 000764Pneumonia, 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
Affiliations:
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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><wicri:noRegion>Daejeon 34943</wicri:noRegion></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">000779</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000779</idno><idno type="wicri:Area/Pmc/Curation">000779</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000779</idno><idno type="wicri:Area/Pmc/Checkpoint">000180</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000180</idno><idno type="wicri:Area/Ncbi/Merge">000612</idno><idno type="wicri:Area/Ncbi/Curation">000612</idno><idno type="wicri:Area/Ncbi/Checkpoint">000612</idno><idno type="wicri:Area/Main/Merge">000765</idno><idno type="wicri:Area/Main/Curation">000763</idno><idno type="wicri:Area/Main/Exploration">000763</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><wicri:noRegion>Daejeon 34943</wicri:noRegion></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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