Association of COPD exacerbation frequency with gene expression of pattern recognition receptors in inflammatory cells in induced sputum
Identifieur interne : 000741 ( Istex/Curation ); précédent : 000740; suivant : 000742Association of COPD exacerbation frequency with gene expression of pattern recognition receptors in inflammatory cells in induced sputum
Auteurs : Daisuke Kinose [Japon] ; Emiko Ogawa [Japon] ; Megumi Kudo [Japon] ; Satoshi Marumo [Japon] ; Hirofumi Kiyokawa [Japon] ; Yuma Hoshino [Japon] ; Toyohiro Hirai [Japon] ; Kazuo Chin [Japon] ; Shigeo Muro [Japon] ; Michiaki Mishima [Japon]Source :
- The Clinical Respiratory Journal [ 1752-6981 ] ; 2016-01.
Abstract
Background: Bacteria and viruses are major causes of chronic obstructive pulmonary disease (COPD) exacerbations. Molecular components of these pathogens are recognized by pattern‐recognition receptors (PRRs) expressed by various cells in the airway, which leads to initiation of inflammatory processes. Expression levels of PRRs in airway inflammatory cells are expected to affect susceptibility to COPD exacerbation. Aims: This prospective observational study was conducted to detect any association between exacerbation and PRR expression. Methods: Thirty‐one male COPD patients were recruited. At baseline, clinical history, lung function measurements, peripheral blood samples and induced sputum were obtained. Using sputum samples, we performed gene expression analysis of TLR2, TLR3, TLR4, NOD1, NOD2, RIG‐I and MDA‐5 by quantitative reverse transcription‐polymerase chain reaction in addition to quantitative bacterial culture. COPD exacerbations were assessed based on Anthonisen's criteria using symptom diaries for the following 1‐year period. Results: During 1‐year follow‐up period, 13 patients experienced at least one exacerbation, but 18 patients did not. Those with exacerbations tended to be more severe COPD and showed larger neutrophil fraction in their induced sputum. Among PRRs, only TLR3 gene expression was increased in COPD patients with exacerbation compared with those without exacerbations. Multivariate logistic regression analysis including neutrophil fraction and TLR3 gene expression as predictor variables demonstrated that only an increase of neutrophil fraction, but not TLR3 gene expression, was a significant predictor for COPD exacerbation. Conclusion: TLR3 expression in inflammatory cells might affect the susceptibility to COPD exacerbation.
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DOI: 10.1111/crj.12171
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of Medical Science, Otsu, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Health Administration Center and Division of Respiratory Medicine, Department of Medicine, Shiga University of Medical Science, Otsu</wicri:regionArea></affiliation><affiliation><mods:affiliation>Emiko Ogawa, MD, PhD, Health Administration Center, Shiga University of Medical Science, Seta‐Tsukinowa‐cho, Otsu, 520‐2192 Shiga, JapanTel: +81 77 548 2087Fax: +81 77 548 2087email:</mods:affiliation><wicri:noCountry code="subField">2087email:</wicri:noCountry></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: eogawa@belle.shiga-med.ac.jp</mods:affiliation><country wicri:rule="url">Japon</country></affiliation></author><author><name sortKey="Kudo, Megumi" sort="Kudo, Megumi" uniqKey="Kudo M" first="Megumi" last="Kudo">Megumi Kudo</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, 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xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Mishima, Michiaki" sort="Mishima, Michiaki" uniqKey="Mishima M" first="Michiaki" last="Mishima">Michiaki Mishima</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:94F27A970F6FC3B47ED89F596AFC6157509AD2DA</idno><date when="2016" year="2016">2016</date><idno type="doi">10.1111/crj.12171</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-V7Z7HK2J-2/fulltext.pdf</idno><idno 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wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Hoshino, Yuma" sort="Hoshino, Yuma" uniqKey="Hoshino Y" first="Yuma" last="Hoshino">Yuma Hoshino</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Hirai, Toyohiro" sort="Hirai, Toyohiro" uniqKey="Hirai T" first="Toyohiro" last="Hirai">Toyohiro Hirai</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Chin, Kazuo" sort="Chin, Kazuo" uniqKey="Chin K" first="Kazuo" last="Chin">Kazuo Chin</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Care and Sleep Control Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Care and Sleep Control Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Muro, Shigeo" sort="Muro, Shigeo" uniqKey="Muro S" first="Shigeo" last="Muro">Shigeo Muro</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author><author><name sortKey="Mishima, Michiaki" sort="Mishima, Michiaki" uniqKey="Mishima M" first="Michiaki" last="Mishima">Michiaki Mishima</name><affiliation wicri:level="1"><mods:affiliation>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Clinical Respiratory Journal</title><title level="j" type="alt">THE CLINICAL RESPIRATORY JOURNAL</title><idno type="ISSN">1752-6981</idno><idno type="eISSN">1752-699X</idno><imprint><biblScope unit="vol">10</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="11">11</biblScope><biblScope unit="page" to="21">21</biblScope><biblScope unit="page-count">11</biblScope><date type="published" when="2016-01">2016-01</date></imprint><idno type="ISSN">1752-6981</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1752-6981</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Background: Bacteria and viruses are major causes of chronic obstructive pulmonary disease (COPD) exacerbations. Molecular components of these pathogens are recognized by pattern‐recognition receptors (PRRs) expressed by various cells in the airway, which leads to initiation of inflammatory processes. Expression levels of PRRs in airway inflammatory cells are expected to affect susceptibility to COPD exacerbation. Aims: This prospective observational study was conducted to detect any association between exacerbation and PRR expression. Methods: Thirty‐one male COPD patients were recruited. At baseline, clinical history, lung function measurements, peripheral blood samples and induced sputum were obtained. Using sputum samples, we performed gene expression analysis of TLR2, TLR3, TLR4, NOD1, NOD2, RIG‐I and MDA‐5 by quantitative reverse transcription‐polymerase chain reaction in addition to quantitative bacterial culture. COPD exacerbations were assessed based on Anthonisen's criteria using symptom diaries for the following 1‐year period. Results: During 1‐year follow‐up period, 13 patients experienced at least one exacerbation, but 18 patients did not. Those with exacerbations tended to be more severe COPD and showed larger neutrophil fraction in their induced sputum. Among PRRs, only TLR3 gene expression was increased in COPD patients with exacerbation compared with those without exacerbations. Multivariate logistic regression analysis including neutrophil fraction and TLR3 gene expression as predictor variables demonstrated that only an increase of neutrophil fraction, but not TLR3 gene expression, was a significant predictor for COPD exacerbation. Conclusion: TLR3 expression in inflammatory cells might affect the susceptibility to COPD exacerbation.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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