{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T18:14:45Z","timestamp":1780337685685,"version":"3.54.1"},"reference-count":25,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,8,23]],"date-time":"2017-08-23T00:00:00Z","timestamp":1503446400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001868","name":"National Science Council","doi-asserted-by":"publisher","award":["NSC 101\u20102314\u2010B\u2010038\u2013044\u2010MY3"],"award-info":[{"award-number":["NSC 101\u20102314\u2010B\u2010038\u2013044\u2010MY3"]}],"id":[{"id":"10.13039\/501100001868","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001868","name":"National Science Council","doi-asserted-by":"publisher","award":["NSC 102\u20102628\u2010B\u2010038\u2013009\u2010MY3"],"award-info":[{"award-number":["NSC 102\u20102628\u2010B\u2010038\u2013009\u2010MY3"]}],"id":[{"id":"10.13039\/501100001868","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Respirology"],"published-print":{"date-parts":[[2018,1]]},"abstract":"ABSTRACT<\/jats:styled-content><\/jats:title>Background and objective<\/jats:title>Parapneumonic effusion (PPE<\/jats:styled-content>) is commonly caused by Gram\u2010positive bacteria (GPB<\/jats:styled-content>) and often presents with pleural loculation, which is characterized by overproduction of plasminogen activator inhibitor (PAI<\/jats:styled-content>)\u20101. Lipoteichoic acid (LTA<\/jats:styled-content>), a surface adhesion molecule of GPB<\/jats:styled-content>, binds to the pleural mesothelium and triggers inflammation. However, the effects of LTA<\/jats:styled-content> on PAI<\/jats:styled-content>\u20101 expression in PPE<\/jats:styled-content> and underlying mechanisms remain unclear.<\/jats:p><\/jats:sec>Methods<\/jats:title>Thirty consecutive patients with PPE<\/jats:styled-content> were enrolled, including uncomplicated culture negative (CN<\/jats:styled-content>, n<\/jats:italic>\u2009=\u200911), Gram\u2010negative bacteria (GNB<\/jats:styled-content>, n<\/jats:italic>\u2009=\u20097) and GPB<\/jats:styled-content> (n<\/jats:italic>\u2009=\u200912) groups stratified by pleural fluid characteristics and bacteriology, and the effusion PAI<\/jats:styled-content>\u20101 levels were measured. In addition, human pleural mesothelial cells (PMC<\/jats:styled-content>) were treated with LTA<\/jats:styled-content> and the expression of PAI<\/jats:styled-content>\u20101 and activation of signalling pathways were assayed.<\/jats:p><\/jats:sec>Results<\/jats:title>The median levels of PAI<\/jats:styled-content>\u20101 were significantly higher in GPB<\/jats:styled-content> (160.5\u2009ng\/mL<\/jats:styled-content>) and GNB<\/jats:styled-content> (117.0\u2009ng\/mL<\/jats:styled-content>) groups than in the uncomplicated CN<\/jats:styled-content> (58.0\u2009ng\/mL<\/jats:styled-content>) group. In human PMC<\/jats:styled-content>, LTA<\/jats:styled-content> markedly upregulated PAI<\/jats:styled-content>\u20101 mRNA<\/jats:styled-content> and protein expression and enhanced elaboration of Toll\u2010like receptor 2 (TLR2<\/jats:styled-content>). Furthermore, LTA<\/jats:styled-content> increased c\u2010Jun N\u2010terminal kinase (JNK<\/jats:styled-content>) phosphorylation, induced activating transcription factor 2 (ATF2<\/jats:styled-content>)\/c\u2010Jun nuclear translocation and activated PAI<\/jats:styled-content>\u20101 promoter activity. Pretreatment with TLR2 siRNA<\/jats:styled-content> significantly inhibited LTA<\/jats:styled-content>\u2010induced JNK<\/jats:styled-content> phosphorylation and PAI<\/jats:styled-content>\u20101 protein expression.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Culture\u2010positive PPE<\/jats:styled-content>, especially that caused by GPB<\/jats:styled-content>, has a significantly higher level of PAI<\/jats:styled-content>\u20101 than uncomplicated CN PPE<\/jats:styled-content>. LTA<\/jats:styled-content> upregulates PAI<\/jats:styled-content>\u20101 expression through activation of TLR2<\/jats:styled-content>\/JNK<\/jats:styled-content>\/activator protein 1 (AP<\/jats:styled-content>\u20101) pathway in human PMC<\/jats:styled-content>. Better understanding of the modulation of PAI<\/jats:styled-content>\u20101 synthesis by LTA<\/jats:styled-content> in PPE<\/jats:styled-content> may provide potential therapies for infected pleural effusions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/resp.13148","type":"journal-article","created":{"date-parts":[[2017,8,24]],"date-time":"2017-08-24T00:08:44Z","timestamp":1503533324000},"page":"89-95","source":"Crossref","is-referenced-by-count":11,"title":["Lipoteichoic acid upregulates plasminogen activator inhibitor\u20101 expression in parapneumonic effusions"],"prefix":"10.1111","volume":"23","author":[{"given":"Kai\u2010Ling","family":"Lee","sequence":"first","affiliation":[{"name":"Division of Pulmonary Medicine, Department of Internal Medicine Taipei Medical University Hospital Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei\u2010Lin","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nursing Mackay Junior College of Medicine, Nursing, and Management Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ray\u2010Jade","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Surgery, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan"},{"name":"Division of General Surgery, Department of Surgery Taipei Medical University Hospital Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin S.","family":"Lai","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Medicine, Department of Internal Medicine Taipei Medical University Hospital Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0656-976X","authenticated-orcid":false,"given":"Chi\u2010Li","family":"Chung","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Medicine, Department of Internal Medicine Taipei Medical University Hospital Taipei Taiwan"},{"name":"Division of Thoracic Medicine, Department of Internal Medicine, School of Medicine and School of Respiratory Therapy, College of Medicine Taipei Medical University Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,8,23]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1843.2003.00539.x"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(03)00242-5"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1843.2002.00404.x"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb\/7.4.414"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2005.03.015"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0053169"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1001647"},{"key":"e_1_2_8_9_1","first-page":"950","article-title":"Lipoteichoic acid and peptidoglycan from Staphylococcus aureus synergistically induce neutrophil influx into the lungs of mice","volume":"10","author":"Leemans JC","year":"2003","journal-title":"Clin. 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