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Therapeutic potential of BLT1 antagonist for COPD: involvement of inducing autophagy and ameliorating inflammation

Identifieur interne : 000290 ( Pmc/Checkpoint ); précédent : 000289; suivant : 000291

Therapeutic potential of BLT1 antagonist for COPD: involvement of inducing autophagy and ameliorating inflammation

Auteurs : Li Zhang [République populaire de Chine] ; Jingwen Huang [République populaire de Chine] ; Ran Dong [République populaire de Chine] ; Yun Feng [République populaire de Chine] ; Min Zhou [République populaire de Chine]

Source :

RBID : PMC:6732561

Abstract

Purpose

Leukotriene B4 (LTB4) is a major pro-inflammatory mediator that leads to the persistence of chronic inflammation in chronic obstructive pulmonary disease (COPD). The purpose of this study was to evaluate therapeutic potential of BLT1 antagonist for cigarette smoke (CS)-induced COPD and to explore the underlying mechanism.

Materials and methods

In vitro, autophagy proteins were determined by Western blotting in RAW264.7 macrophages treated with U75302 (BLT1 antagonist) or autophagy inhibitor in cigarette smoke extract-induced inflammation. In vivo, C57BL/6J mice were randomly divided into three groups: Control group, CS group and CS+U75302 group. After 12-week exposure, histological analysis and lung function tests were performed to evaluate the inflammatory infiltration and emphysema. The expression of inflammatory cytokines was measured by real-time PCR and enzyme-linked immunosorbent assay. Immunohistochemical analysis and Western blotting detected the expression of autophagy-related proteins. Transmission electron microscopy (TEM) showed the alterations of autophagosomes and lysosomes.

Results

Lower levels of inflammatory factors and autophagy markers were detected in U75302-treated cells and mice after CS exposure than control. In vitro, LC3 mRNA expression was elevated when treated with U75302. Autophagy inhibition resulted in augmented inflammatory response and autophagy proteins even with U75302 treatment. Furthermore, BLT1 antagonist decreased the number of lysosomes and autophagosomes in alveolar macrophages of mice and potentially enhanced the expression of transcriptional activation of transcription factor-EB (TFEB) in vitro and vivo.

Conclusion

Insufficient autophagy of macrophages was associated with LTB4-mediated inflammation in CS-exposure models. BLT1 antagonist ameliorated inflammatory response through inducing autophagy.


Url:
DOI: 10.2147/DDDT.S215433
PubMed: 31564828
PubMed Central: 6732561


Affiliations:


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PMC:6732561

Le document en format XML

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<title>Purpose</title>
<p>Leukotriene B4 (LTB4) is a major pro-inflammatory mediator that leads to the persistence of chronic inflammation in chronic obstructive pulmonary disease (COPD). The purpose of this study was to evaluate therapeutic potential of BLT1 antagonist for cigarette smoke (CS)-induced COPD and to explore the underlying mechanism.</p>
</sec>
<sec id="S2002">
<title>Materials and methods</title>
<p>In vitro, autophagy proteins were determined by Western blotting in RAW264.7 macrophages treated with U75302 (BLT1 antagonist) or autophagy inhibitor in cigarette smoke extract-induced inflammation. In vivo, C57BL/6J mice were randomly divided into three groups: Control group, CS group and CS+U75302 group. After 12-week exposure, histological analysis and lung function tests were performed to evaluate the inflammatory infiltration and emphysema. The expression of inflammatory cytokines was measured by real-time PCR and enzyme-linked immunosorbent assay. Immunohistochemical analysis and Western blotting detected the expression of autophagy-related proteins. Transmission electron microscopy (TEM) showed the alterations of autophagosomes and lysosomes.</p>
</sec>
<sec id="S2003">
<title>Results</title>
<p>Lower levels of inflammatory factors and autophagy markers were detected in U75302-treated cells and mice after CS exposure than control. In vitro, LC3 mRNA expression was elevated when treated with U75302. Autophagy inhibition resulted in augmented inflammatory response and autophagy proteins even with U75302 treatment. Furthermore, BLT1 antagonist decreased the number of lysosomes and autophagosomes in alveolar macrophages of mice and potentially enhanced the expression of transcriptional activation of transcription factor-EB (TFEB) in vitro and vivo.</p>
</sec>
<sec id="S2004">
<title>Conclusion</title>
<p>Insufficient autophagy of macrophages was associated with LTB4-mediated inflammation in CS-exposure models. BLT1 antagonist ameliorated inflammatory response through inducing autophagy.</p>
</sec>
</div>
</front>
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<journal-id journal-id-type="nlm-ta">Drug Des Devel Ther</journal-id>
<journal-id journal-id-type="iso-abbrev">Drug Des Devel Ther</journal-id>
<journal-id journal-id-type="publisher-id">DDDT</journal-id>
<journal-id journal-id-type="pmc">dddt</journal-id>
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<journal-title>Drug Design, Development and Therapy</journal-title>
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<issn pub-type="epub">1177-8881</issn>
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<publisher-name>Dove</publisher-name>
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<article-id pub-id-type="pmid">31564828</article-id>
<article-id pub-id-type="pmc">6732561</article-id>
<article-id pub-id-type="publisher-id">215433</article-id>
<article-id pub-id-type="doi">10.2147/DDDT.S215433</article-id>
<article-categories>
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<subject>Original Research</subject>
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<title-group>
<article-title>Therapeutic potential of BLT1 antagonist for COPD: involvement of inducing autophagy and ameliorating inflammation</article-title>
<alt-title alt-title-type="running-authors">Zhang et al</alt-title>
<alt-title alt-title-type="running-title">Zhang et al</alt-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Zhang</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Huang</surname>
<given-names>Jingwen</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Dong</surname>
<given-names>Ran</given-names>
</name>
<xref ref-type="aff" rid="AFF0003">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Feng</surname>
<given-names>Yun</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhou</surname>
<given-names>Min</given-names>
</name>
<xref ref-type="corresp" rid="AN0001"></xref>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<aff id="AFF0001">
<label>1</label>
<institution>Department of Respiratory and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine</institution>
,
<addr-line>Shanghai</addr-line>
,
<country>People’s Republic of China</country>
</aff>
<aff id="AFF0002">
<label>2</label>
<institution>Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine</institution>
,
<addr-line>Shanghai</addr-line>
,
<country>People’s Republic of China</country>
</aff>
<aff id="AFF0003">
<label>3</label>
<institution>Department of Respiratory Medicine, Tongji Hospital, Tongji University School of Medicine</institution>
,
<addr-line>Shanghai</addr-line>
,
<country>People’s Republic of China</country>
</aff>
</contrib-group>
<author-notes>
<corresp id="AN0001">Correspondence: Min Zhou
<institution>Department of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine</institution>
,
<addr-line>No.197 Ruijin Er Road</addr-line>
,
<addr-line>Shanghai</addr-line>
<addr-line>200025</addr-line>
,
<country>People’s Republic of China</country>
<phone>Tel +86 216 437 0045</phone>
<fax>Fax +86 216 467 4301</fax>
Email doctor_zhou_99@163.com</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>04</day>
<month>9</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection">
<year>2019</year>
</pub-date>
<volume>13</volume>
<fpage>3105</fpage>
<lpage>3116</lpage>
<history>
<date date-type="received">
<day>12</day>
<month>5</month>
<year>2019</year>
</date>
<date date-type="accepted">
<day>10</day>
<month>8</month>
<year>2019</year>
</date>
</history>
<permissions>
<copyright-statement>© 2019 Zhang et al.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Zhang et al.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">
<license-p>This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at
<ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>
). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (
<ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
).</license-p>
</license>
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<abstract>
<sec id="S2001">
<title>Purpose</title>
<p>Leukotriene B4 (LTB4) is a major pro-inflammatory mediator that leads to the persistence of chronic inflammation in chronic obstructive pulmonary disease (COPD). The purpose of this study was to evaluate therapeutic potential of BLT1 antagonist for cigarette smoke (CS)-induced COPD and to explore the underlying mechanism.</p>
</sec>
<sec id="S2002">
<title>Materials and methods</title>
<p>In vitro, autophagy proteins were determined by Western blotting in RAW264.7 macrophages treated with U75302 (BLT1 antagonist) or autophagy inhibitor in cigarette smoke extract-induced inflammation. In vivo, C57BL/6J mice were randomly divided into three groups: Control group, CS group and CS+U75302 group. After 12-week exposure, histological analysis and lung function tests were performed to evaluate the inflammatory infiltration and emphysema. The expression of inflammatory cytokines was measured by real-time PCR and enzyme-linked immunosorbent assay. Immunohistochemical analysis and Western blotting detected the expression of autophagy-related proteins. Transmission electron microscopy (TEM) showed the alterations of autophagosomes and lysosomes.</p>
</sec>
<sec id="S2003">
<title>Results</title>
<p>Lower levels of inflammatory factors and autophagy markers were detected in U75302-treated cells and mice after CS exposure than control. In vitro, LC3 mRNA expression was elevated when treated with U75302. Autophagy inhibition resulted in augmented inflammatory response and autophagy proteins even with U75302 treatment. Furthermore, BLT1 antagonist decreased the number of lysosomes and autophagosomes in alveolar macrophages of mice and potentially enhanced the expression of transcriptional activation of transcription factor-EB (TFEB) in vitro and vivo.</p>
</sec>
<sec id="S2004">
<title>Conclusion</title>
<p>Insufficient autophagy of macrophages was associated with LTB4-mediated inflammation in CS-exposure models. BLT1 antagonist ameliorated inflammatory response through inducing autophagy.</p>
</sec>
</abstract>
<kwd-group kwd-group-type="author">
<title>Keywords</title>
<kwd>cigarette smoke</kwd>
<kwd>inflammation</kwd>
<kwd>autophagy</kwd>
<kwd>BLT1 antagonist</kwd>
<kwd>COPD</kwd>
</kwd-group>
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</front>
</pmc>
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<li>République populaire de Chine</li>
</country>
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<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Zhang, Li" sort="Zhang, Li" uniqKey="Zhang L" first="Li" last="Zhang">Li Zhang</name>
</noRegion>
<name sortKey="Dong, Ran" sort="Dong, Ran" uniqKey="Dong R" first="Ran" last="Dong">Ran Dong</name>
<name sortKey="Feng, Yun" sort="Feng, Yun" uniqKey="Feng Y" first="Yun" last="Feng">Yun Feng</name>
<name sortKey="Feng, Yun" sort="Feng, Yun" uniqKey="Feng Y" first="Yun" last="Feng">Yun Feng</name>
<name sortKey="Huang, Jingwen" sort="Huang, Jingwen" uniqKey="Huang J" first="Jingwen" last="Huang">Jingwen Huang</name>
<name sortKey="Huang, Jingwen" sort="Huang, Jingwen" uniqKey="Huang J" first="Jingwen" last="Huang">Jingwen Huang</name>
<name sortKey="Zhang, Li" sort="Zhang, Li" uniqKey="Zhang L" first="Li" last="Zhang">Li Zhang</name>
<name sortKey="Zhou, Min" sort="Zhou, Min" uniqKey="Zhou M" first="Min" last="Zhou">Min Zhou</name>
<name sortKey="Zhou, Min" sort="Zhou, Min" uniqKey="Zhou M" first="Min" last="Zhou">Min Zhou</name>
</country>
</tree>
</affiliations>
</record>

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