Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.
Identifieur interne : 000A49 ( Main/Exploration ); précédent : 000A48; suivant : 000A50Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.
Auteurs : Hongying Zhao [République populaire de Chine] ; Hongguang Chen [République populaire de Chine] ; Meng Xiaoyin [République populaire de Chine] ; Guotao Yang [République populaire de Chine] ; Ying Hu [République populaire de Chine] ; Keliang Xie [République populaire de Chine] ; Yonghao Yu [République populaire de Chine]Source :
- Inflammation [ 1573-2576 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux, Autophagie (physiologie), Bécline-1 (métabolisme), Cytokines (métabolisme), Inflammation (), Lésion pulmonaire aigüe (), Modèles animaux de maladie humaine, Protéine de membrane-2 associée au lysosome (métabolisme), Protéines G rab (métabolisme), Protéines associées aux microtubules, Sepsie (), Sepsie (anatomopathologie), Souris, Taux de survie.
- MESH :
- anatomopathologie : Sepsie.
- métabolisme : Bécline-1, Cytokines, Protéine de membrane-2 associée au lysosome, Protéines G rab.
- physiologie : Autophagie.
- Animaux, Inflammation, Lésion pulmonaire aigüe, Modèles animaux de maladie humaine, Protéines associées aux microtubules, Sepsie, Souris, Taux de survie.
English descriptors
- KwdEn :
- Acute Lung Injury (prevention & control), Animals, Autophagy (physiology), Beclin-1 (metabolism), Cytokines (metabolism), Disease Models, Animal, Inflammation (prevention & control), Lysosomal-Associated Membrane Protein 2 (metabolism), Mice, Microtubule-Associated Proteins, Sepsis (complications), Sepsis (pathology), Survival Rate, rab GTP-Binding Proteins (metabolism).
- MESH :
- chemical , metabolism : Beclin-1, Cytokines, Lysosomal-Associated Membrane Protein 2, rab GTP-Binding Proteins.
- complications : Sepsis.
- pathology : Sepsis.
- physiology : Autophagy.
- prevention & control : Acute Lung Injury, Inflammation.
- Animals, Disease Models, Animal, Mice, Microtubule-Associated Proteins, Survival Rate.
Abstract
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) undergoes the process of pathological event including lung tissue dysfunction, pulmonary edema, and inflammation in sepsis. Autophagy is a cytoprotective process recognized as one of the major pathways for degradation and recycling of cellular constituents. Autophagy as a protective or maladaptive response was still confused in ALI during sepsis. Acute lung injury was performed by cecal ligation and puncture (CLP). Autophagic inducer rapacymin and inhibitor 3-MA and autophagosomal-lysosome fusion inhibitor bafilomucin (Baf) A1 and chloroquine (CQ) were administrated by intraperitoneal injection at 1 h after CLP operation. Microtubule-associated protein light chain 3 II (LC3II), Beclin 1, Rab7, and lysosome-associated membrane protein type 2 (LAMP2) were detected by western blotting. Seven-day survival rate of septic mice was observed. Histologic scores, lung wet-to-dry (W/D) weight ratio, oxygenation index (PaO2/FiO2), total cells and polymorphonuclear neutrophils (PMN) in bronchial alveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity and cytokine tumor necrosis factor (TNF)-α, high-mobility group box (HMGB)1, interleukin (IL)-6, IL-10, and monocyte chemotactic protein (MCP)1 were measured after sham or ALI operation. ALI induced the increasing expression of autophagy-related protein LC3II, Beclin 1, Rab7, and LAMP2 in CLP operation. Autophagic inducer rapacymin significantly induced the expression of LC3II, Beclin 1, LAMP2, and Rab7 in mice model of CLP, and inhibitor 3-MA reduced expression of LC3II, Beclin 1, LAMP2, and Rab7 expressions in CLP + RAP mice compared to CLP group. Compared with ALI group, Baf and CQ obviously elevated the level of LC3II and Beclin 1, and reduced the LAMP2 and Rab7 expressions in CLP + Baf group and ALI + CQ group. Compared with CLP group, autophagic inducer rapacymin improved the survival rate, histologic scores, lung wet/dry weight ratio, PaO2/FiO2, total cells, and PMNS in BALF and MPO activity and cytokines TNF-α, HMGB1, IL-6, IL-10, and MCP1 in CLP + RAP group, but there were exacerbated above indicators in CLP + 3-MA group, CLP + Baf group, and CLP + CQ group. Autophagy activation participated in the pathophysiologic process of sepsis, and alleviated the cytokine excessive release and lung injury in sepsis.
DOI: 10.1007/s10753-018-00952-5
PubMed: 30645707
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (prevention & control)</term>
<term>Animals</term>
<term>Autophagy (physiology)</term>
<term>Beclin-1 (metabolism)</term>
<term>Cytokines (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Inflammation (prevention & control)</term>
<term>Lysosomal-Associated Membrane Protein 2 (metabolism)</term>
<term>Mice</term>
<term>Microtubule-Associated Proteins</term>
<term>Sepsis (complications)</term>
<term>Sepsis (pathology)</term>
<term>Survival Rate</term>
<term>rab GTP-Binding Proteins (metabolism)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Autophagie (physiologie)</term>
<term>Bécline-1 (métabolisme)</term>
<term>Cytokines (métabolisme)</term>
<term>Inflammation ()</term>
<term>Lésion pulmonaire aigüe ()</term>
<term>Modèles animaux de maladie humaine</term>
<term>Protéine de membrane-2 associée au lysosome (métabolisme)</term>
<term>Protéines G rab (métabolisme)</term>
<term>Protéines associées aux microtubules</term>
<term>Sepsie ()</term>
<term>Sepsie (anatomopathologie)</term>
<term>Souris</term>
<term>Taux de survie</term>
</keywords>
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<term>Cytokines</term>
<term>Lysosomal-Associated Membrane Protein 2</term>
<term>rab GTP-Binding Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Sepsie</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Sepsis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term>
<term>Cytokines</term>
<term>Protéine de membrane-2 associée au lysosome</term>
<term>Protéines G rab</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Sepsis</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term>
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<term>Lésion pulmonaire aigüe</term>
<term>Modèles animaux de maladie humaine</term>
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<front><div type="abstract" xml:lang="en">Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) undergoes the process of pathological event including lung tissue dysfunction, pulmonary edema, and inflammation in sepsis. Autophagy is a cytoprotective process recognized as one of the major pathways for degradation and recycling of cellular constituents. Autophagy as a protective or maladaptive response was still confused in ALI during sepsis. Acute lung injury was performed by cecal ligation and puncture (CLP). Autophagic inducer rapacymin and inhibitor 3-MA and autophagosomal-lysosome fusion inhibitor bafilomucin (Baf) A1 and chloroquine (CQ) were administrated by intraperitoneal injection at 1 h after CLP operation. Microtubule-associated protein light chain 3 II (LC3II), Beclin 1, Rab7, and lysosome-associated membrane protein type 2 (LAMP2) were detected by western blotting. Seven-day survival rate of septic mice was observed. Histologic scores, lung wet-to-dry (W/D) weight ratio, oxygenation index (PaO<sub>2</sub>
/FiO<sub>2</sub>
), total cells and polymorphonuclear neutrophils (PMN) in bronchial alveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity and cytokine tumor necrosis factor (TNF)-α, high-mobility group box (HMGB)1, interleukin (IL)-6, IL-10, and monocyte chemotactic protein (MCP)1 were measured after sham or ALI operation. ALI induced the increasing expression of autophagy-related protein LC3II, Beclin 1, Rab7, and LAMP2 in CLP operation. Autophagic inducer rapacymin significantly induced the expression of LC3II, Beclin 1, LAMP2, and Rab7 in mice model of CLP, and inhibitor 3-MA reduced expression of LC3II, Beclin 1, LAMP2, and Rab7 expressions in CLP + RAP mice compared to CLP group. Compared with ALI group, Baf and CQ obviously elevated the level of LC3II and Beclin 1, and reduced the LAMP2 and Rab7 expressions in CLP + Baf group and ALI + CQ group. Compared with CLP group, autophagic inducer rapacymin improved the survival rate, histologic scores, lung wet/dry weight ratio, PaO<sub>2</sub>
/FiO<sub>2</sub>
, total cells, and PMNS in BALF and MPO activity and cytokines TNF-α, HMGB1, IL-6, IL-10, and MCP1 in CLP + RAP group, but there were exacerbated above indicators in CLP + 3-MA group, CLP + Baf group, and CLP + CQ group. Autophagy activation participated in the pathophysiologic process of sepsis, and alleviated the cytokine excessive release and lung injury in sepsis.</div>
</front>
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<affiliations><list><country><li>République populaire de Chine</li>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhao, Hongying" sort="Zhao, Hongying" uniqKey="Zhao H" first="Hongying" last="Zhao">Hongying Zhao</name>
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<name sortKey="Chen, Hongguang" sort="Chen, Hongguang" uniqKey="Chen H" first="Hongguang" last="Chen">Hongguang Chen</name>
<name sortKey="Hu, Ying" sort="Hu, Ying" uniqKey="Hu Y" first="Ying" last="Hu">Ying Hu</name>
<name sortKey="Xiaoyin, Meng" sort="Xiaoyin, Meng" uniqKey="Xiaoyin M" first="Meng" last="Xiaoyin">Meng Xiaoyin</name>
<name sortKey="Xie, Keliang" sort="Xie, Keliang" uniqKey="Xie K" first="Keliang" last="Xie">Keliang Xie</name>
<name sortKey="Yang, Guotao" sort="Yang, Guotao" uniqKey="Yang G" first="Guotao" last="Yang">Guotao Yang</name>
<name sortKey="Yu, Yonghao" sort="Yu, Yonghao" uniqKey="Yu Y" first="Yonghao" last="Yu">Yonghao Yu</name>
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