Inhibition of glycolysis alleviates lipopolysaccharide‐induced acute lung injury in a mouse model
Gluconic metabolic reprogramming, immune response, and inflammation are intimately linked. Glycolysis involves in the pathologic progress in acute and chronic inflammatory diseases. However, the involvement of glycolysis in the acute lung injury (ALI) is still unclear. This study investigated the ro...
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| Veröffentlicht in: | Journal of cellular physiology 2019-04, Vol.234 (4), p.4641-4654 |
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| creator | Zhong, Wen‐Jing Yang, Hui‐Hui Guan, Xin‐Xin Xiong, Jian‐Bing Sun, Chen‐Chen Zhang, Chen‐Yu Luo, Xiao‐Qin Zhang, Yan‐Feng Zhang, Jun Duan, Jia‐Xi Zhou, Yong Guan, Cha‐Xiang |
| description | Gluconic metabolic reprogramming, immune response, and inflammation are intimately linked. Glycolysis involves in the pathologic progress in acute and chronic inflammatory diseases. However, the involvement of glycolysis in the acute lung injury (ALI) is still unclear. This study investigated the role of glycolysis in an animal model of ALI. First, we found that lactate content in serum was remarkably increased in ALI patients and a murine model induced by intratracheal administration of lipopolysaccharide (LPS). The key proteins involving in glycolysis were robustly elevated, including HK2,
PKM2, and
HIF‐1α. Intriguingly, inhibition of glycolysis by 2‐deoxyglucose (2‐DG) pronouncedly attenuated the lung tissue pathological injury, accumulation of neutrophil, oxidative stress, expression of proinflammatory factors in the lung of ALI mice induced by LPS. The 2‐DG treatment also strongly suppressed the activation of the NOD‐like receptor (NLR) family and pyrin domain‐containing protein 3 (NLRP3) inflammasome. Furthermore, we investigated the role of glycolysis in the inflammatory response of primary murine macrophages activated by LPS in vitro. We found that the 2‐DG treatment remarkably reduced the expression of proinflammatory factors induced by LPS, including tumor necrosis factor‐α messenger RNA (mRNA), pro‐interleukin (IL)‐1β mRNA, pro‐IL‐18 mRNA, NLRP3 mRNA, caspase‐1 mRNA, and IL‐1β protein. Altogether, these data provide a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in ALI. This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.
This article provides a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in acute lung injury (ALI). This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI. |
| doi_str_mv | 10.1002/jcp.27261 |
| format | Article |
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PKM2, and
HIF‐1α. Intriguingly, inhibition of glycolysis by 2‐deoxyglucose (2‐DG) pronouncedly attenuated the lung tissue pathological injury, accumulation of neutrophil, oxidative stress, expression of proinflammatory factors in the lung of ALI mice induced by LPS. The 2‐DG treatment also strongly suppressed the activation of the NOD‐like receptor (NLR) family and pyrin domain‐containing protein 3 (NLRP3) inflammasome. Furthermore, we investigated the role of glycolysis in the inflammatory response of primary murine macrophages activated by LPS in vitro. We found that the 2‐DG treatment remarkably reduced the expression of proinflammatory factors induced by LPS, including tumor necrosis factor‐α messenger RNA (mRNA), pro‐interleukin (IL)‐1β mRNA, pro‐IL‐18 mRNA, NLRP3 mRNA, caspase‐1 mRNA, and IL‐1β protein. Altogether, these data provide a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in ALI. This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.
This article provides a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in acute lung injury (ALI). This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.27261</identifier><identifier>PMID: 30256406</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>2‐deoxyglucose ; acute lung injury ; Acute Lung Injury - chemically induced ; Acute Lung Injury - metabolism ; Acute Lung Injury - pathology ; Acute Lung Injury - prevention & control ; Animal models ; Animals ; Anti-Inflammatory Agents - pharmacology ; Bioaccumulation ; Case-Control Studies ; Caspase ; Cells, Cultured ; Deoxyglucose ; Deoxyglucose - pharmacology ; Disease Models, Animal ; Glycolysis ; Glycolysis - drug effects ; Humans ; Immune response ; Immune system ; Inflammasomes ; Inflammation Mediators - metabolism ; Inflammatory diseases ; Inflammatory response ; Injuries ; Interleukins ; Lactic acid ; Lipopolysaccharides ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lungs ; Macrophages ; Macrophages, Peritoneal - drug effects ; Macrophages, Peritoneal - metabolism ; Macrophages, Peritoneal - pathology ; Male ; Metabolism ; Mice, Inbred C57BL ; mRNA ; Neutrophil Infiltration - drug effects ; Neutrophils - drug effects ; Neutrophils - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Oxidative stress ; Oxidative Stress - drug effects ; Proteins ; Pyrin protein ; Ribonucleic acid ; RNA ; Rodents ; Time Factors ; Trachea</subject><ispartof>Journal of cellular physiology, 2019-04, Vol.234 (4), p.4641-4654</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4191-fa976efc1c74d0519b293ea7d361c895dc26f91e2d44888ad2c1f41a224c707a3</citedby><cites>FETCH-LOGICAL-c4191-fa976efc1c74d0519b293ea7d361c895dc26f91e2d44888ad2c1f41a224c707a3</cites><orcidid>0000-0002-7348-2376 ; 0000-0002-8505-8724</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.27261$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.27261$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30256406$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhong, Wen‐Jing</creatorcontrib><creatorcontrib>Yang, Hui‐Hui</creatorcontrib><creatorcontrib>Guan, Xin‐Xin</creatorcontrib><creatorcontrib>Xiong, Jian‐Bing</creatorcontrib><creatorcontrib>Sun, Chen‐Chen</creatorcontrib><creatorcontrib>Zhang, Chen‐Yu</creatorcontrib><creatorcontrib>Luo, Xiao‐Qin</creatorcontrib><creatorcontrib>Zhang, Yan‐Feng</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Duan, Jia‐Xi</creatorcontrib><creatorcontrib>Zhou, Yong</creatorcontrib><creatorcontrib>Guan, Cha‐Xiang</creatorcontrib><title>Inhibition of glycolysis alleviates lipopolysaccharide‐induced acute lung injury in a mouse model</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Gluconic metabolic reprogramming, immune response, and inflammation are intimately linked. Glycolysis involves in the pathologic progress in acute and chronic inflammatory diseases. However, the involvement of glycolysis in the acute lung injury (ALI) is still unclear. This study investigated the role of glycolysis in an animal model of ALI. First, we found that lactate content in serum was remarkably increased in ALI patients and a murine model induced by intratracheal administration of lipopolysaccharide (LPS). The key proteins involving in glycolysis were robustly elevated, including HK2,
PKM2, and
HIF‐1α. Intriguingly, inhibition of glycolysis by 2‐deoxyglucose (2‐DG) pronouncedly attenuated the lung tissue pathological injury, accumulation of neutrophil, oxidative stress, expression of proinflammatory factors in the lung of ALI mice induced by LPS. The 2‐DG treatment also strongly suppressed the activation of the NOD‐like receptor (NLR) family and pyrin domain‐containing protein 3 (NLRP3) inflammasome. Furthermore, we investigated the role of glycolysis in the inflammatory response of primary murine macrophages activated by LPS in vitro. We found that the 2‐DG treatment remarkably reduced the expression of proinflammatory factors induced by LPS, including tumor necrosis factor‐α messenger RNA (mRNA), pro‐interleukin (IL)‐1β mRNA, pro‐IL‐18 mRNA, NLRP3 mRNA, caspase‐1 mRNA, and IL‐1β protein. Altogether, these data provide a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in ALI. This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.
This article provides a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in acute lung injury (ALI). This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.</description><subject>2‐deoxyglucose</subject><subject>acute lung injury</subject><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - pathology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Animal models</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Bioaccumulation</subject><subject>Case-Control Studies</subject><subject>Caspase</subject><subject>Cells, Cultured</subject><subject>Deoxyglucose</subject><subject>Deoxyglucose - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Glycolysis</subject><subject>Glycolysis - drug effects</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Inflammasomes</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammatory diseases</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Interleukins</subject><subject>Lactic acid</subject><subject>Lipopolysaccharides</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Macrophages</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Macrophages, Peritoneal - pathology</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice, Inbred C57BL</subject><subject>mRNA</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - metabolism</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Proteins</subject><subject>Pyrin protein</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Time Factors</subject><subject>Trachea</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM9KxDAQh4Mouq4efAEJeNFDNZOmaXOUxT8rgh70XLLJVLNk29psld58BJ_RJzG66kHwMj-Y-fgxfITsATsGxvjJ3LTHPOcS1sgImMoTITO-TkbxBonKBGyR7RDmjDGl0nSTbKWMZ1IwOSJmWj-6mVu6pqZNRR_8YBo_BBeo9h6fnV5ioN61Tfu51sY86s5ZfH99c7XtDVqqTb9E6vv6gbp63ndDDKrpoukDxmnR75CNSvuAu985JvfnZ3eTy-T65mI6Ob1OjAAFSaVVLrEyYHJhWQZqxlWKOrepBFOozBouKwXIrRBFUWjLDVQCNOfC5CzX6ZgcrnrbrnnqMSzLhQsGvdc1xm9KDhAdMRkdjMnBH3Te9F0dv4uU5GmRS5FF6mhFma4JocOqbDu30N1QAis_zZfRfPllPrL73439bIH2l_xRHYGTFfDiPA7_N5VXk9tV5QdHII5q</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Zhong, Wen‐Jing</creator><creator>Yang, Hui‐Hui</creator><creator>Guan, Xin‐Xin</creator><creator>Xiong, Jian‐Bing</creator><creator>Sun, Chen‐Chen</creator><creator>Zhang, Chen‐Yu</creator><creator>Luo, Xiao‐Qin</creator><creator>Zhang, Yan‐Feng</creator><creator>Zhang, Jun</creator><creator>Duan, Jia‐Xi</creator><creator>Zhou, Yong</creator><creator>Guan, Cha‐Xiang</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7348-2376</orcidid><orcidid>https://orcid.org/0000-0002-8505-8724</orcidid></search><sort><creationdate>201904</creationdate><title>Inhibition of glycolysis alleviates lipopolysaccharide‐induced acute lung injury in a mouse model</title><author>Zhong, Wen‐Jing ; Yang, Hui‐Hui ; Guan, Xin‐Xin ; Xiong, Jian‐Bing ; Sun, Chen‐Chen ; Zhang, Chen‐Yu ; Luo, Xiao‐Qin ; Zhang, Yan‐Feng ; Zhang, Jun ; Duan, Jia‐Xi ; Zhou, Yong ; Guan, Cha‐Xiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4191-fa976efc1c74d0519b293ea7d361c895dc26f91e2d44888ad2c1f41a224c707a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>2‐deoxyglucose</topic><topic>acute lung injury</topic><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - pathology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Animal models</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Bioaccumulation</topic><topic>Case-Control Studies</topic><topic>Caspase</topic><topic>Cells, Cultured</topic><topic>Deoxyglucose</topic><topic>Deoxyglucose - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Glycolysis</topic><topic>Glycolysis - drug effects</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Inflammasomes</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammatory diseases</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Interleukins</topic><topic>Lactic acid</topic><topic>Lipopolysaccharides</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Macrophages</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Macrophages, Peritoneal - pathology</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice, Inbred C57BL</topic><topic>mRNA</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Proteins</topic><topic>Pyrin protein</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Rodents</topic><topic>Time Factors</topic><topic>Trachea</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhong, Wen‐Jing</creatorcontrib><creatorcontrib>Yang, Hui‐Hui</creatorcontrib><creatorcontrib>Guan, Xin‐Xin</creatorcontrib><creatorcontrib>Xiong, Jian‐Bing</creatorcontrib><creatorcontrib>Sun, Chen‐Chen</creatorcontrib><creatorcontrib>Zhang, Chen‐Yu</creatorcontrib><creatorcontrib>Luo, Xiao‐Qin</creatorcontrib><creatorcontrib>Zhang, Yan‐Feng</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Duan, Jia‐Xi</creatorcontrib><creatorcontrib>Zhou, Yong</creatorcontrib><creatorcontrib>Guan, Cha‐Xiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhong, Wen‐Jing</au><au>Yang, Hui‐Hui</au><au>Guan, Xin‐Xin</au><au>Xiong, Jian‐Bing</au><au>Sun, Chen‐Chen</au><au>Zhang, Chen‐Yu</au><au>Luo, Xiao‐Qin</au><au>Zhang, Yan‐Feng</au><au>Zhang, Jun</au><au>Duan, Jia‐Xi</au><au>Zhou, Yong</au><au>Guan, Cha‐Xiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of glycolysis alleviates lipopolysaccharide‐induced acute lung injury in a mouse model</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-04</date><risdate>2019</risdate><volume>234</volume><issue>4</issue><spage>4641</spage><epage>4654</epage><pages>4641-4654</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Gluconic metabolic reprogramming, immune response, and inflammation are intimately linked. Glycolysis involves in the pathologic progress in acute and chronic inflammatory diseases. However, the involvement of glycolysis in the acute lung injury (ALI) is still unclear. This study investigated the role of glycolysis in an animal model of ALI. First, we found that lactate content in serum was remarkably increased in ALI patients and a murine model induced by intratracheal administration of lipopolysaccharide (LPS). The key proteins involving in glycolysis were robustly elevated, including HK2,
PKM2, and
HIF‐1α. Intriguingly, inhibition of glycolysis by 2‐deoxyglucose (2‐DG) pronouncedly attenuated the lung tissue pathological injury, accumulation of neutrophil, oxidative stress, expression of proinflammatory factors in the lung of ALI mice induced by LPS. The 2‐DG treatment also strongly suppressed the activation of the NOD‐like receptor (NLR) family and pyrin domain‐containing protein 3 (NLRP3) inflammasome. Furthermore, we investigated the role of glycolysis in the inflammatory response of primary murine macrophages activated by LPS in vitro. We found that the 2‐DG treatment remarkably reduced the expression of proinflammatory factors induced by LPS, including tumor necrosis factor‐α messenger RNA (mRNA), pro‐interleukin (IL)‐1β mRNA, pro‐IL‐18 mRNA, NLRP3 mRNA, caspase‐1 mRNA, and IL‐1β protein. Altogether, these data provide a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in ALI. This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.
This article provides a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in acute lung injury (ALI). This study suggests glycolytic inhibition as an effective anti‐inflammatory strategy in treating ALI.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30256406</pmid><doi>10.1002/jcp.27261</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-7348-2376</orcidid><orcidid>https://orcid.org/0000-0002-8505-8724</orcidid></addata></record> |
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| subjects | 2‐deoxyglucose acute lung injury Acute Lung Injury - chemically induced Acute Lung Injury - metabolism Acute Lung Injury - pathology Acute Lung Injury - prevention & control Animal models Animals Anti-Inflammatory Agents - pharmacology Bioaccumulation Case-Control Studies Caspase Cells, Cultured Deoxyglucose Deoxyglucose - pharmacology Disease Models, Animal Glycolysis Glycolysis - drug effects Humans Immune response Immune system Inflammasomes Inflammation Mediators - metabolism Inflammatory diseases Inflammatory response Injuries Interleukins Lactic acid Lipopolysaccharides Lung - drug effects Lung - metabolism Lung - pathology Lungs Macrophages Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - pathology Male Metabolism Mice, Inbred C57BL mRNA Neutrophil Infiltration - drug effects Neutrophils - drug effects Neutrophils - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Oxidative stress Oxidative Stress - drug effects Proteins Pyrin protein Ribonucleic acid RNA Rodents Time Factors Trachea |
| title | Inhibition of glycolysis alleviates lipopolysaccharide‐induced acute lung injury in a mouse model |
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