Recent advances in endotoxin tolerance
Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage...
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| Veröffentlicht in: | Journal of cellular biochemistry 2019-01, Vol.120 (1), p.56-70 |
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| creator | Liu, Dan Cao, Shousong Zhou, Yejiang Xiong, Yuxia |
| description | Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically. |
| doi_str_mv | 10.1002/jcb.27547 |
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The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.27547</identifier><identifier>PMID: 30246452</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Apoptosis - immunology ; Cancer ; Cell surface ; Chromatin ; chromatin modification and gene reprogramming ; CXCL10 protein ; Cystic fibrosis ; Cytokines ; Diseases ; Endotoxemia ; endotoxin (lipopolysaccharide) ; Endotoxin shock ; endotoxin tolerance ; Endotoxins ; Growth factors ; host defense ; Humans ; Immune system ; Immunological tolerance ; Inflammation ; Inflammation - immunology ; Inflammation - pathology ; Interleukins ; Ischemia ; Lethal dose ; Lipopolysaccharides ; Lipopolysaccharides - immunology ; Lipopolysaccharides - toxicity ; Liver ; microRNAs ; miRNA ; Molecular modelling ; negative regulate factors ; Proteins ; Regulatory mechanisms (biology) ; Reperfusion ; Sepsis ; Shock, Septic - immunology ; Shock, Septic - pathology ; Signal processing ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - immunology ; Signaling ; TLR4 protein ; Toll-like receptors ; Transforming growth factor ; Transforming growth factor-b ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Journal of cellular biochemistry, 2019-01, Vol.120 (1), p.56-70</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4547-6fd3948fc040b026bdb1e85f0ddf5f1cdd8e4275ec79b3612d53b27ca0fcebd93</citedby><cites>FETCH-LOGICAL-c4547-6fd3948fc040b026bdb1e85f0ddf5f1cdd8e4275ec79b3612d53b27ca0fcebd93</cites><orcidid>0000-0001-9116-5326</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%2Fjcb.27547$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.27547$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30246452$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Cao, Shousong</creatorcontrib><creatorcontrib>Zhou, Yejiang</creatorcontrib><creatorcontrib>Xiong, Yuxia</creatorcontrib><title>Recent advances in endotoxin tolerance</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Cancer</subject><subject>Cell surface</subject><subject>Chromatin</subject><subject>chromatin modification and gene reprogramming</subject><subject>CXCL10 protein</subject><subject>Cystic fibrosis</subject><subject>Cytokines</subject><subject>Diseases</subject><subject>Endotoxemia</subject><subject>endotoxin (lipopolysaccharide)</subject><subject>Endotoxin shock</subject><subject>endotoxin tolerance</subject><subject>Endotoxins</subject><subject>Growth factors</subject><subject>host defense</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunological tolerance</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Inflammation - pathology</subject><subject>Interleukins</subject><subject>Ischemia</subject><subject>Lethal dose</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Liver</subject><subject>microRNAs</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>negative regulate factors</subject><subject>Proteins</subject><subject>Regulatory mechanisms (biology)</subject><subject>Reperfusion</subject><subject>Sepsis</subject><subject>Shock, Septic - immunology</subject><subject>Shock, Septic - pathology</subject><subject>Signal processing</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - immunology</subject><subject>Signaling</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Transforming growth factor</subject><subject>Transforming growth factor-b</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtKAzEUBuAgiq3VhS8gBUF0Me3JZS5Z1uKVgiC6DpPkBKZMZ-pkRu3bmzrVheAmCYePP4efkFMKEwrApkujJyyNRbpHhhRkGolEiH0yhJRDxDhlA3Lk_RIApOTskAw4sEBiNiQXz2iwase5fc8rg35cVGOsbN3Wn-HV1iU22_kxOXB56fFkd4_I6-3Ny_w-WjzdPcxni8iI8H2UOMulyJwBARpYoq2mmMUOrHWxo8baDEXYFE0qNU8oszHXLDU5OIPaSj4il33uuqnfOvStWhXeYFnmFdadV4xSmooknIGe_6HLumuqsF1QPGGcSZkFddUr09TeN-jUuilWebNRFNS2PBXKU9_lBXu2S-z0Cu2v_GkrgGkPPooSN_8nqcf5dR_5BZerds8</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Liu, Dan</creator><creator>Cao, Shousong</creator><creator>Zhou, Yejiang</creator><creator>Xiong, Yuxia</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9116-5326</orcidid></search><sort><creationdate>201901</creationdate><title>Recent advances in endotoxin tolerance</title><author>Liu, Dan ; Cao, Shousong ; Zhou, Yejiang ; Xiong, Yuxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4547-6fd3948fc040b026bdb1e85f0ddf5f1cdd8e4275ec79b3612d53b27ca0fcebd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - immunology</topic><topic>Cancer</topic><topic>Cell surface</topic><topic>Chromatin</topic><topic>chromatin modification and gene reprogramming</topic><topic>CXCL10 protein</topic><topic>Cystic fibrosis</topic><topic>Cytokines</topic><topic>Diseases</topic><topic>Endotoxemia</topic><topic>endotoxin (lipopolysaccharide)</topic><topic>Endotoxin shock</topic><topic>endotoxin tolerance</topic><topic>Endotoxins</topic><topic>Growth factors</topic><topic>host defense</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunological tolerance</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Inflammation - pathology</topic><topic>Interleukins</topic><topic>Ischemia</topic><topic>Lethal dose</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - immunology</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Liver</topic><topic>microRNAs</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>negative regulate factors</topic><topic>Proteins</topic><topic>Regulatory mechanisms (biology)</topic><topic>Reperfusion</topic><topic>Sepsis</topic><topic>Shock, Septic - immunology</topic><topic>Shock, Septic - pathology</topic><topic>Signal processing</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - immunology</topic><topic>Signaling</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Transforming growth factor</topic><topic>Transforming growth factor-b</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Cao, Shousong</creatorcontrib><creatorcontrib>Zhou, Yejiang</creatorcontrib><creatorcontrib>Xiong, Yuxia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Dan</au><au>Cao, Shousong</au><au>Zhou, Yejiang</au><au>Xiong, Yuxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recent advances in endotoxin tolerance</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2019-01</date><risdate>2019</risdate><volume>120</volume><issue>1</issue><spage>56</spage><epage>70</epage><pages>56-70</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30246452</pmid><doi>10.1002/jcb.27547</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-9116-5326</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - immunology Cancer Cell surface Chromatin chromatin modification and gene reprogramming CXCL10 protein Cystic fibrosis Cytokines Diseases Endotoxemia endotoxin (lipopolysaccharide) Endotoxin shock endotoxin tolerance Endotoxins Growth factors host defense Humans Immune system Immunological tolerance Inflammation Inflammation - immunology Inflammation - pathology Interleukins Ischemia Lethal dose Lipopolysaccharides Lipopolysaccharides - immunology Lipopolysaccharides - toxicity Liver microRNAs miRNA Molecular modelling negative regulate factors Proteins Regulatory mechanisms (biology) Reperfusion Sepsis Shock, Septic - immunology Shock, Septic - pathology Signal processing Signal transduction Signal Transduction - drug effects Signal Transduction - immunology Signaling TLR4 protein Toll-like receptors Transforming growth factor Transforming growth factor-b Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Recent advances in endotoxin tolerance |
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