LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation
Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic inte...
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| Veröffentlicht in: | Molecular medicine reports 2018-04, Vol.17 (4), p.5484-5491 |
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| creator | Liu, Xuefang Yin, Sugai Chen, Yulong Wu, Yaosong Zheng, Wanchun Dong, Haoran Bai, Yan Qin, Yanqin Li, Jiansheng Feng, Suxiang Zhao, Peng |
| description | Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation. |
| doi_str_mv | 10.3892/mmr.2018.8542 |
| format | Article |
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The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8542</identifier><identifier>PMID: 29393460</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Activator protein 1 ; Bacterial infections ; Biomarkers ; Biotechnology ; Cell activation ; Cell culture ; Cell Line ; Cell Survival ; Chronic obstructive pulmonary disease ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Deoxyribonucleic acid ; DNA ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelium ; Gene Expression Regulation - drug effects ; Gram-negative bacteria ; Humans ; Inflammation ; Inflammation Mediators - metabolism ; Interleukin 6 ; Interleukin 8 ; Intracellular signalling ; Janus kinase ; Kinases ; Lipopolysaccharides ; Lipopolysaccharides - immunology ; Lipopolysaccharides - pharmacology ; Lung carcinoma ; Lung diseases ; Macrophages ; Macrophages - immunology ; Macrophages - metabolism ; MAP kinase ; Metalloproteinase ; NF-kappa B - metabolism ; NF-κB protein ; Nuclear transport ; Phosphorylation ; Protein Binding ; Protein expression ; Protein kinase ; Proteins ; Respiratory Mucosa - immunology ; Respiratory Mucosa - metabolism ; Respiratory tract ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism ; Tissue inhibitor of metalloproteinases ; Transcription Factor AP-1 - metabolism ; Transcription factors ; Tumor necrosis factor-TNF</subject><ispartof>Molecular medicine reports, 2018-04, Vol.17 (4), p.5484-5491</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2752-a21fefed5b540a4c0c746d5468546e023819542cc604ba9caefd124b0ef2fca83</citedby><cites>FETCH-LOGICAL-c2752-a21fefed5b540a4c0c746d5468546e023819542cc604ba9caefd124b0ef2fca83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29393460$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xuefang</creatorcontrib><creatorcontrib>Yin, Sugai</creatorcontrib><creatorcontrib>Chen, Yulong</creatorcontrib><creatorcontrib>Wu, Yaosong</creatorcontrib><creatorcontrib>Zheng, Wanchun</creatorcontrib><creatorcontrib>Dong, Haoran</creatorcontrib><creatorcontrib>Bai, Yan</creatorcontrib><creatorcontrib>Qin, Yanqin</creatorcontrib><creatorcontrib>Li, Jiansheng</creatorcontrib><creatorcontrib>Feng, Suxiang</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><title>LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation.</description><subject>Activator protein 1</subject><subject>Bacterial infections</subject><subject>Biomarkers</subject><subject>Biotechnology</subject><subject>Cell activation</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelium</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gram-negative bacteria</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Intracellular signalling</subject><subject>Janus kinase</subject><subject>Kinases</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lung carcinoma</subject><subject>Lung diseases</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>MAP kinase</subject><subject>Metalloproteinase</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Phosphorylation</subject><subject>Protein Binding</subject><subject>Protein expression</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Respiratory Mucosa - immunology</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory tract</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tissue inhibitor of metalloproteinases</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-TNF</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNo9kLtOAzEQRS0E4hEoaZElWjbYXu_DZUC8pAiQCPVq4p0lhn1h7wLp6Kn4HT6Cj-BLcCBQzWh0517dQ8guZ8MwVeKwquxQMJ4O00iKFbLJE8WDkDG5utyFUskG2XLunrE4EpFaJxtChSqUMdskb-Prm6_Xd1PnvcactrYxdVFCVUHX2DnV8655MDVSfGktOmeampqazvoKagrGPsOcYmu6GZYGSqqxLB2FOqcVaNu0M7hDR58M0MtTn_L5cXRAbyajSUgbS0fX_sQp6M48Qeedt8laAaXDneUckNvTk8nxeTC-Ors4Ho0DLZJIBCB4gQXm0TSSDKRmOpFxHsnYE4iRiTDlyrPQOmZyCkoDFjkXcsqwEIWGNByQ_V9f3_axR9dl901vax-ZLUiqNIm9y4AEvypfxDmLRdZaU4GdZ5xlC_SZR__zkC3Qe_3e0rWfVpj_q_9Yh9_h24Qz</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Liu, Xuefang</creator><creator>Yin, Sugai</creator><creator>Chen, Yulong</creator><creator>Wu, Yaosong</creator><creator>Zheng, Wanchun</creator><creator>Dong, Haoran</creator><creator>Bai, Yan</creator><creator>Qin, Yanqin</creator><creator>Li, Jiansheng</creator><creator>Feng, Suxiang</creator><creator>Zhao, Peng</creator><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20180401</creationdate><title>LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation</title><author>Liu, Xuefang ; Yin, Sugai ; Chen, Yulong ; Wu, Yaosong ; Zheng, Wanchun ; Dong, Haoran ; Bai, Yan ; Qin, Yanqin ; Li, Jiansheng ; Feng, Suxiang ; Zhao, Peng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2752-a21fefed5b540a4c0c746d5468546e023819542cc604ba9caefd124b0ef2fca83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activator protein 1</topic><topic>Bacterial infections</topic><topic>Biomarkers</topic><topic>Biotechnology</topic><topic>Cell activation</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelium</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gram-negative bacteria</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Intracellular signalling</topic><topic>Janus kinase</topic><topic>Kinases</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - immunology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lung carcinoma</topic><topic>Lung diseases</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>MAP kinase</topic><topic>Metalloproteinase</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Nuclear transport</topic><topic>Phosphorylation</topic><topic>Protein Binding</topic><topic>Protein expression</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Respiratory Mucosa - immunology</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory tract</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tissue inhibitor of metalloproteinases</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xuefang</creatorcontrib><creatorcontrib>Yin, Sugai</creatorcontrib><creatorcontrib>Chen, Yulong</creatorcontrib><creatorcontrib>Wu, Yaosong</creatorcontrib><creatorcontrib>Zheng, Wanchun</creatorcontrib><creatorcontrib>Dong, Haoran</creatorcontrib><creatorcontrib>Bai, Yan</creatorcontrib><creatorcontrib>Qin, Yanqin</creatorcontrib><creatorcontrib>Li, Jiansheng</creatorcontrib><creatorcontrib>Feng, Suxiang</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xuefang</au><au>Yin, Sugai</au><au>Chen, Yulong</au><au>Wu, Yaosong</au><au>Zheng, Wanchun</au><au>Dong, Haoran</au><au>Bai, Yan</au><au>Qin, Yanqin</au><au>Li, Jiansheng</au><au>Feng, Suxiang</au><au>Zhao, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>17</volume><issue>4</issue><spage>5484</spage><epage>5491</epage><pages>5484-5491</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>29393460</pmid><doi>10.3892/mmr.2018.8542</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Activator protein 1 Bacterial infections Biomarkers Biotechnology Cell activation Cell culture Cell Line Cell Survival Chronic obstructive pulmonary disease Cytokines Cytokines - genetics Cytokines - metabolism Deoxyribonucleic acid DNA Epithelial cells Epithelial Cells - metabolism Epithelium Gene Expression Regulation - drug effects Gram-negative bacteria Humans Inflammation Inflammation Mediators - metabolism Interleukin 6 Interleukin 8 Intracellular signalling Janus kinase Kinases Lipopolysaccharides Lipopolysaccharides - immunology Lipopolysaccharides - pharmacology Lung carcinoma Lung diseases Macrophages Macrophages - immunology Macrophages - metabolism MAP kinase Metalloproteinase NF-kappa B - metabolism NF-κB protein Nuclear transport Phosphorylation Protein Binding Protein expression Protein kinase Proteins Respiratory Mucosa - immunology Respiratory Mucosa - metabolism Respiratory tract Rodents Signal transduction Signal Transduction - drug effects STAT3 Transcription Factor - metabolism Tissue inhibitor of metalloproteinases Transcription Factor AP-1 - metabolism Transcription factors Tumor necrosis factor-TNF |
| title | LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation |
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