Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung
Background/Aims: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been st...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2017-12, Vol.44 (4), p.1526-1536 |
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| creator | Tai, Wenlin Xu, Yiheng Ding, Jiawei Wu, Hanxin Du, Ming Qu, Xiaoyuan Gao, Ling Li, Jinyu Dong, Zhaoxing |
| description | Background/Aims: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). Methods: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. Results: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). Conclusion: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung. |
| doi_str_mv | 10.1159/000485647 |
| format | Article |
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To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). Methods: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. Results: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). Conclusion: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000485647</identifier><identifier>PMID: 29197869</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acute lung injury (ALI) ; Acute Lung Injury - etiology ; Acute Lung Injury - pathology ; Animals ; Biomarkers ; Bleomycin - pharmacology ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchoalveolar Lavage Fluid - cytology ; Care and treatment ; Cells, Cultured ; Chemokines ; Chemokines - genetics ; Chemokines - metabolism ; Collagen ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Development and progression ; Disease Models, Animal ; Fibroblasts ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibrocytes ; Gene expression ; Growth factors ; Health aspects ; Infections ; Laboratory animals ; Leukocytes, Mononuclear - cytology ; Leukocytes, Mononuclear - drug effects ; Lipopolysaccharide (LPS) ; Lipopolysaccharides - toxicity ; Lung - immunology ; Lung - metabolism ; Lung diseases ; Macrophage inflammatory protein 2 (MIP-2) ; Male ; Mice ; Mice, Inbred BALB C ; Mortality ; Multiple organ dysfunction syndrome ; Myeloperoxidase (MPO) ; Neutrophils ; Neutrophils - immunology ; Neutrophils - physiology ; Original Paper ; Peroxidase - metabolism ; Rodents ; Sepsis ; Smooth muscle ; Tumor necrosis factor-TNF ; Wound healing</subject><ispartof>Cellular Physiology and Biochemistry, 2017-12, Vol.44 (4), p.1526-1536</ispartof><rights>2017 The Author(s). Published by S. Karger AG, Basel</rights><rights>2017 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2017 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c596t-c531c8f65baa892934e3ed5473b47da04268615ff892dd4d4f825d31d757a1503</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,861,2096,27616,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29197869$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tai, Wenlin</creatorcontrib><creatorcontrib>Xu, Yiheng</creatorcontrib><creatorcontrib>Ding, Jiawei</creatorcontrib><creatorcontrib>Wu, Hanxin</creatorcontrib><creatorcontrib>Du, Ming</creatorcontrib><creatorcontrib>Qu, Xiaoyuan</creatorcontrib><creatorcontrib>Gao, Ling</creatorcontrib><creatorcontrib>Li, Jinyu</creatorcontrib><creatorcontrib>Dong, Zhaoxing</creatorcontrib><title>Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). Methods: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. Results: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). Conclusion: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung.</description><subject>Acute lung injury (ALI)</subject><subject>Acute Lung Injury - etiology</subject><subject>Acute Lung Injury - pathology</subject><subject>Animals</subject><subject>Biomarkers</subject><subject>Bleomycin - pharmacology</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>Care and treatment</subject><subject>Cells, Cultured</subject><subject>Chemokines</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Fibroblasts</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrocytes</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Infections</subject><subject>Laboratory animals</subject><subject>Leukocytes, Mononuclear - cytology</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Lipopolysaccharide (LPS)</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Lung diseases</subject><subject>Macrophage inflammatory protein 2 (MIP-2)</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mortality</subject><subject>Multiple organ dysfunction syndrome</subject><subject>Myeloperoxidase (MPO)</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - physiology</subject><subject>Original Paper</subject><subject>Peroxidase - metabolism</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Smooth muscle</subject><subject>Tumor necrosis factor-TNF</subject><subject>Wound healing</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkkuP0zAQgCMEYh9w4I5QJC7LoYvt-JVjKSxUqgAhOFuOPW7dTeKu4yD1Z_CPcZtSJIQsjT3jb56aoniB0S3GrH6LEKKScSoeFZeYEjyrhZCP8xthNpO1FBfF1TBsUVZFTZ4WF6TGtZC8vix-3fkmBrNPMJTzDlofok5Qzs2Y5Wrs1-Wy345xXzb78j2YCHrwR6NrddfpFPLXYp_Cve-h1L0tFxvoJm0FP6EdjsZvYEdz8PsMY4pht_FtTmHGbmx18qEvfV-mzZTwWfHE6XaA56f7uvhx9-H74tNs9eXjcjFfzQyrecqywkY6zhqtZU3qikIFllFRNVRYjSjhkmPmXP60llrqJGG2wlYwoTFD1XWxnOLaoLdqF32n414F7dXREOJa6Zi8aUFZl31MU1uuJaVENEjjhiBqcSPz3A-xbqZYuxgeRhiS6vxgoG11D2EcVJ42qRBnnGf09T_oNoyxz50qgrHAlEspMnU7UWud8_vehRS1ycdC503owflsn_NKMELwsYI3k4OJYRgiuHNHGKnDkqjzkmT21amEsenAnsk_W_G3xnsd1xDPwOLruymE2lmXqZf_pU5ZfgPgastk</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Tai, Wenlin</creator><creator>Xu, Yiheng</creator><creator>Ding, Jiawei</creator><creator>Wu, Hanxin</creator><creator>Du, Ming</creator><creator>Qu, Xiaoyuan</creator><creator>Gao, Ling</creator><creator>Li, Jinyu</creator><creator>Dong, Zhaoxing</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>IAO</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20171201</creationdate><title>Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung</title><author>Tai, Wenlin ; Xu, Yiheng ; Ding, Jiawei ; Wu, Hanxin ; Du, Ming ; Qu, Xiaoyuan ; Gao, Ling ; Li, Jinyu ; Dong, Zhaoxing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c596t-c531c8f65baa892934e3ed5473b47da04268615ff892dd4d4f825d31d757a1503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acute lung injury (ALI)</topic><topic>Acute Lung Injury - etiology</topic><topic>Acute Lung Injury - pathology</topic><topic>Animals</topic><topic>Biomarkers</topic><topic>Bleomycin - pharmacology</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>Care and treatment</topic><topic>Cells, Cultured</topic><topic>Chemokines</topic><topic>Chemokines - genetics</topic><topic>Chemokines - metabolism</topic><topic>Collagen</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>Fibroblasts</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrocytes</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Infections</topic><topic>Laboratory animals</topic><topic>Leukocytes, Mononuclear - cytology</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Lipopolysaccharide (LPS)</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung - immunology</topic><topic>Lung - metabolism</topic><topic>Lung diseases</topic><topic>Macrophage inflammatory protein 2 (MIP-2)</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mortality</topic><topic>Multiple organ dysfunction syndrome</topic><topic>Myeloperoxidase (MPO)</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - physiology</topic><topic>Original Paper</topic><topic>Peroxidase - metabolism</topic><topic>Rodents</topic><topic>Sepsis</topic><topic>Smooth muscle</topic><topic>Tumor necrosis factor-TNF</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tai, Wenlin</creatorcontrib><creatorcontrib>Xu, Yiheng</creatorcontrib><creatorcontrib>Ding, Jiawei</creatorcontrib><creatorcontrib>Wu, Hanxin</creatorcontrib><creatorcontrib>Du, Ming</creatorcontrib><creatorcontrib>Qu, Xiaoyuan</creatorcontrib><creatorcontrib>Gao, Ling</creatorcontrib><creatorcontrib>Li, Jinyu</creatorcontrib><creatorcontrib>Dong, Zhaoxing</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</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>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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tai, Wenlin</au><au>Xu, Yiheng</au><au>Ding, Jiawei</au><au>Wu, Hanxin</au><au>Du, Ming</au><au>Qu, Xiaoyuan</au><au>Gao, Ling</au><au>Li, Jinyu</au><au>Dong, Zhaoxing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>44</volume><issue>4</issue><spage>1526</spage><epage>1536</epage><pages>1526-1536</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). Methods: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. Results: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). Conclusion: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29197869</pmid><doi>10.1159/000485647</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute lung injury (ALI) Acute Lung Injury - etiology Acute Lung Injury - pathology Animals Biomarkers Bleomycin - pharmacology Bronchoalveolar Lavage Fluid - chemistry Bronchoalveolar Lavage Fluid - cytology Care and treatment Cells, Cultured Chemokines Chemokines - genetics Chemokines - metabolism Collagen Cytokines Cytokines - genetics Cytokines - metabolism Development and progression Disease Models, Animal Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism Fibrocytes Gene expression Growth factors Health aspects Infections Laboratory animals Leukocytes, Mononuclear - cytology Leukocytes, Mononuclear - drug effects Lipopolysaccharide (LPS) Lipopolysaccharides - toxicity Lung - immunology Lung - metabolism Lung diseases Macrophage inflammatory protein 2 (MIP-2) Male Mice Mice, Inbred BALB C Mortality Multiple organ dysfunction syndrome Myeloperoxidase (MPO) Neutrophils Neutrophils - immunology Neutrophils - physiology Original Paper Peroxidase - metabolism Rodents Sepsis Smooth muscle Tumor necrosis factor-TNF Wound healing |
| title | Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung |
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