Lack of T-bet reduces monocytic interleukin-12 formation and accelerates thrombus resolution in deep vein thrombosis
The role of leukocytes in deep vein thrombosis (DVT) resolution is incompletely understood. We determined how depletion of lysozyme positive (LysM + ) cells and a switched-off type 1 immune response influences thrombus resolution. DVT was induced in 12-week-old male mice by inferior vena cava (IVC)...
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| Veröffentlicht in: | Scientific reports 2018-02, Vol.8 (1), p.3013-10, Article 3013 |
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| creator | Schönfelder, Tanja Brandt, Moritz Kossmann, Sabine Knopp, Tanja Münzel, Thomas Walter, Ulrich Karbach, Susanne H. Wenzel, Philip |
| description | The role of leukocytes in deep vein thrombosis (DVT) resolution is incompletely understood. We determined how depletion of lysozyme positive (LysM
+
) cells and a switched-off type 1 immune response influences thrombus resolution. DVT was induced in 12-week-old male mice by inferior vena cava (IVC) stenosis. Toxin mediated depletion of myeloid cells improved thrombus resolution in mice with Cre-inducible expression of the diphtheria toxin receptor in LysM
+
cells. This correlated with decreased CD45
+
cells, a population shift of Gr-1
+
to Gr-1
−
CD11b
+
myelomonocytic cells (flow cytometry) and an increase in CC-chemokine ligand 2, interleukin-4 and interleukin-10 mRNA expressions. Tbx21
−/−
mice (lacking transcription factor T-bet and marked by an attenuated type 1 immune response) with DVT had faster thrombus resolution, a reduction of pro-inflammatory Ly6C
hi
monocytes in thrombi and decreased interleukin-12p40 mRNA expression than control mice resulting in increased vascular endothelial growth factor mRNA expression and improved neovascularization of thrombotic veins. Transfer of Tbx21
−/−
bone marrow into irradiated Tbx21
+/+
recipients lead to accelerated thrombus resolution with lower T-bet-dependent interleukin-12p40 mRNA levels following IVC-stenosis. We conclude that inhibition of Tbet
+
interleukin-12 forming myelomonocytic cells accelerated thrombus resolution. Modulating the inflammatory immune response might be an approach to improve therapy of DVT. |
| doi_str_mv | 10.1038/s41598-018-21273-5 |
| format | Article |
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+
) cells and a switched-off type 1 immune response influences thrombus resolution. DVT was induced in 12-week-old male mice by inferior vena cava (IVC) stenosis. Toxin mediated depletion of myeloid cells improved thrombus resolution in mice with Cre-inducible expression of the diphtheria toxin receptor in LysM
+
cells. This correlated with decreased CD45
+
cells, a population shift of Gr-1
+
to Gr-1
−
CD11b
+
myelomonocytic cells (flow cytometry) and an increase in CC-chemokine ligand 2, interleukin-4 and interleukin-10 mRNA expressions. Tbx21
−/−
mice (lacking transcription factor T-bet and marked by an attenuated type 1 immune response) with DVT had faster thrombus resolution, a reduction of pro-inflammatory Ly6C
hi
monocytes in thrombi and decreased interleukin-12p40 mRNA expression than control mice resulting in increased vascular endothelial growth factor mRNA expression and improved neovascularization of thrombotic veins. Transfer of Tbx21
−/−
bone marrow into irradiated Tbx21
+/+
recipients lead to accelerated thrombus resolution with lower T-bet-dependent interleukin-12p40 mRNA levels following IVC-stenosis. We conclude that inhibition of Tbet
+
interleukin-12 forming myelomonocytic cells accelerated thrombus resolution. Modulating the inflammatory immune response might be an approach to improve therapy of DVT.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-21273-5</identifier><identifier>PMID: 29445199</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/31 ; 59 ; 631/250/2500 ; 64 ; 64/60 ; 692/308/575 ; Blood clots ; Bone marrow ; CD11b antigen ; CD45 antigen ; Cytokines ; Diphtheria ; Diphtheria toxin ; Flow cytometry ; Gene expression ; Humanities and Social Sciences ; Immune response ; Inflammation ; Interleukin 10 ; Interleukin 12 ; Interleukin 4 ; Leukocytes ; Lysozyme ; Monocytes ; multidisciplinary ; Myeloid cells ; Rodents ; Science ; Science (multidisciplinary) ; Stenosis ; Thromboembolism ; Thrombosis ; Toxins ; Vascular endothelial growth factor ; Vascularization</subject><ispartof>Scientific reports, 2018-02, Vol.8 (1), p.3013-10, Article 3013</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-bcd72bdaa1d62389d4f240fe9e27af4507132d81efc0892f2d9113223502ad323</citedby><cites>FETCH-LOGICAL-c511t-bcd72bdaa1d62389d4f240fe9e27af4507132d81efc0892f2d9113223502ad323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813037/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813037/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29445199$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schönfelder, Tanja</creatorcontrib><creatorcontrib>Brandt, Moritz</creatorcontrib><creatorcontrib>Kossmann, Sabine</creatorcontrib><creatorcontrib>Knopp, Tanja</creatorcontrib><creatorcontrib>Münzel, Thomas</creatorcontrib><creatorcontrib>Walter, Ulrich</creatorcontrib><creatorcontrib>Karbach, Susanne H.</creatorcontrib><creatorcontrib>Wenzel, Philip</creatorcontrib><title>Lack of T-bet reduces monocytic interleukin-12 formation and accelerates thrombus resolution in deep vein thrombosis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The role of leukocytes in deep vein thrombosis (DVT) resolution is incompletely understood. We determined how depletion of lysozyme positive (LysM
+
) cells and a switched-off type 1 immune response influences thrombus resolution. DVT was induced in 12-week-old male mice by inferior vena cava (IVC) stenosis. Toxin mediated depletion of myeloid cells improved thrombus resolution in mice with Cre-inducible expression of the diphtheria toxin receptor in LysM
+
cells. This correlated with decreased CD45
+
cells, a population shift of Gr-1
+
to Gr-1
−
CD11b
+
myelomonocytic cells (flow cytometry) and an increase in CC-chemokine ligand 2, interleukin-4 and interleukin-10 mRNA expressions. Tbx21
−/−
mice (lacking transcription factor T-bet and marked by an attenuated type 1 immune response) with DVT had faster thrombus resolution, a reduction of pro-inflammatory Ly6C
hi
monocytes in thrombi and decreased interleukin-12p40 mRNA expression than control mice resulting in increased vascular endothelial growth factor mRNA expression and improved neovascularization of thrombotic veins. Transfer of Tbx21
−/−
bone marrow into irradiated Tbx21
+/+
recipients lead to accelerated thrombus resolution with lower T-bet-dependent interleukin-12p40 mRNA levels following IVC-stenosis. We conclude that inhibition of Tbet
+
interleukin-12 forming myelomonocytic cells accelerated thrombus resolution. Modulating the inflammatory immune response might be an approach to improve therapy of DVT.</description><subject>13</subject><subject>13/31</subject><subject>59</subject><subject>631/250/2500</subject><subject>64</subject><subject>64/60</subject><subject>692/308/575</subject><subject>Blood clots</subject><subject>Bone marrow</subject><subject>CD11b antigen</subject><subject>CD45 antigen</subject><subject>Cytokines</subject><subject>Diphtheria</subject><subject>Diphtheria toxin</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Humanities and Social Sciences</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin 12</subject><subject>Interleukin 4</subject><subject>Leukocytes</subject><subject>Lysozyme</subject><subject>Monocytes</subject><subject>multidisciplinary</subject><subject>Myeloid cells</subject><subject>Rodents</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Stenosis</subject><subject>Thromboembolism</subject><subject>Thrombosis</subject><subject>Toxins</subject><subject>Vascular endothelial growth factor</subject><subject>Vascularization</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUFrFTEQxxdRbKn9Ah4k4MVLajLZvN1cBClqhQde6jlkk9k27W7yTLKFfvvmva21ejAQZsj85j8Z_k3zlrMzzkT_Mbdcqp4y3lPg0AkqXzTHwFpJQQC8fJYfNac537B6JKiWq9fNUY2t5EodN2Vr7C2JI7mkAxaS0C0WM5ljiPa-eEt8KJgmXG59oBzIGNNsio-BmOCIsRYnTKbUlnKd4jwsuWrkOC0HxgfiEHfkDmu2AjH7_KZ5NZop4-ljPGl-fv1yeX5Btz--fT__vKVWcl7oYF0HgzOGuw2IXrl2hJaNqBA6M7aSdVyA6zmOlvUKRnCK1xcQkoFxAsRJ82nV3S3DjM5iKMlMepf8bNK9jsbrvyvBX-ureKdlzwUTXRX48CiQ4q8Fc9Gzz3XlyQSMS9bAGLQ9bDaqou__QW_ikkJd70Dt70ZWClbKpphzwvHpM5zpva969VVXX_XBV71vevd8jaeW3y5WQKxArqVwhenP7P_IPgA6qK98</recordid><startdate>20180214</startdate><enddate>20180214</enddate><creator>Schönfelder, Tanja</creator><creator>Brandt, Moritz</creator><creator>Kossmann, Sabine</creator><creator>Knopp, Tanja</creator><creator>Münzel, Thomas</creator><creator>Walter, Ulrich</creator><creator>Karbach, Susanne H.</creator><creator>Wenzel, Philip</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</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>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180214</creationdate><title>Lack of T-bet reduces monocytic interleukin-12 formation and accelerates thrombus resolution in deep vein thrombosis</title><author>Schönfelder, Tanja ; Brandt, Moritz ; Kossmann, Sabine ; Knopp, Tanja ; Münzel, Thomas ; Walter, Ulrich ; Karbach, Susanne H. ; Wenzel, Philip</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-bcd72bdaa1d62389d4f240fe9e27af4507132d81efc0892f2d9113223502ad323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13</topic><topic>13/31</topic><topic>59</topic><topic>631/250/2500</topic><topic>64</topic><topic>64/60</topic><topic>692/308/575</topic><topic>Blood clots</topic><topic>Bone marrow</topic><topic>CD11b antigen</topic><topic>CD45 antigen</topic><topic>Cytokines</topic><topic>Diphtheria</topic><topic>Diphtheria toxin</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Humanities and Social Sciences</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Interleukin 12</topic><topic>Interleukin 4</topic><topic>Leukocytes</topic><topic>Lysozyme</topic><topic>Monocytes</topic><topic>multidisciplinary</topic><topic>Myeloid cells</topic><topic>Rodents</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Stenosis</topic><topic>Thromboembolism</topic><topic>Thrombosis</topic><topic>Toxins</topic><topic>Vascular endothelial growth factor</topic><topic>Vascularization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schönfelder, Tanja</creatorcontrib><creatorcontrib>Brandt, Moritz</creatorcontrib><creatorcontrib>Kossmann, Sabine</creatorcontrib><creatorcontrib>Knopp, Tanja</creatorcontrib><creatorcontrib>Münzel, Thomas</creatorcontrib><creatorcontrib>Walter, Ulrich</creatorcontrib><creatorcontrib>Karbach, Susanne H.</creatorcontrib><creatorcontrib>Wenzel, Philip</creatorcontrib><collection>Springer Nature OA Free Journals</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>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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>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>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schönfelder, Tanja</au><au>Brandt, Moritz</au><au>Kossmann, Sabine</au><au>Knopp, Tanja</au><au>Münzel, Thomas</au><au>Walter, Ulrich</au><au>Karbach, Susanne H.</au><au>Wenzel, Philip</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of T-bet reduces monocytic interleukin-12 formation and accelerates thrombus resolution in deep vein thrombosis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-02-14</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>3013</spage><epage>10</epage><pages>3013-10</pages><artnum>3013</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The role of leukocytes in deep vein thrombosis (DVT) resolution is incompletely understood. We determined how depletion of lysozyme positive (LysM
+
) cells and a switched-off type 1 immune response influences thrombus resolution. DVT was induced in 12-week-old male mice by inferior vena cava (IVC) stenosis. Toxin mediated depletion of myeloid cells improved thrombus resolution in mice with Cre-inducible expression of the diphtheria toxin receptor in LysM
+
cells. This correlated with decreased CD45
+
cells, a population shift of Gr-1
+
to Gr-1
−
CD11b
+
myelomonocytic cells (flow cytometry) and an increase in CC-chemokine ligand 2, interleukin-4 and interleukin-10 mRNA expressions. Tbx21
−/−
mice (lacking transcription factor T-bet and marked by an attenuated type 1 immune response) with DVT had faster thrombus resolution, a reduction of pro-inflammatory Ly6C
hi
monocytes in thrombi and decreased interleukin-12p40 mRNA expression than control mice resulting in increased vascular endothelial growth factor mRNA expression and improved neovascularization of thrombotic veins. Transfer of Tbx21
−/−
bone marrow into irradiated Tbx21
+/+
recipients lead to accelerated thrombus resolution with lower T-bet-dependent interleukin-12p40 mRNA levels following IVC-stenosis. We conclude that inhibition of Tbet
+
interleukin-12 forming myelomonocytic cells accelerated thrombus resolution. Modulating the inflammatory immune response might be an approach to improve therapy of DVT.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29445199</pmid><doi>10.1038/s41598-018-21273-5</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 13 13/31 59 631/250/2500 64 64/60 692/308/575 Blood clots Bone marrow CD11b antigen CD45 antigen Cytokines Diphtheria Diphtheria toxin Flow cytometry Gene expression Humanities and Social Sciences Immune response Inflammation Interleukin 10 Interleukin 12 Interleukin 4 Leukocytes Lysozyme Monocytes multidisciplinary Myeloid cells Rodents Science Science (multidisciplinary) Stenosis Thromboembolism Thrombosis Toxins Vascular endothelial growth factor Vascularization |
| title | Lack of T-bet reduces monocytic interleukin-12 formation and accelerates thrombus resolution in deep vein thrombosis |
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