Interferon-β induces hepatocyte growth factor in monocytes of multiple sclerosis patients
Interferon-β is a first-line therapy used to prevent relapses in relapsing-remitting multiple sclerosis. The clinical benefit of interferon-β in relapsing-remitting multiple sclerosis is attributed to its immunomodulatory effects on inflammatory mediators and T cell reactivity. Here, we evaluated th...
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| Veröffentlicht in: | PloS one 2012-11, Vol.7 (11), p.e49882 |
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| creator | Molnarfi, Nicolas Benkhoucha, Mahdia Bjarnadóttir, Kristbjörg Juillard, Catherine Lalive, Patrice H |
| description | Interferon-β is a first-line therapy used to prevent relapses in relapsing-remitting multiple sclerosis. The clinical benefit of interferon-β in relapsing-remitting multiple sclerosis is attributed to its immunomodulatory effects on inflammatory mediators and T cell reactivity. Here, we evaluated the production of hepatocyte growth factor, a neuroprotective and neuroinflammation-suppressive mediator, by peripheral blood mononuclear cells collected from interferon-β--treated relapsing-remitting multiple sclerosis patients, relapsing remitting multiple sclerosis patients not treated with interferon-β, and healthy volunteers. Using intracellular flow cytometry analysis, increased production of hepatocyte growth factor was observed in circulating CD14(+) monocytes from patients undergoing long-term treatment with interferon-β versus untreated patients. Complementary in vitro studies confirmed that treatment with interferon-β induced rapid and transient transcription of the hepatocyte growth factor gene in CD14(+) monocytes and that intracellular and secreted monocytic hepatocyte growth factor protein levels were markedly stimulated by interferon-β treatment. Additional exploration revealed that "pro-inflammatory" (CD14(+)CD16(+)) monocytes produced similar levels of hepatocyte growth factor in response to interferon-β as "classical" (CD14(+)CD16(-)) monocytes, and that CD14(+) monocytes but not CD4(+) T cells express the hepatocyte growth factor receptor c-Met. Our findings suggest that interferon-β may mediate some of its therapeutic effects in relapsing-remitting multiple sclerosis through the induction of hepatocyte growth factor by blood monocytes by coupling immune regulation and neuroprotection. |
| doi_str_mv | 10.1371/journal.pone.0049882 |
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The clinical benefit of interferon-β in relapsing-remitting multiple sclerosis is attributed to its immunomodulatory effects on inflammatory mediators and T cell reactivity. Here, we evaluated the production of hepatocyte growth factor, a neuroprotective and neuroinflammation-suppressive mediator, by peripheral blood mononuclear cells collected from interferon-β--treated relapsing-remitting multiple sclerosis patients, relapsing remitting multiple sclerosis patients not treated with interferon-β, and healthy volunteers. Using intracellular flow cytometry analysis, increased production of hepatocyte growth factor was observed in circulating CD14(+) monocytes from patients undergoing long-term treatment with interferon-β versus untreated patients. Complementary in vitro studies confirmed that treatment with interferon-β induced rapid and transient transcription of the hepatocyte growth factor gene in CD14(+) monocytes and that intracellular and secreted monocytic hepatocyte growth factor protein levels were markedly stimulated by interferon-β treatment. Additional exploration revealed that "pro-inflammatory" (CD14(+)CD16(+)) monocytes produced similar levels of hepatocyte growth factor in response to interferon-β as "classical" (CD14(+)CD16(-)) monocytes, and that CD14(+) monocytes but not CD4(+) T cells express the hepatocyte growth factor receptor c-Met. Our findings suggest that interferon-β may mediate some of its therapeutic effects in relapsing-remitting multiple sclerosis through the induction of hepatocyte growth factor by blood monocytes by coupling immune regulation and neuroprotection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0049882</identifier><identifier>PMID: 23166786</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Biology ; Blood ; Blotting, Western ; c-Met protein ; CD14 antigen ; CD16 antigen ; CD4 antigen ; Cytometry ; Enzyme-Linked Immunosorbent Assay ; Exploration ; Female ; Flow Cytometry ; Gene Expression Regulation - drug effects ; Growth factors ; Hepatocyte growth factor ; Hepatocyte Growth Factor - biosynthesis ; Hospitals ; Humans ; Immunology ; Immunomodulation ; Immunoregulation ; Inflammation ; Interferon ; Interferon-beta - pharmacology ; Interferon-beta - therapeutic use ; Intracellular ; Laboratories ; Leukocytes (mononuclear) ; Leukocytes, Mononuclear - metabolism ; Lymphocytes ; Lymphocytes T ; Male ; Medicine ; Middle Aged ; Monocytes ; Multiple sclerosis ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - metabolism ; Nervous system ; Neurodegeneration ; Neurology ; Neuroprotection ; Neurosciences ; Pathology ; Patients ; Peripheral blood mononuclear cells ; Proto-Oncogene Proteins c-met - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; Switzerland ; Transcription ; β-Interferon</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e49882</ispartof><rights>2012 Molnarfi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Molnarfi et al 2012 Molnarfi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-1bc0dab515cef4540c8b14f7e981e3b8dc284bd1dce55f69c2bf66e2ca1c85ad3</citedby><cites>FETCH-LOGICAL-c526t-1bc0dab515cef4540c8b14f7e981e3b8dc284bd1dce55f69c2bf66e2ca1c85ad3</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/PMC3498184/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498184/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23166786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Weber, Martin Sebastian</contributor><creatorcontrib>Molnarfi, Nicolas</creatorcontrib><creatorcontrib>Benkhoucha, Mahdia</creatorcontrib><creatorcontrib>Bjarnadóttir, Kristbjörg</creatorcontrib><creatorcontrib>Juillard, Catherine</creatorcontrib><creatorcontrib>Lalive, Patrice H</creatorcontrib><title>Interferon-β induces hepatocyte growth factor in monocytes of multiple sclerosis patients</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Interferon-β is a first-line therapy used to prevent relapses in relapsing-remitting multiple sclerosis. The clinical benefit of interferon-β in relapsing-remitting multiple sclerosis is attributed to its immunomodulatory effects on inflammatory mediators and T cell reactivity. Here, we evaluated the production of hepatocyte growth factor, a neuroprotective and neuroinflammation-suppressive mediator, by peripheral blood mononuclear cells collected from interferon-β--treated relapsing-remitting multiple sclerosis patients, relapsing remitting multiple sclerosis patients not treated with interferon-β, and healthy volunteers. Using intracellular flow cytometry analysis, increased production of hepatocyte growth factor was observed in circulating CD14(+) monocytes from patients undergoing long-term treatment with interferon-β versus untreated patients. Complementary in vitro studies confirmed that treatment with interferon-β induced rapid and transient transcription of the hepatocyte growth factor gene in CD14(+) monocytes and that intracellular and secreted monocytic hepatocyte growth factor protein levels were markedly stimulated by interferon-β treatment. Additional exploration revealed that "pro-inflammatory" (CD14(+)CD16(+)) monocytes produced similar levels of hepatocyte growth factor in response to interferon-β as "classical" (CD14(+)CD16(-)) monocytes, and that CD14(+) monocytes but not CD4(+) T cells express the hepatocyte growth factor receptor c-Met. Our findings suggest that interferon-β may mediate some of its therapeutic effects in relapsing-remitting multiple sclerosis through the induction of hepatocyte growth factor by blood monocytes by coupling immune regulation and neuroprotection.</description><subject>Adult</subject><subject>Biology</subject><subject>Blood</subject><subject>Blotting, Western</subject><subject>c-Met protein</subject><subject>CD14 antigen</subject><subject>CD16 antigen</subject><subject>CD4 antigen</subject><subject>Cytometry</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Exploration</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Growth factors</subject><subject>Hepatocyte growth factor</subject><subject>Hepatocyte Growth Factor - biosynthesis</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunology</subject><subject>Immunomodulation</subject><subject>Immunoregulation</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon-beta - 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drug effects</topic><topic>Growth factors</topic><topic>Hepatocyte growth factor</topic><topic>Hepatocyte Growth Factor - biosynthesis</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunology</topic><topic>Immunomodulation</topic><topic>Immunoregulation</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interferon-beta - pharmacology</topic><topic>Interferon-beta - therapeutic use</topic><topic>Intracellular</topic><topic>Laboratories</topic><topic>Leukocytes (mononuclear)</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medicine</topic><topic>Middle Aged</topic><topic>Monocytes</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - drug therapy</topic><topic>Multiple Sclerosis - metabolism</topic><topic>Nervous system</topic><topic>Neurodegeneration</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Pathology</topic><topic>Patients</topic><topic>Peripheral blood mononuclear cells</topic><topic>Proto-Oncogene Proteins c-met - 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The clinical benefit of interferon-β in relapsing-remitting multiple sclerosis is attributed to its immunomodulatory effects on inflammatory mediators and T cell reactivity. Here, we evaluated the production of hepatocyte growth factor, a neuroprotective and neuroinflammation-suppressive mediator, by peripheral blood mononuclear cells collected from interferon-β--treated relapsing-remitting multiple sclerosis patients, relapsing remitting multiple sclerosis patients not treated with interferon-β, and healthy volunteers. Using intracellular flow cytometry analysis, increased production of hepatocyte growth factor was observed in circulating CD14(+) monocytes from patients undergoing long-term treatment with interferon-β versus untreated patients. Complementary in vitro studies confirmed that treatment with interferon-β induced rapid and transient transcription of the hepatocyte growth factor gene in CD14(+) monocytes and that intracellular and secreted monocytic hepatocyte growth factor protein levels were markedly stimulated by interferon-β treatment. Additional exploration revealed that "pro-inflammatory" (CD14(+)CD16(+)) monocytes produced similar levels of hepatocyte growth factor in response to interferon-β as "classical" (CD14(+)CD16(-)) monocytes, and that CD14(+) monocytes but not CD4(+) T cells express the hepatocyte growth factor receptor c-Met. Our findings suggest that interferon-β may mediate some of its therapeutic effects in relapsing-remitting multiple sclerosis through the induction of hepatocyte growth factor by blood monocytes by coupling immune regulation and neuroprotection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23166786</pmid><doi>10.1371/journal.pone.0049882</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Biology Blood Blotting, Western c-Met protein CD14 antigen CD16 antigen CD4 antigen Cytometry Enzyme-Linked Immunosorbent Assay Exploration Female Flow Cytometry Gene Expression Regulation - drug effects Growth factors Hepatocyte growth factor Hepatocyte Growth Factor - biosynthesis Hospitals Humans Immunology Immunomodulation Immunoregulation Inflammation Interferon Interferon-beta - pharmacology Interferon-beta - therapeutic use Intracellular Laboratories Leukocytes (mononuclear) Leukocytes, Mononuclear - metabolism Lymphocytes Lymphocytes T Male Medicine Middle Aged Monocytes Multiple sclerosis Multiple Sclerosis - drug therapy Multiple Sclerosis - metabolism Nervous system Neurodegeneration Neurology Neuroprotection Neurosciences Pathology Patients Peripheral blood mononuclear cells Proto-Oncogene Proteins c-met - metabolism Reverse Transcriptase Polymerase Chain Reaction Rodents Switzerland Transcription β-Interferon |
| title | Interferon-β induces hepatocyte growth factor in monocytes of multiple sclerosis patients |
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