Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins
Sixty, relapsing remitting (RR) multiple sclerosis (MS) patients, who underwent treatment with glatiramer acetate (GA), interferon (IFN)-beta 1a, and immunoglobulins (Igs) (20 per treatment group), were assessed for levels of brain-derived neurotrophic factor (BDNF) in the supernatants of unstimulat...
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| Veröffentlicht in: | Multiple sclerosis 2007-04, Vol.13 (3), p.313-331 |
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| creator | Sarchielli, P Zaffaroni, M Floridi, A Greco, L Candeliere, A Mattioni, A Tenaglia, S Di Filippo, M Calabresi, P |
| description | Sixty, relapsing remitting (RR) multiple sclerosis (MS) patients, who underwent treatment with glatiramer acetate (GA), interferon (IFN)-beta 1a, and immunoglobulins (Igs) (20 per treatment group), were assessed for levels of brain-derived neurotrophic factor (BDNF) in the supernatants of unstimulated and stimulated peripheral blood mononuclear cells (PBMCs) in the first year of treatment. Phytohemagglutinin (PHA), anti-OKT3 antibody, myelin basic protein (MPB) and GA were used as stimuli. Cytokine responses by ELISPOT and lymphoproliferative responses were also assessed. The GA-treated MS patient group showed a progressive increase in BDNF levels, from baseline to month three; thereafter, the levels remained stable and significantly greater compared with baseline and controls (ANOVA=P |
| doi_str_mv | 10.1177/1352458506070146 |
| format | Article |
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Phytohemagglutinin (PHA), anti-OKT3 antibody, myelin basic protein (MPB) and GA were used as stimuli. Cytokine responses by ELISPOT and lymphoproliferative responses were also assessed. The GA-treated MS patient group showed a progressive increase in BDNF levels, from baseline to month three; thereafter, the levels remained stable and significantly greater compared with baseline and controls (ANOVA=P<0.001). IFN-beta 1a had no effect on BDNF production, whereas Igs induced a slight decrease (ANOVA=P<0.04). ELISPOT analysis revealed a significant decrease of IFN-gamma, an increase of interleukin (IL)-4 and IL-5 in GA-treated MS patients, and an increase of IL-10 in patients treated with IFN-beta 1a and GA. No significant correlation was found between BDNF secretion in the supernatants of PBMCs and cytokine response, lesional load, and measures of atrophy. Increased BDNF production related to GA treatment can have implications for understanding the mechanism of action of this immunomodulatory agent, in light of evidence suggesting its effects in promoting neuroprotective immunity in MS patients; however, a clinically measurable effect, especially in terms of an impact on actual disease progression, remains to be established.</description><identifier>ISSN: 1352-4585</identifier><identifier>DOI: 10.1177/1352458506070146</identifier><identifier>PMID: 17439900</identifier><language>eng</language><publisher>England</publisher><subject>Adjuvants, Immunologic - therapeutic use ; Adult ; Brain - anatomy & histology ; Brain - pathology ; Brain-Derived Neurotrophic Factor - blood ; Female ; Follow-Up Studies ; Glatiramer Acetate ; Humans ; Immunoglobulins - therapeutic use ; Interferon beta-1a ; Interferon-beta - therapeutic use ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - physiology ; Lymphocyte Activation ; Lymphocyte Count ; Magnetic Resonance Imaging ; Male ; Multiple Sclerosis, Relapsing-Remitting - blood ; Multiple Sclerosis, Relapsing-Remitting - drug therapy ; Peptides - therapeutic use ; Time Factors</subject><ispartof>Multiple sclerosis, 2007-04, Vol.13 (3), p.313-331</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17439900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sarchielli, P</creatorcontrib><creatorcontrib>Zaffaroni, M</creatorcontrib><creatorcontrib>Floridi, A</creatorcontrib><creatorcontrib>Greco, L</creatorcontrib><creatorcontrib>Candeliere, A</creatorcontrib><creatorcontrib>Mattioni, A</creatorcontrib><creatorcontrib>Tenaglia, S</creatorcontrib><creatorcontrib>Di Filippo, M</creatorcontrib><creatorcontrib>Calabresi, P</creatorcontrib><title>Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins</title><title>Multiple sclerosis</title><addtitle>Mult Scler</addtitle><description>Sixty, relapsing remitting (RR) multiple sclerosis (MS) patients, who underwent treatment with glatiramer acetate (GA), interferon (IFN)-beta 1a, and immunoglobulins (Igs) (20 per treatment group), were assessed for levels of brain-derived neurotrophic factor (BDNF) in the supernatants of unstimulated and stimulated peripheral blood mononuclear cells (PBMCs) in the first year of treatment. Phytohemagglutinin (PHA), anti-OKT3 antibody, myelin basic protein (MPB) and GA were used as stimuli. Cytokine responses by ELISPOT and lymphoproliferative responses were also assessed. The GA-treated MS patient group showed a progressive increase in BDNF levels, from baseline to month three; thereafter, the levels remained stable and significantly greater compared with baseline and controls (ANOVA=P<0.001). IFN-beta 1a had no effect on BDNF production, whereas Igs induced a slight decrease (ANOVA=P<0.04). ELISPOT analysis revealed a significant decrease of IFN-gamma, an increase of interleukin (IL)-4 and IL-5 in GA-treated MS patients, and an increase of IL-10 in patients treated with IFN-beta 1a and GA. No significant correlation was found between BDNF secretion in the supernatants of PBMCs and cytokine response, lesional load, and measures of atrophy. Increased BDNF production related to GA treatment can have implications for understanding the mechanism of action of this immunomodulatory agent, in light of evidence suggesting its effects in promoting neuroprotective immunity in MS patients; however, a clinically measurable effect, especially in terms of an impact on actual disease progression, remains to be established.</description><subject>Adjuvants, Immunologic - therapeutic use</subject><subject>Adult</subject><subject>Brain - anatomy & histology</subject><subject>Brain - pathology</subject><subject>Brain-Derived Neurotrophic Factor - blood</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Glatiramer Acetate</subject><subject>Humans</subject><subject>Immunoglobulins - therapeutic use</subject><subject>Interferon beta-1a</subject><subject>Interferon-beta - therapeutic use</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - physiology</subject><subject>Lymphocyte Activation</subject><subject>Lymphocyte Count</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Multiple Sclerosis, Relapsing-Remitting - blood</subject><subject>Multiple Sclerosis, Relapsing-Remitting - drug therapy</subject><subject>Peptides - therapeutic use</subject><subject>Time Factors</subject><issn>1352-4585</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtP5TAQhV2AlsduvxWaioqAnThxXCLES0Jii936ynYm9xo5dvADdH_d_jVyedRUI53zzRkdDSG_GT1nTIgL1rQ1b_uWdlRQxrs9criTqp12QI5SeqKUCtG0P8gBE7yRktJD8v9PDEMx2QYPYQQdlfXVgNG-4AAeSww5hnljDYzK5BBBb2EKPvhiHKoIBp1Lu81ZZYs-J3i1eQNTcdnODiEtWAzJJsgRVV5C3_21W_CoJoygDObFOAPrM8ZxoX2lFwmYOgPlB9jY9QaGkPD9jp2m4sPaBV2c9ekn2R-VS_jrcx6TfzfXf6_uqofH2_ury4dqZoLmqu17ITSnmnHecVNLrho0oq9riR3XppV8FGxELTk3gmnFe1lLo4XusaZj2xyT04_cOYbngimvJpt25ZXHUNJK0Ea2tP4eZLLjfcP4Ap58gkVPOKzmaCcVt6uv3zRvv6KT2A</recordid><startdate>200704</startdate><enddate>200704</enddate><creator>Sarchielli, P</creator><creator>Zaffaroni, M</creator><creator>Floridi, A</creator><creator>Greco, L</creator><creator>Candeliere, A</creator><creator>Mattioni, A</creator><creator>Tenaglia, S</creator><creator>Di Filippo, M</creator><creator>Calabresi, P</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200704</creationdate><title>Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins</title><author>Sarchielli, P ; Zaffaroni, M ; Floridi, A ; Greco, L ; Candeliere, A ; Mattioni, A ; Tenaglia, S ; Di Filippo, M ; Calabresi, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p170t-58877b40b14464c294a3ec78229e64bc594f71feb944c71ba48929cb7b8e20f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adjuvants, Immunologic - therapeutic use</topic><topic>Adult</topic><topic>Brain - anatomy & histology</topic><topic>Brain - pathology</topic><topic>Brain-Derived Neurotrophic Factor - blood</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Glatiramer Acetate</topic><topic>Humans</topic><topic>Immunoglobulins - therapeutic use</topic><topic>Interferon beta-1a</topic><topic>Interferon-beta - therapeutic use</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - physiology</topic><topic>Lymphocyte Activation</topic><topic>Lymphocyte Count</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Multiple Sclerosis, Relapsing-Remitting - blood</topic><topic>Multiple Sclerosis, Relapsing-Remitting - drug therapy</topic><topic>Peptides - therapeutic use</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sarchielli, P</creatorcontrib><creatorcontrib>Zaffaroni, M</creatorcontrib><creatorcontrib>Floridi, A</creatorcontrib><creatorcontrib>Greco, L</creatorcontrib><creatorcontrib>Candeliere, A</creatorcontrib><creatorcontrib>Mattioni, A</creatorcontrib><creatorcontrib>Tenaglia, S</creatorcontrib><creatorcontrib>Di Filippo, M</creatorcontrib><creatorcontrib>Calabresi, P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Multiple sclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sarchielli, P</au><au>Zaffaroni, M</au><au>Floridi, A</au><au>Greco, L</au><au>Candeliere, A</au><au>Mattioni, A</au><au>Tenaglia, S</au><au>Di Filippo, M</au><au>Calabresi, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins</atitle><jtitle>Multiple sclerosis</jtitle><addtitle>Mult Scler</addtitle><date>2007-04</date><risdate>2007</risdate><volume>13</volume><issue>3</issue><spage>313</spage><epage>331</epage><pages>313-331</pages><issn>1352-4585</issn><abstract>Sixty, relapsing remitting (RR) multiple sclerosis (MS) patients, who underwent treatment with glatiramer acetate (GA), interferon (IFN)-beta 1a, and immunoglobulins (Igs) (20 per treatment group), were assessed for levels of brain-derived neurotrophic factor (BDNF) in the supernatants of unstimulated and stimulated peripheral blood mononuclear cells (PBMCs) in the first year of treatment. Phytohemagglutinin (PHA), anti-OKT3 antibody, myelin basic protein (MPB) and GA were used as stimuli. Cytokine responses by ELISPOT and lymphoproliferative responses were also assessed. The GA-treated MS patient group showed a progressive increase in BDNF levels, from baseline to month three; thereafter, the levels remained stable and significantly greater compared with baseline and controls (ANOVA=P<0.001). IFN-beta 1a had no effect on BDNF production, whereas Igs induced a slight decrease (ANOVA=P<0.04). ELISPOT analysis revealed a significant decrease of IFN-gamma, an increase of interleukin (IL)-4 and IL-5 in GA-treated MS patients, and an increase of IL-10 in patients treated with IFN-beta 1a and GA. No significant correlation was found between BDNF secretion in the supernatants of PBMCs and cytokine response, lesional load, and measures of atrophy. Increased BDNF production related to GA treatment can have implications for understanding the mechanism of action of this immunomodulatory agent, in light of evidence suggesting its effects in promoting neuroprotective immunity in MS patients; however, a clinically measurable effect, especially in terms of an impact on actual disease progression, remains to be established.</abstract><cop>England</cop><pmid>17439900</pmid><doi>10.1177/1352458506070146</doi><tpages>19</tpages></addata></record> |
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| subjects | Adjuvants, Immunologic - therapeutic use Adult Brain - anatomy & histology Brain - pathology Brain-Derived Neurotrophic Factor - blood Female Follow-Up Studies Glatiramer Acetate Humans Immunoglobulins - therapeutic use Interferon beta-1a Interferon-beta - therapeutic use Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - physiology Lymphocyte Activation Lymphocyte Count Magnetic Resonance Imaging Male Multiple Sclerosis, Relapsing-Remitting - blood Multiple Sclerosis, Relapsing-Remitting - drug therapy Peptides - therapeutic use Time Factors |
| title | Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins |
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