Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis

Background: Sargramostim, granulocyte macrophage colony‐stimulating factor (GM‐CSF), a hematopoietic growth factor, stimulates cells of the intestinal innate immune system. Clinical trials show that sargramostim induces clinical response and remission in patients with active Crohn's disease. To...

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Veröffentlicht in:Inflammatory bowel diseases 2008-01, Vol.14 (1), p.88-99
Hauptverfasser: Sainathan, Satheesh K., Hanna, Eyad M., Gong, Qingqing, Bishnupuri, Kumar S., Luo, Qizhi, Colonna, Marco, White, Frances V., Croze, Ed, Houchen, Courtney, Anant, Shrikant, Dieckgraefe, Brian K.
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container_end_page 99
container_issue 1
container_start_page 88
container_title Inflammatory bowel diseases
container_volume 14
creator Sainathan, Satheesh K.
Hanna, Eyad M.
Gong, Qingqing
Bishnupuri, Kumar S.
Luo, Qizhi
Colonna, Marco
White, Frances V.
Croze, Ed
Houchen, Courtney
Anant, Shrikant
Dieckgraefe, Brian K.
description Background: Sargramostim, granulocyte macrophage colony‐stimulating factor (GM‐CSF), a hematopoietic growth factor, stimulates cells of the intestinal innate immune system. Clinical trials show that sargramostim induces clinical response and remission in patients with active Crohn's disease. To study the mechanism, we examined the effects of GM‐CSF in the dextran sulfate sodium (DSS)‐induced acute colitis model. We hypothesized that GM‐CSF may work through effects on dendritic cells (DCs). Methods: Acute colitis was induced in Balb/c mice by administration of DSS in drinking water. Mice were treated with daily GM‐CSF or phosphate‐buffered saline (PBS). To probe the role of plasmacytoid DCs (pDCs) in the response to GM‐CSF, we further examined the effects of monoclonal antibody 440c, which is specific for a sialic acid‐binding immunoglobulin (Ig)‐like lectin expressed on pDCs. Results: GM‐CSF ameliorates acute DSS‐induced colitis, resulting in significantly improved clinical parameters and histology. Microarray analysis showed reduced expression of proinflammatory genes including TNF‐α and IL1‐β; the results were further confirmed by real‐time reverse‐transcriptase polymerase chain reaction and serum Bio‐plex analysis. GM‐CSF treatment significantly expands pDCs and type 1 IFN production. Administration of mAb 440c completely blocked the therapeutic effect of GM‐CSF. GM‐CSF is also effective in RAG1−/− mice, demonstrating activity‐independent effects on T and B cells. IFN‐β administration mimics the therapeutic effect of GM‐CSF in DSS‐treated mice. GM‐CSF increases systemic and mucosal type 1 IFN expression and exhibits synergy with pDC activators, such as microbial cytosine‐phosphate‐guanosine (CpG) DNA. Conclusions: GM‐CSF is effective in the treatment of DSS colitis in a mechanism involving the 440c+ pDC population. (Inflamm Bowel Dis 2007)
doi_str_mv 10.1002/ibd.20279
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Clinical trials show that sargramostim induces clinical response and remission in patients with active Crohn's disease. To study the mechanism, we examined the effects of GM‐CSF in the dextran sulfate sodium (DSS)‐induced acute colitis model. We hypothesized that GM‐CSF may work through effects on dendritic cells (DCs). Methods: Acute colitis was induced in Balb/c mice by administration of DSS in drinking water. Mice were treated with daily GM‐CSF or phosphate‐buffered saline (PBS). To probe the role of plasmacytoid DCs (pDCs) in the response to GM‐CSF, we further examined the effects of monoclonal antibody 440c, which is specific for a sialic acid‐binding immunoglobulin (Ig)‐like lectin expressed on pDCs. Results: GM‐CSF ameliorates acute DSS‐induced colitis, resulting in significantly improved clinical parameters and histology. Microarray analysis showed reduced expression of proinflammatory genes including TNF‐α and IL1‐β; the results were further confirmed by real‐time reverse‐transcriptase polymerase chain reaction and serum Bio‐plex analysis. GM‐CSF treatment significantly expands pDCs and type 1 IFN production. Administration of mAb 440c completely blocked the therapeutic effect of GM‐CSF. GM‐CSF is also effective in RAG1−/− mice, demonstrating activity‐independent effects on T and B cells. IFN‐β administration mimics the therapeutic effect of GM‐CSF in DSS‐treated mice. GM‐CSF increases systemic and mucosal type 1 IFN expression and exhibits synergy with pDC activators, such as microbial cytosine‐phosphate‐guanosine (CpG) DNA. Conclusions: GM‐CSF is effective in the treatment of DSS colitis in a mechanism involving the 440c+ pDC population. 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Clinical trials show that sargramostim induces clinical response and remission in patients with active Crohn's disease. To study the mechanism, we examined the effects of GM‐CSF in the dextran sulfate sodium (DSS)‐induced acute colitis model. We hypothesized that GM‐CSF may work through effects on dendritic cells (DCs). Methods: Acute colitis was induced in Balb/c mice by administration of DSS in drinking water. Mice were treated with daily GM‐CSF or phosphate‐buffered saline (PBS). To probe the role of plasmacytoid DCs (pDCs) in the response to GM‐CSF, we further examined the effects of monoclonal antibody 440c, which is specific for a sialic acid‐binding immunoglobulin (Ig)‐like lectin expressed on pDCs. Results: GM‐CSF ameliorates acute DSS‐induced colitis, resulting in significantly improved clinical parameters and histology. Microarray analysis showed reduced expression of proinflammatory genes including TNF‐α and IL1‐β; the results were further confirmed by real‐time reverse‐transcriptase polymerase chain reaction and serum Bio‐plex analysis. GM‐CSF treatment significantly expands pDCs and type 1 IFN production. Administration of mAb 440c completely blocked the therapeutic effect of GM‐CSF. GM‐CSF is also effective in RAG1−/− mice, demonstrating activity‐independent effects on T and B cells. IFN‐β administration mimics the therapeutic effect of GM‐CSF in DSS‐treated mice. GM‐CSF increases systemic and mucosal type 1 IFN expression and exhibits synergy with pDC activators, such as microbial cytosine‐phosphate‐guanosine (CpG) DNA. Conclusions: GM‐CSF is effective in the treatment of DSS colitis in a mechanism involving the 440c+ pDC population. 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Hanna, Eyad M. ; Gong, Qingqing ; Bishnupuri, Kumar S. ; Luo, Qizhi ; Colonna, Marco ; White, Frances V. ; Croze, Ed ; Houchen, Courtney ; Anant, Shrikant ; Dieckgraefe, Brian K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4459-410a01fb4c83e93d46c780a1ec0069a60e3e81dc602cfdfba8a114088a27c4ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Clinical trials</topic><topic>Colitis</topic><topic>Colitis - chemically induced</topic><topic>Colitis - immunology</topic><topic>Colitis - pathology</topic><topic>Colitis - physiopathology</topic><topic>Colon - pathology</topic><topic>CpG islands</topic><topic>Crohn's disease</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Dextran sulfate</topic><topic>Dextran Sulfate - toxicity</topic><topic>dextran sulfate sodium</topic><topic>Drinking water</topic><topic>DSS</topic><topic>Female</topic><topic>GM‐CSF</topic><topic>Granulocyte-macrophage colony-stimulating factor</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - immunology</topic><topic>Growth factors</topic><topic>Hemopoiesis</topic><topic>Homeodomain Proteins - genetics</topic><topic>Immune system</topic><topic>Immunoglobulins</topic><topic>Inflammatory bowel diseases</topic><topic>Interferon</topic><topic>Interferon Type I - immunology</topic><topic>Interleukin 1</topic><topic>Interleukin-1beta - genetics</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine</topic><topic>Lectins</topic><topic>Lymphocytes B</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Monoclonal antibodies</topic><topic>Mucosa</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Polymerase chain reaction</topic><topic>Probes</topic><topic>RAG1 protein</topic><topic>Recombinant Proteins</topic><topic>Remission</topic><topic>sargramostim</topic><topic>Sodium</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sainathan, Satheesh K.</creatorcontrib><creatorcontrib>Hanna, Eyad M.</creatorcontrib><creatorcontrib>Gong, Qingqing</creatorcontrib><creatorcontrib>Bishnupuri, Kumar S.</creatorcontrib><creatorcontrib>Luo, Qizhi</creatorcontrib><creatorcontrib>Colonna, Marco</creatorcontrib><creatorcontrib>White, Frances V.</creatorcontrib><creatorcontrib>Croze, Ed</creatorcontrib><creatorcontrib>Houchen, Courtney</creatorcontrib><creatorcontrib>Anant, Shrikant</creatorcontrib><creatorcontrib>Dieckgraefe, Brian K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Inflammatory bowel diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sainathan, Satheesh K.</au><au>Hanna, Eyad M.</au><au>Gong, Qingqing</au><au>Bishnupuri, Kumar S.</au><au>Luo, Qizhi</au><au>Colonna, Marco</au><au>White, Frances V.</au><au>Croze, Ed</au><au>Houchen, Courtney</au><au>Anant, Shrikant</au><au>Dieckgraefe, Brian K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis</atitle><jtitle>Inflammatory bowel diseases</jtitle><addtitle>Inflamm Bowel Dis</addtitle><date>2008-01</date><risdate>2008</risdate><volume>14</volume><issue>1</issue><spage>88</spage><epage>99</epage><pages>88-99</pages><issn>1078-0998</issn><eissn>1536-4844</eissn><abstract>Background: Sargramostim, granulocyte macrophage colony‐stimulating factor (GM‐CSF), a hematopoietic growth factor, stimulates cells of the intestinal innate immune system. Clinical trials show that sargramostim induces clinical response and remission in patients with active Crohn's disease. To study the mechanism, we examined the effects of GM‐CSF in the dextran sulfate sodium (DSS)‐induced acute colitis model. We hypothesized that GM‐CSF may work through effects on dendritic cells (DCs). Methods: Acute colitis was induced in Balb/c mice by administration of DSS in drinking water. Mice were treated with daily GM‐CSF or phosphate‐buffered saline (PBS). To probe the role of plasmacytoid DCs (pDCs) in the response to GM‐CSF, we further examined the effects of monoclonal antibody 440c, which is specific for a sialic acid‐binding immunoglobulin (Ig)‐like lectin expressed on pDCs. Results: GM‐CSF ameliorates acute DSS‐induced colitis, resulting in significantly improved clinical parameters and histology. Microarray analysis showed reduced expression of proinflammatory genes including TNF‐α and IL1‐β; the results were further confirmed by real‐time reverse‐transcriptase polymerase chain reaction and serum Bio‐plex analysis. GM‐CSF treatment significantly expands pDCs and type 1 IFN production. Administration of mAb 440c completely blocked the therapeutic effect of GM‐CSF. GM‐CSF is also effective in RAG1−/− mice, demonstrating activity‐independent effects on T and B cells. IFN‐β administration mimics the therapeutic effect of GM‐CSF in DSS‐treated mice. GM‐CSF increases systemic and mucosal type 1 IFN expression and exhibits synergy with pDC activators, such as microbial cytosine‐phosphate‐guanosine (CpG) DNA. Conclusions: GM‐CSF is effective in the treatment of DSS colitis in a mechanism involving the 440c+ pDC population. (Inflamm Bowel Dis 2007)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17932977</pmid><doi>10.1002/ibd.20279</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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source Wiley Online Library - AutoHoldings Journals; MEDLINE; Oxford University Press Journals All Titles (1996-Current)
subjects Animal models
Animals
Clinical trials
Colitis
Colitis - chemically induced
Colitis - immunology
Colitis - pathology
Colitis - physiopathology
Colon - pathology
CpG islands
Crohn's disease
Dendritic cells
Dendritic Cells - immunology
Dextran sulfate
Dextran Sulfate - toxicity
dextran sulfate sodium
Drinking water
DSS
Female
GM‐CSF
Granulocyte-macrophage colony-stimulating factor
Granulocyte-Macrophage Colony-Stimulating Factor - immunology
Growth factors
Hemopoiesis
Homeodomain Proteins - genetics
Immune system
Immunoglobulins
Inflammatory bowel diseases
Interferon
Interferon Type I - immunology
Interleukin 1
Interleukin-1beta - genetics
Intestinal Mucosa - pathology
Intestine
Lectins
Lymphocytes B
Mice
Mice, Inbred BALB C
Mice, Knockout
Monoclonal antibodies
Mucosa
Oligonucleotide Array Sequence Analysis
Polymerase chain reaction
Probes
RAG1 protein
Recombinant Proteins
Remission
sargramostim
Sodium
Tumor Necrosis Factor-alpha - genetics
title Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis
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