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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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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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4565141</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>902334133</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4459-410a01fb4c83e93d46c780a1ec0069a60e3e81dc602cfdfba8a114088a27c4ca3</originalsourceid><addsrcrecordid>eNp1kctO3DAUhq2qqDNcFrxAlV3FImDHnsTeVCp3pJFYAGvrjHMyY-TEUztpmR2PwDPyJBhmROkCeWFL_vSdX-cnZJ_RQ0ZpcWRn9WFBi0p9IWM24WUupBBf05tWMqdKyRHZjvE-oemob2TEKsULVVVjAhcBusF5s-oxa8EEv1zAHDPjne9Wz49Psbft4KC33TxrwPQ-ZNCisz5AjzE7vblJkO3qwWCd4cMSg22x68G9Kmxv4y7ZasBF3NvcO-Tu_Oz25DKfXl9cnfya5kaIicoFo0BZMxNGclS8FqWpJAWGhtJSQUmRo2S1KWlhmrqZgQTGBJUSisoIA3yH_Fx7l8OsxdqkEAGcXqY8EFbag9X__3R2oef-jxaTcsIES4IfG0HwvweMvW5tNOgcdOiHqBUtOE8cT-TBmkzrijFg8z6FUf3aiE6N6LdGEvv9Y6x_5KaCBBytgb_W4epzk746Pl0rXwC0nZqv</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>902334133</pqid></control><display><type>article</type><title>Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis</title><source>Wiley Online Library - AutoHoldings Journals</source><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><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.</creator><creatorcontrib>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.</creatorcontrib><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)</description><identifier>ISSN: 1078-0998</identifier><identifier>EISSN: 1536-4844</identifier><identifier>DOI: 10.1002/ibd.20279</identifier><identifier>PMID: 17932977</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>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</subject><ispartof>Inflammatory bowel diseases, 2008-01, Vol.14 (1), p.88-99</ispartof><rights>Copyright © 2007 Crohn's & Colitis Foundation of America, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4459-410a01fb4c83e93d46c780a1ec0069a60e3e81dc602cfdfba8a114088a27c4ca3</citedby><cites>FETCH-LOGICAL-c4459-410a01fb4c83e93d46c780a1ec0069a60e3e81dc602cfdfba8a114088a27c4ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fibd.20279$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fibd.20279$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,781,785,886,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17932977$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><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><title>Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis</title><title>Inflammatory bowel diseases</title><addtitle>Inflamm Bowel Dis</addtitle><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)</description><subject>Animal models</subject><subject>Animals</subject><subject>Clinical trials</subject><subject>Colitis</subject><subject>Colitis - chemically induced</subject><subject>Colitis - immunology</subject><subject>Colitis - pathology</subject><subject>Colitis - physiopathology</subject><subject>Colon - pathology</subject><subject>CpG islands</subject><subject>Crohn's disease</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Dextran sulfate</subject><subject>Dextran Sulfate - toxicity</subject><subject>dextran sulfate sodium</subject><subject>Drinking water</subject><subject>DSS</subject><subject>Female</subject><subject>GM‐CSF</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - immunology</subject><subject>Growth factors</subject><subject>Hemopoiesis</subject><subject>Homeodomain Proteins - genetics</subject><subject>Immune system</subject><subject>Immunoglobulins</subject><subject>Inflammatory bowel diseases</subject><subject>Interferon</subject><subject>Interferon Type I - immunology</subject><subject>Interleukin 1</subject><subject>Interleukin-1beta - genetics</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine</subject><subject>Lectins</subject><subject>Lymphocytes B</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Monoclonal antibodies</subject><subject>Mucosa</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Polymerase chain reaction</subject><subject>Probes</subject><subject>RAG1 protein</subject><subject>Recombinant Proteins</subject><subject>Remission</subject><subject>sargramostim</subject><subject>Sodium</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>1078-0998</issn><issn>1536-4844</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctO3DAUhq2qqDNcFrxAlV3FImDHnsTeVCp3pJFYAGvrjHMyY-TEUztpmR2PwDPyJBhmROkCeWFL_vSdX-cnZJ_RQ0ZpcWRn9WFBi0p9IWM24WUupBBf05tWMqdKyRHZjvE-oemob2TEKsULVVVjAhcBusF5s-oxa8EEv1zAHDPjne9Wz49Psbft4KC33TxrwPQ-ZNCisz5AjzE7vblJkO3qwWCd4cMSg22x68G9Kmxv4y7ZasBF3NvcO-Tu_Oz25DKfXl9cnfya5kaIicoFo0BZMxNGclS8FqWpJAWGhtJSQUmRo2S1KWlhmrqZgQTGBJUSisoIA3yH_Fx7l8OsxdqkEAGcXqY8EFbag9X__3R2oef-jxaTcsIES4IfG0HwvweMvW5tNOgcdOiHqBUtOE8cT-TBmkzrijFg8z6FUf3aiE6N6LdGEvv9Y6x_5KaCBBytgb_W4epzk746Pl0rXwC0nZqv</recordid><startdate>200801</startdate><enddate>200801</enddate><creator>Sainathan, Satheesh K.</creator><creator>Hanna, Eyad M.</creator><creator>Gong, Qingqing</creator><creator>Bishnupuri, Kumar S.</creator><creator>Luo, Qizhi</creator><creator>Colonna, Marco</creator><creator>White, Frances V.</creator><creator>Croze, Ed</creator><creator>Houchen, Courtney</creator><creator>Anant, Shrikant</creator><creator>Dieckgraefe, Brian K.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><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>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>200801</creationdate><title>Granulocyte macrophage colony‐stimulating factor ameliorates DSS‐induced experimental colitis</title><author>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.</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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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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