Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease
Background and Aims Fibrosis is a major complication of inflammatory bowel disease (IBD), which may be mediated by the intestinal fibroblast. Our aim was to isolate and characterize mucosal fibroblasts from histologically normal intestine (control), ulcerative colitis (UC), inflamed Crohn's dis...
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| Veröffentlicht in: | Inflammatory bowel diseases 2001-08, Vol.7 (3), p.226-236 |
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| creator | Lawrance, Ian Craig Maxwell, Lesley Doe, William |
| description | Background and Aims
Fibrosis is a major complication of inflammatory bowel disease (IBD), which may be mediated by the intestinal fibroblast. Our aim was to isolate and characterize mucosal fibroblasts from histologically normal intestine (control), ulcerative colitis (UC), inflamed Crohn's disease (CD), and fibrosed CD intestine.
Methods
Fibroblasts were characterized by light and electron microscopy and immunohistochemistry. Fibroblast collagen secretion and proliferation were determined by 3H‐proline and 3H‐thymidine incorporation, and the effects of exposure to interleukin (IL)‐1β, basic fibroblast growth factor (bFGF), platelet‐derived growth factor (PDGF), transforming growth factor (TGF)‐β1, insulin‐like growth factor (IGF)‐1, and macrophage colony stimulating factor (M‐CSF) were determined.
Results
No difference in doubling time was observed between the fibroblast populations from UC and CD intestine. All proliferated faster than fibroblasts from control intestine. Collagen secretion from IBD fibroblasts, independent of type, was increased compared with control fibroblasts and PDGF, bFGF, and TGF‐β1‐induced collagen secretion from IBD fibroblasts.
Conclusions
These results suggest the presence of an activated subpopulation of fibroblasts in both UC and CD tissue irrespective of the presence of tissue fibrosis or disease type. |
| doi_str_mv | 10.1097/00054725-200108000-00008 |
| format | Article |
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Fibrosis is a major complication of inflammatory bowel disease (IBD), which may be mediated by the intestinal fibroblast. Our aim was to isolate and characterize mucosal fibroblasts from histologically normal intestine (control), ulcerative colitis (UC), inflamed Crohn's disease (CD), and fibrosed CD intestine.
Methods
Fibroblasts were characterized by light and electron microscopy and immunohistochemistry. Fibroblast collagen secretion and proliferation were determined by 3H‐proline and 3H‐thymidine incorporation, and the effects of exposure to interleukin (IL)‐1β, basic fibroblast growth factor (bFGF), platelet‐derived growth factor (PDGF), transforming growth factor (TGF)‐β1, insulin‐like growth factor (IGF)‐1, and macrophage colony stimulating factor (M‐CSF) were determined.
Results
No difference in doubling time was observed between the fibroblast populations from UC and CD intestine. All proliferated faster than fibroblasts from control intestine. Collagen secretion from IBD fibroblasts, independent of type, was increased compared with control fibroblasts and PDGF, bFGF, and TGF‐β1‐induced collagen secretion from IBD fibroblasts.
Conclusions
These results suggest the presence of an activated subpopulation of fibroblasts in both UC and CD tissue irrespective of the presence of tissue fibrosis or disease type.</description><identifier>ISSN: 1078-0998</identifier><identifier>EISSN: 1536-4844</identifier><identifier>DOI: 10.1097/00054725-200108000-00008</identifier><identifier>PMID: 11515849</identifier><language>eng</language><publisher>Philadelphia: Lippincott Williams & Wilkins, Inc</publisher><subject>Actins - biosynthesis ; Adult ; Colitis, Ulcerative - metabolism ; Colitis, Ulcerative - pathology ; Collagen ; Collagen - metabolism ; Colonies ; Crohn Disease - metabolism ; Crohn Disease - pathology ; Crohn's disease ; Cytokines ; Cytokines - metabolism ; Desmin - biosynthesis ; Electron microscopy ; Female ; Fibroblast ; Fibroblast growth factor 2 ; Fibroblasts ; Fibroblasts - metabolism ; Fibrosis ; Humans ; Immunohistochemistry ; Inflammation ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Inflammatory Bowel Diseases - metabolism ; Inflammatory Bowel Diseases - pathology ; Insulin-like growth factors ; Interleukins ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine ; Macrophage colony-stimulating factor ; Macrophages ; Male ; Middle Aged ; Mucosa ; Platelet-derived growth factor ; Transforming growth factor ; Ulcerative colitis ; Vimentin - biosynthesis</subject><ispartof>Inflammatory bowel diseases, 2001-08, Vol.7 (3), p.226-236</ispartof><rights>Copyright © 2001 Crohn's & Colitis Foundation of America, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1097%2F00054725-200108000-00008$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1097%2F00054725-200108000-00008$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11515849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lawrance, Ian Craig</creatorcontrib><creatorcontrib>Maxwell, Lesley</creatorcontrib><creatorcontrib>Doe, William</creatorcontrib><title>Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease</title><title>Inflammatory bowel diseases</title><addtitle>Inflamm Bowel Dis</addtitle><description>Background and Aims
Fibrosis is a major complication of inflammatory bowel disease (IBD), which may be mediated by the intestinal fibroblast. Our aim was to isolate and characterize mucosal fibroblasts from histologically normal intestine (control), ulcerative colitis (UC), inflamed Crohn's disease (CD), and fibrosed CD intestine.
Methods
Fibroblasts were characterized by light and electron microscopy and immunohistochemistry. Fibroblast collagen secretion and proliferation were determined by 3H‐proline and 3H‐thymidine incorporation, and the effects of exposure to interleukin (IL)‐1β, basic fibroblast growth factor (bFGF), platelet‐derived growth factor (PDGF), transforming growth factor (TGF)‐β1, insulin‐like growth factor (IGF)‐1, and macrophage colony stimulating factor (M‐CSF) were determined.
Results
No difference in doubling time was observed between the fibroblast populations from UC and CD intestine. All proliferated faster than fibroblasts from control intestine. Collagen secretion from IBD fibroblasts, independent of type, was increased compared with control fibroblasts and PDGF, bFGF, and TGF‐β1‐induced collagen secretion from IBD fibroblasts.
Conclusions
These results suggest the presence of an activated subpopulation of fibroblasts in both UC and CD tissue irrespective of the presence of tissue fibrosis or disease type.</description><subject>Actins - biosynthesis</subject><subject>Adult</subject><subject>Colitis, Ulcerative - metabolism</subject><subject>Colitis, Ulcerative - pathology</subject><subject>Collagen</subject><subject>Collagen - metabolism</subject><subject>Colonies</subject><subject>Crohn Disease - metabolism</subject><subject>Crohn Disease - pathology</subject><subject>Crohn's disease</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Desmin - biosynthesis</subject><subject>Electron microscopy</subject><subject>Female</subject><subject>Fibroblast</subject><subject>Fibroblast growth factor 2</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Inflammatory Bowel Diseases - metabolism</subject><subject>Inflammatory Bowel Diseases - pathology</subject><subject>Insulin-like growth factors</subject><subject>Interleukins</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine</subject><subject>Macrophage colony-stimulating factor</subject><subject>Macrophages</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mucosa</subject><subject>Platelet-derived growth factor</subject><subject>Transforming growth factor</subject><subject>Ulcerative colitis</subject><subject>Vimentin - biosynthesis</subject><issn>1078-0998</issn><issn>1536-4844</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUlPxSAQx4nRuH8Fw0lP1WEpLUd9romJF--EwtSgtDxLX8z79uJ-M0Bm-0GG-RNCGZwy0M0ZANSy4XXFARi0JazKgXaD7LJaqEq2Um4WH5q2Aq3bHbKX8zMAL0tvkx3Gala3Uu-Sl_M444SeTpiXacxIU0_DOGOew2gjHVYu5WL70E2pizbPmc6JLqf0mXnCMTjq1nN6CSPmcrPsPtphsHOa1rRLbxipDxltxgOy1duY8fDb7pPH66vHxW11_3Bztzi_r5a89FppRHBKcQHee82Kj171Uih02taguG9qZBq9k9px20neM9YhgOsUNij2ycnXs6XJ11X5iBlCdhijHTGtstHAhRCqlYU8_pdsGGNSqw_w6BtcdQN6s5zCYKe1-ZljARZfwFuIuP6rg_nQy_zoZX71Mp96mbuLS9GUuAEBrXgHKdiLMQ</recordid><startdate>200108</startdate><enddate>200108</enddate><creator>Lawrance, Ian Craig</creator><creator>Maxwell, Lesley</creator><creator>Doe, William</creator><general>Lippincott Williams & Wilkins, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>200108</creationdate><title>Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease</title><author>Lawrance, Ian Craig ; Maxwell, Lesley ; Doe, William</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2998-9ee0c66230ddd910c6ed6f436ec9a5062d75e19edc49c2ab42f11be00cb6e7e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Actins - biosynthesis</topic><topic>Adult</topic><topic>Colitis, Ulcerative - metabolism</topic><topic>Colitis, Ulcerative - pathology</topic><topic>Collagen</topic><topic>Collagen - metabolism</topic><topic>Colonies</topic><topic>Crohn Disease - metabolism</topic><topic>Crohn Disease - pathology</topic><topic>Crohn's disease</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Desmin - biosynthesis</topic><topic>Electron microscopy</topic><topic>Female</topic><topic>Fibroblast</topic><topic>Fibroblast growth factor 2</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Inflammatory Bowel Diseases - metabolism</topic><topic>Inflammatory Bowel Diseases - pathology</topic><topic>Insulin-like growth factors</topic><topic>Interleukins</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine</topic><topic>Macrophage colony-stimulating factor</topic><topic>Macrophages</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mucosa</topic><topic>Platelet-derived growth factor</topic><topic>Transforming growth factor</topic><topic>Ulcerative colitis</topic><topic>Vimentin - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lawrance, Ian Craig</creatorcontrib><creatorcontrib>Maxwell, Lesley</creatorcontrib><creatorcontrib>Doe, William</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Inflammatory bowel diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lawrance, Ian Craig</au><au>Maxwell, Lesley</au><au>Doe, William</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease</atitle><jtitle>Inflammatory bowel diseases</jtitle><addtitle>Inflamm Bowel Dis</addtitle><date>2001-08</date><risdate>2001</risdate><volume>7</volume><issue>3</issue><spage>226</spage><epage>236</epage><pages>226-236</pages><issn>1078-0998</issn><eissn>1536-4844</eissn><abstract>Background and Aims
Fibrosis is a major complication of inflammatory bowel disease (IBD), which may be mediated by the intestinal fibroblast. Our aim was to isolate and characterize mucosal fibroblasts from histologically normal intestine (control), ulcerative colitis (UC), inflamed Crohn's disease (CD), and fibrosed CD intestine.
Methods
Fibroblasts were characterized by light and electron microscopy and immunohistochemistry. Fibroblast collagen secretion and proliferation were determined by 3H‐proline and 3H‐thymidine incorporation, and the effects of exposure to interleukin (IL)‐1β, basic fibroblast growth factor (bFGF), platelet‐derived growth factor (PDGF), transforming growth factor (TGF)‐β1, insulin‐like growth factor (IGF)‐1, and macrophage colony stimulating factor (M‐CSF) were determined.
Results
No difference in doubling time was observed between the fibroblast populations from UC and CD intestine. All proliferated faster than fibroblasts from control intestine. Collagen secretion from IBD fibroblasts, independent of type, was increased compared with control fibroblasts and PDGF, bFGF, and TGF‐β1‐induced collagen secretion from IBD fibroblasts.
Conclusions
These results suggest the presence of an activated subpopulation of fibroblasts in both UC and CD tissue irrespective of the presence of tissue fibrosis or disease type.</abstract><cop>Philadelphia</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>11515849</pmid><doi>10.1097/00054725-200108000-00008</doi><tpages>11</tpages></addata></record> |
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| ispartof | Inflammatory bowel diseases, 2001-08, Vol.7 (3), p.226-236 |
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| source | Wiley-Blackwell Journals; MEDLINE; Oxford Academic |
| subjects | Actins - biosynthesis Adult Colitis, Ulcerative - metabolism Colitis, Ulcerative - pathology Collagen Collagen - metabolism Colonies Crohn Disease - metabolism Crohn Disease - pathology Crohn's disease Cytokines Cytokines - metabolism Desmin - biosynthesis Electron microscopy Female Fibroblast Fibroblast growth factor 2 Fibroblasts Fibroblasts - metabolism Fibrosis Humans Immunohistochemistry Inflammation Inflammatory bowel disease Inflammatory bowel diseases Inflammatory Bowel Diseases - metabolism Inflammatory Bowel Diseases - pathology Insulin-like growth factors Interleukins Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Intestine Macrophage colony-stimulating factor Macrophages Male Middle Aged Mucosa Platelet-derived growth factor Transforming growth factor Ulcerative colitis Vimentin - biosynthesis |
| title | Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease |
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