Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines

Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS‐induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS...

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Published in	Clinical and experimental immunology Vol. 114; no. 3; pp. 385 - 391
Main Authors	DIELEMAN, L. A, PALMEN, M. J. H. J, AKOL, H, BLOEMENA, E, PENA, A. S, MEUWISSEN, S. G. M, VAN REES, E. P
Format	Journal Article
Language	English
Published	Oxford BSL Blackwell Science Ltd 01.12.1998 Blackwell Oxford University Press Blackwell Publishing Ltd
Subjects	Animals Biological and medical sciences Chronic Disease colitis Colitis - chemically induced Colitis - immunology Colitis - pathology Cytokines - metabolism Dextran Sulfate dextran sulphate Disease Models, Animal Female Gastroenterology. Liver. Pancreas. Abdomen IL‐4 Interferon-gamma - metabolism interferon‐gamma Interleukin-4 - metabolism Interleukin-5 - metabolism Lymphocytes Medical sciences Mice Original Other diseases. Semiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Th1 Cells - immunology Th2 Cells - immunology Pathophysiology Cytokine Rodentia Th1 lymphocyte Helper cell Cellular immunity Inflammation Cell subpopulation Dextran Vertebrata Interleukin 4 Experimental disease Mammalia Interleukin 5 Mouse Animal Sodium sulfate T-Lymphocyte Digestive diseases Intestinal disease Th2 lymphocyte Inflammatory cell Colitis Gamma interferon
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Abstract	Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS‐induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2–5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon‐gamma (IFN‐γ), IL‐4 and IL‐5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4+ T cells. These CD4+ T cells showed a focal increase of IFN‐γ and IL‐4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS‐induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis.
AbstractList	Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS-induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2-5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon-gamma (IFN- gamma ), IL-4 and IL-5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4 super(+) T cells. These CD4 super(+) T cells showed a focal increase of IFN- gamma and IL-4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS-induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis. Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS-induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2-5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon-gamma (IFN-gamma), IL-4 and IL-5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4+ T cells. These CD4+ T cells showed a focal increase of IFN-gamma and IL-4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS-induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis. SUMMARY Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS-induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2–5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon-gamma (IFN-γ), IL-4 and IL-5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4+ T cells. These CD4+ T cells showed a focal increase of IFN-γ and IL-4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS-induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis. Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS-induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2–5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon-gamma (IFN-γ), IL-4 and IL-5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4 + T cells. These CD4 + T cells showed a focal increase of IFN-γ and IL-4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS-induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis. Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS‐induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2–5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon‐gamma (IFN‐γ), IL‐4 and IL‐5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4+ T cells. These CD4+ T cells showed a focal increase of IFN‐γ and IL‐4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS‐induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis.
Author	PEÑA Bloemena Palmen Dieleman Akol Meuwissen Van Rees
Author_xml	– sequence: 1 givenname: L. A surname: DIELEMAN fullname: DIELEMAN, L. A organization: Department of Gastroenterology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 2 givenname: M. J. H. J surname: PALMEN fullname: PALMEN, M. J. H. J organization: Department of Cell Biology/Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 3 givenname: H surname: AKOL fullname: AKOL, H organization: Department of Cell Biology/Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 4 givenname: E surname: BLOEMENA fullname: BLOEMENA, E organization: Department of Pathology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 5 givenname: A. S surname: PENA fullname: PENA, A. S organization: Department of Gastroenterology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 6 givenname: S. G. M surname: MEUWISSEN fullname: MEUWISSEN, S. G. M organization: Department of Gastroenterology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands – sequence: 7 givenname: E. P surname: VAN REES fullname: VAN REES, E. P organization: Department of Cell Biology/Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1590417$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/9844047$$D View this record in MEDLINE/PubMed
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Keywords	Pathophysiology Cytokine Rodentia Th1 lymphocyte Helper cell Cellular immunity Inflammation Cell subpopulation Dextran Vertebrata Interleukin 4 Experimental disease Mammalia Interleukin 5 Mouse Animal Sodium sulfate T-Lymphocyte Digestive diseases Intestinal disease Th2 lymphocyte Inflammatory cell Colitis Gamma interferon
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References	Ohkusa T (b16_335) 1995; 56 Wallace JL (b15_334) 1985; 30 Cooper H (b2_321) 1993; 69 Mullin G (b23_342) 1992; 102 Mullin GE (b28_347) 1996; 2 McDonald SAC (b27_346) 1997; 91 Graham RC (b4_323) 1966; 14 b25_344 Sartor RB (b22_341) 1994; 106 Reynolds DS (b12_331) 1987; 139 Yamada T (b14_333) 1992; 102 Desreumaux P (b30_349) 1997; 112 Sartor RB (b18_337) 1993; 104 b9_328 Berg DJ (b24_343) 1996; 98 Dieleman LA (b3_322) 1994; 107 Faulds P (b19_338) 1993; 45 Stevcea L (b29_348) 1996; 110 Coffman RL (b8_327) 1985; 69 Karttunnnen R (b26_345) 1994; 47 Pierres A (b6_325) 1984; 132 b17_336 Claassen E (b11_330) 1986; 34 Takahashi I (b31_350) 1997; 112 Murthy SN (b20_339) 1993; 38 Mosmann TR (b21_340) 1989; 46 Kraal G (b5_324) 1987; 26 Ledbetter JA (b7_326) 1979; 47 Dieleman LA (b13_332) 1996; 271 Schumacher JH (b10_329) 1988; 141 Okayasu I (b1_320) 1990; 98
References_xml	– volume: 69 start-page: 5 year: 1985 ident: b8_327 publication-title: Immunol Rev doi: 10.1111/j.1600-065X.1983.tb00446.x contributor: fullname: Coffman RL – volume: 141 start-page: 1576 year: 1988 ident: b10_329 publication-title: J Immunol doi: 10.4049/jimmunol.141.5.1576 contributor: fullname: Schumacher JH – volume: 69 start-page: 238 year: 1993 ident: b2_321 publication-title: Lab Invest contributor: fullname: Cooper H – volume: 47 start-page: 1015 year: 1994 ident: b26_345 publication-title: J Clin Pathol doi: 10.1136/jcp.47.11.1015 contributor: fullname: Karttunnnen R – volume: 271 start-page: G130 year: 1996 ident: b13_332 publication-title: Am J Physiol doi: 10.1152/ajpcell.1996.271.1.C130 contributor: fullname: Dieleman LA – volume: 112 start-page: 1876 year: 1997 ident: b31_350 publication-title: Gastroenterology doi: 10.1053/gast.1997.v112.pm9178680 contributor: fullname: Takahashi I – volume: 2 start-page: 16 year: 1996 ident: b28_347 publication-title: Inflammatory Bowel Dis doi: 10.1097/00054725-199603000-00004 contributor: fullname: Mullin GE – volume: 91 start-page: 73 year: 1997 ident: b27_346 publication-title: Immunology doi: 10.1046/j.1365-2567.1997.00217.x contributor: fullname: McDonald SAC – volume: 112 start-page: 118 year: 1997 ident: b30_349 publication-title: Gastroenterology doi: 10.1016/S0016-5085(97)70116-1 contributor: fullname: Desreumaux P – volume: 98 start-page: 1010 year: 1996 ident: b24_343 publication-title: J Clin Invest doi: 10.1172/JCI118861 contributor: fullname: Berg DJ – volume: 132 start-page: 2775 year: 1984 ident: b6_325 publication-title: J Immunol doi: 10.4049/jimmunol.132.6.2775 contributor: fullname: Pierres A – volume: 30 start-page: 866 year: 1985 ident: b15_334 publication-title: Dig Dis Sci doi: 10.1007/BF01309518 contributor: fullname: Wallace JL – volume: 98 start-page: 694 year: 1990 ident: b1_320 publication-title: Gastroenterology doi: 10.1016/0016-5085(90)90290-H contributor: fullname: Okayasu I – volume: 104 start-page: A7 year: 1993 ident: b18_337 publication-title: Gastroenterology contributor: fullname: Sartor RB – volume: 102 start-page: 1524 year: 1992 ident: b14_333 publication-title: Gastroenterology doi: 10.1016/0016-5085(92)91710-L contributor: fullname: Yamada T – volume: 26 start-page: 653 year: 1987 ident: b5_324 publication-title: Scan J Immunol doi: 10.1111/j.1365-3083.1987.tb02301.x contributor: fullname: Kraal G – volume: 106 start-page: 533 year: 1994 ident: b22_341 publication-title: Gastroenterology doi: 10.1016/0016-5085(94)90614-9 contributor: fullname: Sartor RB – volume: 107 start-page: 1643 year: 1994 ident: b3_322 publication-title: Gastroenterology doi: 10.1016/0016-5085(94)90803-6 contributor: fullname: Dieleman LA – volume: 110 start-page: A1019 year: 1996 ident: b29_348 publication-title: Gastroenterology contributor: fullname: Stevcea L – volume: 47 start-page: 63 year: 1979 ident: b7_326 publication-title: Immunol Rev doi: 10.1111/j.1600-065X.1979.tb00289.x contributor: fullname: Ledbetter JA – ident: b25_344 doi: 10.1084/jem.178.5.1607 – volume: 14 start-page: 291 year: 1966 ident: b4_323 publication-title: J Histochem Cytochem doi: 10.1177/14.4.291 contributor: fullname: Graham RC – volume: 102 start-page: 1620 year: 1992 ident: b23_342 publication-title: Gastroenterology doi: 10.1016/0016-5085(92)91722-G contributor: fullname: Mullin G – volume: 45 start-page: 953 year: 1993 ident: b19_338 publication-title: Drugs doi: 10.2165/00003495-199345060-00007 contributor: fullname: Faulds P – volume: 46 start-page: 111 year: 1989 ident: b21_340 publication-title: Adv Immunol doi: 10.1016/S0065-2776(08)60652-5 contributor: fullname: Mosmann TR – volume: 139 start-page: 767 year: 1987 ident: b12_331 publication-title: J Immunol doi: 10.4049/jimmunol.139.3.767 contributor: fullname: Reynolds DS – ident: b17_336 doi: 10.1046/j.1365-2249.1998.00564.x – ident: b9_328 doi: 10.1016/0022-1759(93)90361-A – volume: 38 start-page: 1722 year: 1993 ident: b20_339 publication-title: Dig Dis Sci doi: 10.1007/BF01303184 contributor: fullname: Murthy SN – volume: 34 start-page: 423 year: 1986 ident: b11_330 publication-title: J Histochem Cytochem doi: 10.1177/34.4.2419394 contributor: fullname: Claassen E – volume: 56 start-page: 159 year: 1995 ident: b16_335 publication-title: Digestion doi: 10.1159/000201236 contributor: fullname: Ohkusa T
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Snippet	Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of... SUMMARY Oral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase...
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StartPage	385
SubjectTerms	Animals Biological and medical sciences Chronic Disease colitis Colitis - chemically induced Colitis - immunology Colitis - pathology Cytokines - metabolism Dextran Sulfate dextran sulphate Disease Models, Animal Female Gastroenterology. Liver. Pancreas. Abdomen IL‐4 Interferon-gamma - metabolism interferon‐gamma Interleukin-4 - metabolism Interleukin-5 - metabolism Lymphocytes Medical sciences Mice Original Other diseases. Semiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Th1 Cells - immunology Th2 Cells - immunology
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Title	Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines
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