Dextran sodium sulfate (DSS) induces necrotizing enterocolitis-like lesions in neonatal mice
Necrotizing enterocolitis (NEC) is an inflammatory bowel disease of preterm human newborns with yet unresolved etiology. An established neonatal murine model for NEC employs oral administration of lipopolysaccharides (LPS) combined with hypoxia/hypothermia. In adult mice, feeding dextran sodium sulf...
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| creator | Ginzel, Marco Feng, Xiaoyan Kuebler, Joachim F Klemann, Christian Yu, Yi von Wasielewski, Reinhard Park, Joon-Keun Hornef, Mathias W Vieten, Gertrud Ure, Benno M Kaussen, Torsten Gosemann, Jan Hendrik Mayer, Steffi Suttkus, Anne Lacher, Martin |
| description | Necrotizing enterocolitis (NEC) is an inflammatory bowel disease of preterm human newborns with yet unresolved etiology. An established neonatal murine model for NEC employs oral administration of lipopolysaccharides (LPS) combined with hypoxia/hypothermia. In adult mice, feeding dextran sodium sulfate (DSS) represents a well-established model for experimental inflammatory bowel disease. Here we investigated the effect of DSS administration on the neonatal murine intestine in comparison with the established NEC model.
3-day-old C57BL/6J mice were either fed formula containing DSS or LPS. LPS treated animals were additionally stressed by hypoxia/hypothermia twice daily. After 72 h, mice were euthanized, their intestinal tissue harvested and analyzed by histology, qRT-PCR and flow cytometry. For comparison, adult C57BL/6J mice were fed with DSS for 8 days and examined likewise. Untreated, age matched animals served as controls.
Adult mice treated with DSS exhibited colonic inflammation with significantly increased Cxcl2 mRNA expression. In contrast, tissue inflammation in neonatal mice treated with DSS or LPS plus hypoxia/hypothermia was present in colon and small intestine as well. Comparative analysis of neonatal mice revealed a significantly increased lesion size and intestinal Cxcl2 mRNA expression after DSS exposure. Whereas LPS administration mainly induced local neutrophil recruitment, DSS treated animals displayed increased monocytes/macrophages infiltration.
Our study demonstrates the potential of DSS to induce NEC-like lesions accompanied by a significant humoral and cellular immune response in the small and large intestine of neonatal mice. The new model therefore represents a good alternative to LPS plus hypoxia/hypothermia administration requiring no additional physical stress. |
| doi_str_mv | 10.1371/journal.pone.0182732 |
| format | Article |
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3-day-old C57BL/6J mice were either fed formula containing DSS or LPS. LPS treated animals were additionally stressed by hypoxia/hypothermia twice daily. After 72 h, mice were euthanized, their intestinal tissue harvested and analyzed by histology, qRT-PCR and flow cytometry. For comparison, adult C57BL/6J mice were fed with DSS for 8 days and examined likewise. Untreated, age matched animals served as controls.
Adult mice treated with DSS exhibited colonic inflammation with significantly increased Cxcl2 mRNA expression. In contrast, tissue inflammation in neonatal mice treated with DSS or LPS plus hypoxia/hypothermia was present in colon and small intestine as well. Comparative analysis of neonatal mice revealed a significantly increased lesion size and intestinal Cxcl2 mRNA expression after DSS exposure. Whereas LPS administration mainly induced local neutrophil recruitment, DSS treated animals displayed increased monocytes/macrophages infiltration.
Our study demonstrates the potential of DSS to induce NEC-like lesions accompanied by a significant humoral and cellular immune response in the small and large intestine of neonatal mice. The new model therefore represents a good alternative to LPS plus hypoxia/hypothermia administration requiring no additional physical stress.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0182732</identifier><identifier>PMID: 28817583</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animal models ; Animals ; Animals, Newborn ; Apoptosis ; Biology and Life Sciences ; Colon ; Comparative analysis ; Cytometry ; Development and progression ; Dextran ; Dextran Sulfate - toxicity ; Dextrans ; Disease Models, Animal ; Drinking water ; Enterocolitis ; Enterocolitis, Necrotizing - etiology ; Enterocolitis, Necrotizing - pathology ; Etiology ; Feeding ; Flow cytometry ; Gangrene ; Gastroenterology ; Gastrointestinal diseases ; Gene expression ; Histology ; Hypothermia ; Hypoxia ; Immune response ; Immune response (cell-mediated) ; Immune response (humoral) ; Immune system ; Immunology ; Infiltration ; Inflammation ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Intestinal Mucosa - drug effects ; Large intestine ; Lesions ; Lipopolysaccharides ; Macrophages ; Macrophages - pathology ; Medical research ; Medical schools ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Monocytes ; Necrosis ; Necrotizing enterocolitis ; Neonates ; Neutrophil Infiltration ; Neutrophils ; Newborn babies ; Oral administration ; Pathogenesis ; Pediatrics ; Physical stress ; Physiological aspects ; Physiology ; Polymerase chain reaction ; Recruitment ; Research and Analysis Methods ; Risk factors ; Rodents ; Small intestine ; Sodium ; Sodium sulfate ; Sulfates ; Surgery</subject><ispartof>PloS one, 2017-08, Vol.12 (8), p.e0182732-e0182732</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Ginzel et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Ginzel et al 2017 Ginzel et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c593t-f955eac1d9586f010ae8a9bb43171d7e7f69bd71a27042d29b1d56c1333a26273</citedby><cites>FETCH-LOGICAL-c593t-f955eac1d9586f010ae8a9bb43171d7e7f69bd71a27042d29b1d56c1333a26273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560643/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560643/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28817583$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ginzel, Marco</creatorcontrib><creatorcontrib>Feng, Xiaoyan</creatorcontrib><creatorcontrib>Kuebler, Joachim F</creatorcontrib><creatorcontrib>Klemann, Christian</creatorcontrib><creatorcontrib>Yu, Yi</creatorcontrib><creatorcontrib>von Wasielewski, Reinhard</creatorcontrib><creatorcontrib>Park, Joon-Keun</creatorcontrib><creatorcontrib>Hornef, Mathias W</creatorcontrib><creatorcontrib>Vieten, Gertrud</creatorcontrib><creatorcontrib>Ure, Benno M</creatorcontrib><creatorcontrib>Kaussen, Torsten</creatorcontrib><creatorcontrib>Gosemann, Jan Hendrik</creatorcontrib><creatorcontrib>Mayer, Steffi</creatorcontrib><creatorcontrib>Suttkus, Anne</creatorcontrib><creatorcontrib>Lacher, Martin</creatorcontrib><title>Dextran sodium sulfate (DSS) induces necrotizing enterocolitis-like lesions in neonatal mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Necrotizing enterocolitis (NEC) is an inflammatory bowel disease of preterm human newborns with yet unresolved etiology. An established neonatal murine model for NEC employs oral administration of lipopolysaccharides (LPS) combined with hypoxia/hypothermia. In adult mice, feeding dextran sodium sulfate (DSS) represents a well-established model for experimental inflammatory bowel disease. Here we investigated the effect of DSS administration on the neonatal murine intestine in comparison with the established NEC model.
3-day-old C57BL/6J mice were either fed formula containing DSS or LPS. LPS treated animals were additionally stressed by hypoxia/hypothermia twice daily. After 72 h, mice were euthanized, their intestinal tissue harvested and analyzed by histology, qRT-PCR and flow cytometry. For comparison, adult C57BL/6J mice were fed with DSS for 8 days and examined likewise. Untreated, age matched animals served as controls.
Adult mice treated with DSS exhibited colonic inflammation with significantly increased Cxcl2 mRNA expression. In contrast, tissue inflammation in neonatal mice treated with DSS or LPS plus hypoxia/hypothermia was present in colon and small intestine as well. Comparative analysis of neonatal mice revealed a significantly increased lesion size and intestinal Cxcl2 mRNA expression after DSS exposure. Whereas LPS administration mainly induced local neutrophil recruitment, DSS treated animals displayed increased monocytes/macrophages infiltration.
Our study demonstrates the potential of DSS to induce NEC-like lesions accompanied by a significant humoral and cellular immune response in the small and large intestine of neonatal mice. The new model therefore represents a good alternative to LPS plus hypoxia/hypothermia administration requiring no additional physical stress.</description><subject>Analysis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Colon</subject><subject>Comparative analysis</subject><subject>Cytometry</subject><subject>Development and progression</subject><subject>Dextran</subject><subject>Dextran Sulfate - toxicity</subject><subject>Dextrans</subject><subject>Disease Models, Animal</subject><subject>Drinking water</subject><subject>Enterocolitis</subject><subject>Enterocolitis, Necrotizing - etiology</subject><subject>Enterocolitis, Necrotizing - pathology</subject><subject>Etiology</subject><subject>Feeding</subject><subject>Flow cytometry</subject><subject>Gangrene</subject><subject>Gastroenterology</subject><subject>Gastrointestinal diseases</subject><subject>Gene expression</subject><subject>Histology</subject><subject>Hypothermia</subject><subject>Hypoxia</subject><subject>Immune response</subject><subject>Immune response (cell-mediated)</subject><subject>Immune response (humoral)</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Large intestine</subject><subject>Lesions</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Macrophages - pathology</subject><subject>Medical research</subject><subject>Medical schools</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocytes</subject><subject>Necrosis</subject><subject>Necrotizing enterocolitis</subject><subject>Neonates</subject><subject>Neutrophil Infiltration</subject><subject>Neutrophils</subject><subject>Newborn babies</subject><subject>Oral administration</subject><subject>Pathogenesis</subject><subject>Pediatrics</subject><subject>Physical stress</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Polymerase chain reaction</subject><subject>Recruitment</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Small intestine</subject><subject>Sodium</subject><subject>Sodium sulfate</subject><subject>Sulfates</subject><subject>Surgery</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkktv1DAUhSMEoqXwDxBEYlMWGfyI7XiDVLU8KlViUdghWY59M3hw7MFOEPDr8TBp1UFVFo7s7x773Huq6jlGK0wFfrOJcwrar7YxwArhjghKHlTHWFLScILowzv_R9WTnDcIMdpx_rg6Il2HBevocfX1An5NSYc6R-vmsc6zH_QE9enF9fXr2gU7G8h1AJPi5P64sK4hTJCiid5NLjfefYfaQ3Yx5IIXMgY9aV-PzsDT6tGgfYZny3pSfXn_7vP5x-bq04fL87OrxjBJp2aQjIE22ErW8QFhpKHTsu9bigW2AsTAZW8F1kSgllgie2wZN5hSqgkvvk-ql3vdrY9ZLY3JqthHbVu8kkJc7gkb9UZtkxt1-q2idurfRkxrpdPkjAeFqJaYMCEZom1rpRScS5CA-NCDAVy03i63zf0I1pSGJO0PRA9Pgvum1vGnYowj3tIicLoIpPhjhjyp0WUD3uvSvXl5d7cbaUFf_Yfe726h1roYcGGI5V6zE1VnDGHBEcJtoVb3UOWzUIZVUjS4sn9Q0O4LyvBzTjDcesRI7TJ48xi1y6BaMljKXtztz23RTejoX5xg2EU</recordid><startdate>20170817</startdate><enddate>20170817</enddate><creator>Ginzel, 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Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ginzel, Marco</au><au>Feng, Xiaoyan</au><au>Kuebler, Joachim F</au><au>Klemann, Christian</au><au>Yu, Yi</au><au>von Wasielewski, Reinhard</au><au>Park, Joon-Keun</au><au>Hornef, Mathias W</au><au>Vieten, Gertrud</au><au>Ure, Benno M</au><au>Kaussen, Torsten</au><au>Gosemann, Jan Hendrik</au><au>Mayer, Steffi</au><au>Suttkus, Anne</au><au>Lacher, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dextran sodium sulfate (DSS) induces necrotizing enterocolitis-like lesions in neonatal mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-08-17</date><risdate>2017</risdate><volume>12</volume><issue>8</issue><spage>e0182732</spage><epage>e0182732</epage><pages>e0182732-e0182732</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Necrotizing enterocolitis (NEC) is an inflammatory bowel disease of preterm human newborns with yet unresolved etiology. An established neonatal murine model for NEC employs oral administration of lipopolysaccharides (LPS) combined with hypoxia/hypothermia. In adult mice, feeding dextran sodium sulfate (DSS) represents a well-established model for experimental inflammatory bowel disease. Here we investigated the effect of DSS administration on the neonatal murine intestine in comparison with the established NEC model.
3-day-old C57BL/6J mice were either fed formula containing DSS or LPS. LPS treated animals were additionally stressed by hypoxia/hypothermia twice daily. After 72 h, mice were euthanized, their intestinal tissue harvested and analyzed by histology, qRT-PCR and flow cytometry. For comparison, adult C57BL/6J mice were fed with DSS for 8 days and examined likewise. Untreated, age matched animals served as controls.
Adult mice treated with DSS exhibited colonic inflammation with significantly increased Cxcl2 mRNA expression. In contrast, tissue inflammation in neonatal mice treated with DSS or LPS plus hypoxia/hypothermia was present in colon and small intestine as well. Comparative analysis of neonatal mice revealed a significantly increased lesion size and intestinal Cxcl2 mRNA expression after DSS exposure. Whereas LPS administration mainly induced local neutrophil recruitment, DSS treated animals displayed increased monocytes/macrophages infiltration.
Our study demonstrates the potential of DSS to induce NEC-like lesions accompanied by a significant humoral and cellular immune response in the small and large intestine of neonatal mice. The new model therefore represents a good alternative to LPS plus hypoxia/hypothermia administration requiring no additional physical stress.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28817583</pmid><doi>10.1371/journal.pone.0182732</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-08, Vol.12 (8), p.e0182732-e0182732 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1930442882 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Analysis Animal models Animals Animals, Newborn Apoptosis Biology and Life Sciences Colon Comparative analysis Cytometry Development and progression Dextran Dextran Sulfate - toxicity Dextrans Disease Models, Animal Drinking water Enterocolitis Enterocolitis, Necrotizing - etiology Enterocolitis, Necrotizing - pathology Etiology Feeding Flow cytometry Gangrene Gastroenterology Gastrointestinal diseases Gene expression Histology Hypothermia Hypoxia Immune response Immune response (cell-mediated) Immune response (humoral) Immune system Immunology Infiltration Inflammation Inflammatory bowel disease Inflammatory bowel diseases Intestinal Mucosa - drug effects Large intestine Lesions Lipopolysaccharides Macrophages Macrophages - pathology Medical research Medical schools Medicine and Health Sciences Mice Mice, Inbred C57BL Monocytes Necrosis Necrotizing enterocolitis Neonates Neutrophil Infiltration Neutrophils Newborn babies Oral administration Pathogenesis Pediatrics Physical stress Physiological aspects Physiology Polymerase chain reaction Recruitment Research and Analysis Methods Risk factors Rodents Small intestine Sodium Sodium sulfate Sulfates Surgery |
| title | Dextran sodium sulfate (DSS) induces necrotizing enterocolitis-like lesions in neonatal mice |
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