File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Systemic tumor necrosis factor-alpha production in experimental colitis

TitleSystemic tumor necrosis factor-alpha production in experimental colitis
Authors
Issue Date1992
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116
Citation
Digestive Diseases And Sciences, 1992, v. 37 n. 11, p. 1738-1745 How to Cite?
AbstractTumor necrosis factor-alpha (TNF) is a cytokine released by mononuclear cells in response to inflammation and sepsis. Since the biological effects of TNF are consistent with the systemic and nal features of ulcerative colitis, the role of TNF was examined in a rabbit model of chronic colitis. Peripheral blood mononuclear cells were isolated, stimulated with lipopolysaccharide, and cultured supernatants assayed for TNF levels using a cytotoxic assay on mouse fibrosarcoma L929 cells. Basal levels of TNF production by mononuclear cells from 13 normal rabbits (124.3 units/ml ± 27.1 units/ml, mean ± SE) were not different from nine rabbits with colitis (83.6 units/ml ± 24.4 units/ml, P > 0.05). Treatment with lipopolysaccharide (100 μg/ml) induced increased TNF production by mononuclear cells isolated from both normals (672.0 units/ml ± 197.5 units/ml, P < 0.05) and rabbits with colitis (1114.0 units/ml ± 489.6 units/ml, P < 0.05). However, at all lipopolysaccharide concentrations stimulated TNF levels were comparable in experimental and control groups (P > 0.05). In light of the role of leukotrienes in inflammation, a separate group of rabbits with colitis was investigated following treatment with an oral leukotriene B4 receptor antagonist. Serum TNF levels in 15 control rabbits (32.5 units/ml ± 7.6 units/ml, mean ± SE) were not significantly different from rabbits with colitis receiving either leukotriene B4 receptor antagonist (35.7 units/ml ± 9.2 units/ml, N = 13) or vehicle alone (50.3 units/ml ± 10.2 units/ml, N = 14) (ANOVA, P > 0.05). These data indicate that systemic levels of TNF are not elevated in this experimental model of chronic colitis. Therefore, other inflammatory mediators with biological functions parallel to those of TNF are likely to mediate the systemic manifestations of colitis.
Persistent Identifierhttp://hdl.handle.net/10722/170252
ISSN
2015 Impact Factor: 2.516
2015 SCImago Journal Rankings: 0.995
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMack, DRen_US
dc.contributor.authorLau, ASen_US
dc.contributor.authorSherman, PMen_US
dc.date.accessioned2012-10-30T06:06:59Z-
dc.date.available2012-10-30T06:06:59Z-
dc.date.issued1992en_US
dc.identifier.citationDigestive Diseases And Sciences, 1992, v. 37 n. 11, p. 1738-1745en_US
dc.identifier.issn0163-2116en_US
dc.identifier.urihttp://hdl.handle.net/10722/170252-
dc.description.abstractTumor necrosis factor-alpha (TNF) is a cytokine released by mononuclear cells in response to inflammation and sepsis. Since the biological effects of TNF are consistent with the systemic and nal features of ulcerative colitis, the role of TNF was examined in a rabbit model of chronic colitis. Peripheral blood mononuclear cells were isolated, stimulated with lipopolysaccharide, and cultured supernatants assayed for TNF levels using a cytotoxic assay on mouse fibrosarcoma L929 cells. Basal levels of TNF production by mononuclear cells from 13 normal rabbits (124.3 units/ml ± 27.1 units/ml, mean ± SE) were not different from nine rabbits with colitis (83.6 units/ml ± 24.4 units/ml, P > 0.05). Treatment with lipopolysaccharide (100 μg/ml) induced increased TNF production by mononuclear cells isolated from both normals (672.0 units/ml ± 197.5 units/ml, P < 0.05) and rabbits with colitis (1114.0 units/ml ± 489.6 units/ml, P < 0.05). However, at all lipopolysaccharide concentrations stimulated TNF levels were comparable in experimental and control groups (P > 0.05). In light of the role of leukotrienes in inflammation, a separate group of rabbits with colitis was investigated following treatment with an oral leukotriene B4 receptor antagonist. Serum TNF levels in 15 control rabbits (32.5 units/ml ± 7.6 units/ml, mean ± SE) were not significantly different from rabbits with colitis receiving either leukotriene B4 receptor antagonist (35.7 units/ml ± 9.2 units/ml, N = 13) or vehicle alone (50.3 units/ml ± 10.2 units/ml, N = 14) (ANOVA, P > 0.05). These data indicate that systemic levels of TNF are not elevated in this experimental model of chronic colitis. Therefore, other inflammatory mediators with biological functions parallel to those of TNF are likely to mediate the systemic manifestations of colitis.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116en_US
dc.relation.ispartofDigestive Diseases and Sciencesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBenzopyrans - Administration & Dosageen_US
dc.subject.meshCells, Cultured - Drug Effects - Metabolismen_US
dc.subject.meshColitis, Ulcerative - Blood - Chemically Induced - Drug Therapyen_US
dc.subject.meshDinitrochlorobenzeneen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEscherichia Colien_US
dc.subject.meshLeukocytes, Mononuclear - Drug Effects - Metabolismen_US
dc.subject.meshLeukotriene B4 - Antagonists & Inhibitorsen_US
dc.subject.meshLipopolysaccharides - Pharmacologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshReceptors, Immunologic - Drug Effectsen_US
dc.subject.meshReceptors, Leukotriene B4en_US
dc.subject.meshTumor Necrosis Factor-Alpha - Analysis - Biosynthesis - Drug Effectsen_US
dc.titleSystemic tumor necrosis factor-alpha production in experimental colitisen_US
dc.typeArticleen_US
dc.identifier.emailLau, AS:asylau@hku.hken_US
dc.identifier.authorityLau, AS=rp00474en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF01299868en_US
dc.identifier.pmid1330461-
dc.identifier.scopuseid_2-s2.0-0026484749en_US
dc.identifier.volume37en_US
dc.identifier.issue11en_US
dc.identifier.spage1738en_US
dc.identifier.epage1745en_US
dc.identifier.isiWOS:A1992JY62400018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMack, DR=7102096227en_US
dc.identifier.scopusauthoridLau, AS=7202626202en_US
dc.identifier.scopusauthoridSherman, PM=7203008320en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats