http://purl.uniprot.org/citations/18202111 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18202111 | http://www.w3.org/2000/01/rdf-schema#comment | "Although macrophages are considered a critical factor in determining the severity of acute inflammatory responses in the gut, recent evidence has indicated that macrophages may also play a counterinflammatory role. In this study, we examined the role of a macrophage subset in two models of colitis. Macrophage colony-stimulating factor (M-CSF)-deficient osteopetrotic mice (op/op) and M-CSF-expressing heterozygote (+/?) mice were studied following the induction of colitis by either dinitrobenzene sulfonic acid (DNBS) or dextran sulfate sodium (DSS). DNBS induced a severe colitis in M-CSF-deficient op/op mice compared with +/? mice. This was associated with increased mortality and more severe macroscopic and microscopic injury. Colonic tissue myeloperoxidase (MPO) activity as well as concentrations of TNF-alpha, IL-1beta, and IL-6 were higher and IL-10 lower in op/op mice with DNBS colitis. The severity of inflammation and mortality was attenuated in op/op mice that had received human recombinant M-CSF prior to the induction of colitis. In contrast, op/op mice appeared less vulnerable to colitis induced by DSS. Macroscopic damage, microscopic injury, MPO activity, and tissue concentrations of TNF-alpha, IL-1beta, and IL-6 were all lower in op/op mice compared with +/? mice with DSS colitis, and no changes were seen in IL-10. Macrophage inflammatory protein-1alpha concentrations were increased in op/op but not +/? mice following colitis induced by DNBS but not DSS. These results indicate that M-CSF-dependent macrophages may play either a pro- or counterinflammatory role in acute experimental colitis, depending on the stimulus used to induce colitis."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpgi.00453.2007"xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Collins S."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Vallance B.A."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Hogaboam C.M."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Galeazzi F."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Ghia J.E."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/author | "Ford D.C."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/name | "Am J Physiol Gastrointest Liver Physiol"xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/pages | "G770-7"xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/title | "Role of M-CSF-dependent macrophages in colitis is driven by the nature of the inflammatory stimulus."xsd:string |
http://purl.uniprot.org/citations/18202111 | http://purl.uniprot.org/core/volume | "294"xsd:string |
http://purl.uniprot.org/citations/18202111 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18202111 |
http://purl.uniprot.org/citations/18202111 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18202111 |
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