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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2004-3-19
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pubmed:abstractText |
Down-regulation of receptors involved in the recognition or transmission of inflammatory signals and a reduced responsiveness support the concept that macrophages are 'desensitized' during their differentiation in the intestinal mucosa. During inflammatory bowel disease (IBD) intestinal macrophages (IMACs) change to a reactive or 'aggressive' type. After having established a method of isolation and purification of IMACs, message for cathepsin D was one of the mRNAs we found to be up-regulated in a subtractive hybridization of Crohn's disease (CD) macrophages versus IMACs from control mucosa. The expression of cathepsin D in intestinal mucosa was analysed by immunohistochemistry in biopsies from IBD and control patients and in a mouse model of dextran sulphate sodium (DSS)-induced acute and chronic colitis. IMACs were isolated and purified from normal and inflamed mucosa by immunomagnetic beads armed with a CD33 antibody. RT-PCR was performed for cathepsin D mRNA. Results were confirmed by Northern blot and flow cytometrical analysis. Immunohistochemistry revealed a significant increase in the cathepsin D protein expression in inflamed intestinal mucosa from IBD patients compared to non-inflamed mucosa. No cathepsin D polymerase chain reaction (PCR) product could be obtained with mRNA from CD33-positive IMACs from normal mucosa. Reverse transcription (RT)-PCR showed an induction of mRNA for cathepsin D in purified IMACs from IBD patients. Northern blot and flow cytometry analysis confirmed these results. Cathepsin D protein was also found in intestinal mucosa in acute and chronic DSS-colitis but was absent in normal mucosa. This study shows that expression of cathepsin D is induced in inflammation-associated IMACs. The presence of cathepsin D might contribute to the mucosal damage in IBD.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
136
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
157-67
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:15030527-Acute Disease,
pubmed-meshheading:15030527-Animals,
pubmed-meshheading:15030527-Cathepsin D,
pubmed-meshheading:15030527-Chronic Disease,
pubmed-meshheading:15030527-Dextran Sulfate,
pubmed-meshheading:15030527-Female,
pubmed-meshheading:15030527-Immunoenzyme Techniques,
pubmed-meshheading:15030527-Inflammatory Bowel Diseases,
pubmed-meshheading:15030527-Intestinal Mucosa,
pubmed-meshheading:15030527-Macrophages,
pubmed-meshheading:15030527-Mice,
pubmed-meshheading:15030527-Mice, Inbred BALB C,
pubmed-meshheading:15030527-RNA, Messenger,
pubmed-meshheading:15030527-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15030527-Up-Regulation
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pubmed:year |
2004
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pubmed:articleTitle |
Cathepsin D is up-regulated in inflammatory bowel disease macrophages.
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pubmed:affiliation |
Department of Internal Medicine I, University of Regensburg, Regensburg, Germany. martin.hausmann@klinik.uni-regensburg.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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