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Modulation of Beta 2, Beta 3, and AlphavBeta3 Integrins in Chronic Experimental Colitis Induced by Iodoacetamide and Enteropathogenic E. coliββ
Author(s) -
Jurjus Abdo Romanos,
Saliba Jessica L.,
Ghanem Simona,
Jurjus Rosalyn Abdo,
Hussein Inaya Abdallah Hajj
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb15
Subject(s) - iodoacetamide , immunohistochemistry , integrin , pathogenesis , colitis , pathology , medicine , immunology , chemistry , microbiology and biotechnology , receptor , biology , biochemistry , cysteine , enzyme
Many integrins have been implicated in the pathogenesis of inflammatory bowel disease. This work studied the modulation of expression of ß 2 , ß 3 , and αvß 3 integrins in a rat model of IBD. A total of 160 adult male Sprage‐Dawley rats were divided into 4 groups and inoculated intrarectally on a weekly basis, unless otherwise specified, for 56 days with (1) methylcellulose 1% (MC), (2) iodoacetamide 6% (IA), (3) Enteropathogenic E. coli 4x108 colony factor (B), and (4) Iodoacetamide plus E. Coli (IA+B). The treatments were discontinued after 1 month in half of the animals. Daily observation for diarrhea and gross changes was performed. On days 3, 7, 14, 28, 42, and 56 open biopsies were removed from the intestines for RNA extraction, and for microscopy, and immunohistochemistry which was performed for ß 2 , ß 3 , and αvß 3 on paraffin section from the descending colon using FITC conjugated goat antimouse IgG and RNA was extracted for Real Time PCR performed on αvß 3 . Results showed an increased expression 3 to 5 times of ß 2 integrin in the IA and IA+B groups, mostly in the mucosa and submucosa. ß 3 levels were also elevated in the experimental groups of IA and IA+B compared to controls. The highest values were in the combination groups. αvß 3 expression behaved the same way both by immunohistochemistry and RT‐PCR. In conclusion, the chronic release of inflammatory molecules may have caused the precancerous profile of integrins expression.