Abstract
Neutrophil (PMN) localization at the lumenal epithelium surface is a key histological feature of the large intestine of inflammatory bowel disease ((IBD), Crohn's Disease and Ulcerative Colitis) patients. Extracellular matrix proteins (ECM) can affect PMN recruitment and other functions. Periostin, an ECM protein secreted by fibroblasts during cellular injury and tissue repair, was investigated as an adhesive molecule for PMN. Immunofluorescence reveals that periostin similarly to the subepithelial fibroblasts is confined to the base of the crypt epithelium. Flow Cytometry and adhesion results show that intestinal fibroblasts and T84 epithelial cells adhere to periostin and express periostin on the cell surface. Anti‐αvβ3 and anti‐αvβ5 (known integrin receptors for periostin) antibodies inhibit periostin adhesion to fibroblasts and T84 cells. In particular, anti‐αvβ3 and anti‐αvβ5 antibodies inhibit 50% of adhesion. However, anti‐CD11b antibodies inhibit 95% of this adhesion. PMN surface expression of periostin is reduced when PMN are exposed to microbial products and anti‐periostin antibodies inhibit PMN adhesion to fibrinogen (a known ligand for CD11b, a precursor to fibrin, and important in the inflammatory response) by 85%. Thus, PMN adhesion to periostin can be modulated by αvβ3, αvβ5 and CD11b integrins and may play a role in PMN‐epithelial interactions in IBD.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
