title: Poly I:C-induced expression of intercellular adhesion molecule-1 in intestinal epithelial cells.
abstract: Intercellular adhesion molecul-1 (ICAM-1) is a transmembrane glycoprotein belonging to the immunoglobulin superfamily of adhesion molecules and plays perdominant roles in recruitment and trafficking of leucocytes to sites of inflammation. ICAM-1 expression in intestinal epithelial cells (IECs) is enhanced by several stimuli, such as proinflammatory cytokines, bacterial infections or pathogen-associated molecular patterns. One of these stimuli, double-stranded RNA (dsRNA), is a by-product of viral replication and can be recognized by its cognate receptor Toll-like receptor 3 (TLR-3). In spite of expression of both TLR-3 and ICAM-1 in IECs, correlation between TLR-3-signalling and ICAM-1 expression has never been examined in IECs. In the present study, we investigated whether poly I:C, an analogue of dsRNA, can stimulate the expression of ICAM-1 in IEC line, HT-29. Poly I:C-stimulation up-regulated the expression of ICAM-1 mRNA by real-time polymerase chain reaction. Enhanced expression of ICAM-1 was confirmed in protein level by immunofluoresense cell staining and enzyme-linked immunosorbent assay by measuring the released soluble ICAM-1 in culture supernatant. As the stimulation effect was reduced by pre-treatment of the cells with anti-TLR-3 antibody, poly I:C-binding signal was thought to be sensed by TLR-3 on the surface of HT-29. The results of luciferase assay and nuclear factor kappa-b (NF-kappaB) inhibitor treatment experiments indicated that the downstream signal was mainly transduced by transcription factor, NF-kappaB. All these results demonstrated the connection between TLR-3 signalling and ICAM-1 expression in HT-29 cells and indicated the importance of coordinated function of both innate and adaptive immunity against viral infections.
authors.affiliation: Department of Pathology, Nihon University School of Dentistry, Tokyo, Japan.
authors.forename: D
authors.initials: D
authors.lastname: Omagari
authors.forename: Y
authors.initials: Y
authors.lastname: Mikami
authors.forename: H
authors.initials: H
authors.lastname: Suguro
authors.forename: K
authors.initials: K
authors.lastname: Sunagawa
authors.forename: M
authors.initials: M
authors.lastname: Asano
authors.forename: E
authors.initials: E
authors.lastname: Sanuki
authors.forename: I
authors.initials: I
authors.lastname: Moro
authors.forename: K
authors.initials: K
authors.lastname: Komiyama
mesh_terms: D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D004847:Epithelial Cells / Q000378:metabolism*; D015870:Gene Expression; D019073:HT29 Cells; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D050838:Interferon Regulatory Factor-3 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D011070:Poly I-C / Q000494:pharmacology*; D012333:RNA, Messenger / Q000032:analysis; D013268:Stimulation, Chemical; D015854:Up-Regulation
chemical_list: D050838:Interferon Regulatory Factor-3; D016328:NF-kappa B; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D011070:Poly I-C