E. Nicolis et al., ICAM-1 INDUCTION IN RESPIRATORY CELLS EXPOSED TO A REPLICATION-DEFICIENT RECOMBINANT ADENOVIRUS IN-VITRO AND IN-VIVO, Gene therapy, 5(1), 1998, pp. 131-136
Citations number
32
Categorie Soggetti
Biothechnology & Applied Migrobiology","Genetics & Heredity",Biology,"Medicine, Research & Experimental
Administration of replication-deficient recombinant adenoviruses (Ad)
designed as vectors for gene transfer to the airway tract of rats and
monkeys has been associated with a dose-dependent inflammatory process
a few days after viral exposure. Among the cellular mechanisms possib
ly involved, we investigated the expression of intercellular adhesion
molecule-1 (ICAM-1), which is known to be induced by parainfluenza, ad
enovirus type 5 and respiratory syncytial viruses in vitro. To test th
is hypothesis, an Ad type 5-derived replication-deficient recombinant
vector carrying the expression cassette for the cystic fibrosis gene (
Ad.CFTR) was either incubated with A549 cells (a human-derived lung ep
ithelial cell line) or instilled by bronchoscopic procedures into the
airways of Rhesus monkeys. Ad.CFTR induced expression of ICAM-1 in A54
9 cells and up-regulated with time the basal levels of ICAM-1 mRNA in
lung portions of Rhesus monkeys. These observations indicate that E1-E
3-deleted replication-deficient adenoviral vectors are capable of indu
cing adhesion molecules known to play a role in inflammation.