| Literature DB >> 15733557 |
Takahiko Sasaki1, Mutsuo Yamaya, Hiroyasu Yasuda, Daisuke Inoue, Mitsuhiro Yamada, Hiroshi Kubo, Hidekazu Nishimura, Hidetada Sasaki.
Abstract
To examine the effects of lansoprazole, a proton pump inhibitor, on rhinovirus infection in airways, human tracheal epithelial cells were infected with a major subgroup of rhinoviruses, type 14 rhinovirus. Rhinovirus increased the mRNA expression of intercellular adhesion molecule-1 (ICAM-1) in the cells, the major rhinovirus receptor, and the content of the soluble form of ICAM-1 (sICAM-1) and cytokines in supernatants. Lansoprazole reduced supernatant titers and RNA of rhinovirus, the susceptibility to rhinovirus infection, the ICAM-1 mRNA production, the number and fluorescence intensity of acidic endosomes in the cells, and supernatants sICAM-1 and cytokine concentrations including interleukin-1beta. Antibody to interleukin-1beta reduced baseline and rhinovirus-induced ICAM-1 production. These results suggest that lansoprazole inhibits rhinovirus infection by reducing ICAM-1 via partly endogenous production of interleukin-1beta, and by blocking the rhinovirus RNA entry into the endosomes. Lansoprazole may modulate airway inflammation by reducing the production of cytokines and ICAM-1 in rhinovirus infection.Entities:
Mesh:
Substances:
Year: 2005 PMID: 15733557 DOI: 10.1016/j.ejphar.2004.12.042
Source DB: PubMed Journal: Eur J Pharmacol ISSN: 0014-2999 Impact factor: 4.432