Bovine herpesvirus-1 infection reduces bronchial epithelial cell migration to extracellular matrix proteins

Abstract

Repair of airway epithelium after viral infection involves migration of epithelial cells to cover injured, denuded areas. We determined whether viral infection reduces the capability of bronchial epithelial cells to migrate and to attach to extracellular matrix proteins. Inoculation of bovine bronchial epithelial cells in vitro with bovine herpesvirus-1 reduced their ability to migrate in two different assays of cell migration. When attachment assays were performed, fewer cells attached to both control wells and matrix protein-precoated wells, suggesting that general mechanisms of adherence to substrates were altered by viral infection. Focal contact points of epithelial cells with the underlying matrix were evaluated with epifluorescence microscopy and monoclonal antibodies to vinculin and alpha v, an integrin chain. Disruption of focal contact points was seen early after infection and was prevented by an inhibitor of viral DNA polymerase, phosphonoacetic acid. Cycloheximide did not cause similar disruptions of focal contacts at early time points. Viral infection thus has marked effects on the interactions of bronchial epithelial cells with extracellular matrix and the organization of matrix to cytoskeleton links. The effects appear to be dependent in part on viral replication in the cells and are not simply due to reductions in host cell protein synthesis.

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

“…In an in vitro model, BoHV-1 infection had marked effects on the interactions of bronchial epithelial cells with the extracellular matrix, thus decreasing the cell migration [192].…”

Reorganization of the host cytoskeleton by the intracellular pathogenChlamydia trachomatis

“…For instance inhibition of bronchial epithelial cell migration by bovine herpesvirus-1 infection compromises respiratory epithelial repair after injury contributing to lung disease. 24 In contrast vaccinia virus infection stimulates host cell motility via activation of RhoA by its F11L gene product to facilitate dissemination. 25 Whether Chlamydia inhibits cell motility directly by cytoskeletal disruption or indirectly via sequestration of cell migration regulators such as RhoA, remains to be determined.…”

Chlamydia trachomatisinfection prevents front-rear polarity of migrating HeLa cells

“…Alterations in epithelial cell motility have been linked to the spread of infection and reduced tissue repair during viral infections (Morales et al ., ; Spurzem et al . ). It has been shown previously that Chlamydia infection can block cell migration in an in vitro wound healing assay (Kumar and Valdivia, ).…”

“…Furthermore, epithelial regeneration, wound healing and immune surveillance strongly depend on migration processes (Hackam and Ford, 2002;Gurtner et al, 2008). Alterations in epithelial cell motility have been linked to the spread of infection and reduced tissue repair during viral infections (Morales et al, 2008;Spurzem et al 1995). It has been shown previously that Chlamydia infection can block cell migration in an in vitro wound healing assay (Kumar and Valdivia, 2008a).…”