Due to necessary maintenance, Xenbase will be unavailable from December 24-29, 2014. We apologize for the inconvenience.

Click on this message to dismiss it.
Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-38692
Am J Respir Crit Care Med. December 15, 2008; 178 (12): 1271-81.

Rhinovirus disrupts the barrier function of polarized airway epithelial cells.

Sajjan U , Wang Q , Zhao Y , Gruenert DC , Hershenson MB .


Abstract
Secondary bacterial infection following rhinovirus (RV) infection has been recognized in chronic obstructive pulmonary disease.We sought to understand mechanisms by which RV infection facilitates secondary bacterial infection.Primary human airway epithelial cells grown at air-liquid interface and human bronchial epithelial (16HBE14o-) cells grown as polarized monolayers were infected apically with RV. Transmigration of bacteria (nontypeable Haemophilus influenzae and others) was assessed by colony counting and transmission electron microscopy. Transepithelial resistance (R(T)) was measured by using a voltmeter. The distribution of zona occludins (ZO)-1 was determined by immunohistochemistry and immunoblotting.Epithelial cells infected with RV showed 2-log more bound bacteria than sham-infected cultures, and bacteria were recovered from the basolateral media of RV- but not sham-infected cells. Infection of polarized airway epithelial cell cultures with RV for 24 hours caused a significant decrease in R(T) without causing cell death or apoptosis. Ultraviolet-treated RV did not decrease R(T), suggesting a requirement for viral replication. Reduced R(T) was associated with increased paracellular permeability, as determined by flux of fluorescein isothiocyanate (FITC)-inulin. Neutralizing antibodies to tumor necrosis factor (TNF)-alpha, IFN-gamma and IL-1beta reversed corresponding cytokine-induced reductions in R(T) but not that induced by RV, indicating that the RV effect is independent of these proinflammatory cytokines. Confocal microscopy and immunoblotting revealed the loss of ZO-1 from tight junction complexes in RV-infected cells. Intranasal inoculation of mice with RV1B also caused the loss of ZO-1 from the bronchial epithelium tight junctions in vivo.RV facilitates binding, translocation, and persistence of bacteria by disrupting airway epithelial barrier function.

PubMed ID: 18787220
PMC ID: PMC2599868
Article link: Am J Respir Crit Care Med.
Grant support: HL82550 NHLBI NIH HHS , HL82550 NHLBI NIH HHS , HL82550 NHLBI NIH HHS , HL82550 NHLBI NIH HHS , HL82550 NHLBI NIH HHS , HL82550 NHLBI NIH HHS

Genes referenced: tjp1 tnf
Antibodies referenced:
Morpholinos referenced:

My Xenbase: [ Log-in / Register ]
version: [3.3]


Major funding for Xenbase is provided by the National Institute of Child Health and Human Development, grant P41 HD064556