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Infection and Immunity, December 2000, p. 7202-7208, Vol. 68, No. 12
Cell Imaging Facility and Department of
Biochemistry, School of Medical Sciences, University of Bristol,
Bristol BS8 1TD, United Kingdom,1 and
Departamento de Histologia e Embriologia, Instituto de
Biologia, Universidade Estadual de Campinas, Campinas, SP, 13083-970, Brazil2
Received 3 August 2000/Accepted 15 September 2000
Infection of polarized MDCK epithelial layers by Salmonella
enterica serovar Typhimurium is accompanied by increased tight junction permeability and by contraction of perijunctional
actinomyosin. We localized dysfunctional tight junctions in serovar
Typhimurium-infected MDCK layers by imaging apical-basolateral
intramembrane diffusion of fluorescent lipid and found that loss of the
apical-basolateral diffusion barrier (tight junction fence function)
was most marked in areas of prominent perijunctional contraction. The
protein kinase inhibitor staurosporine prevented perijunctional
contraction but did not reverse the effects of serovar Typhimurium on
tight junction barrier function. Hence, perijunctional contraction is not required for Salmonella-induced tight junction
dysfunction and this epithelial response to infection may be multifactorial.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Localization of Dysfunctional Tight Junctions in
Salmonella enterica Serovar Typhimurium-Infected
Epithelial Layers
and
*
Corresponding author. Mailing address: Cell Imaging
Facility and Department of Biochemistry, School of Medical Sciences,
University of Bristol, Bristol BS8 1TD, United Kingdom. Phone: 44 117 928 7410. Fax: 44 117 928 8274. E-mail:
m.a.jepson{at}bristol.ac.uk.
Present address: Department of Molecular Biology and Biotechnology,
University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN,
United Kingdom.
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