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Infection and Immunity, March 2000, p. 1731-1734, Vol. 68, No. 3
Novavax, Rockville,
Maryland,1 and Department of Biological
Sciences,2 The Biofilm Research
Group,3 and Department of Microbiology
and Infectious Diseases,4 University of
Calgary, Calgary, Alberta, Canada
Received 12 October 1999/Accepted 30 November 1999
Bacterial lipopolysaccharide (LPS) is an important agent of
induction of ocular pathology following corneal injury or wearing of
contaminated contact lenses. The mechanism of LPS uptake through the
corneal epithelium is unclear, and the role played by inflammatory cells in this phenomenon has not been previously assessed. Fluorescein isothiocyanate-labeled LPS from Escherichia coli was
deposited onto the abraded corneas of New Zealand White rabbits.
Epifluorescence microscopy of living excised corneas revealed diffuse
LPS staining in the epithelial and stromal layers only in the vicinity
of the abrasion. In addition, specific cellular uptake of LPS was
suggested by fluorescence staining of cells along the abrasion site. In a second series of experiments, an anti-CD18 polyclonal antibody was
used to block infiltration of polymorphonuclear neutrophils (PMN) into
the cornea. In these experiments, a diffuse distribution of fluorescent
LPS was still observed along the abrasion, but the specific cellular
uptake was abolished. The findings indicate that LPS enters the cornea
via diffuse penetration at sites of injury and that specific cellular
uptake of LPS occurs within the cornea via PMN which have
migrated into the damaged tissue.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Lipopolysaccharide Entry in the Damaged Cornea and
Specific Uptake by Polymorphonuclear Neutrophils
*
Corresponding author. Mailing address: University of
Calgary, 2500 University Dr. NW, Calgary, Alberta, Canada T2N 1N4.
Phone: (403) 220-5278. Fax: (403) 284-1537. E-mail:
dmorck{at}ucalgary.ca.
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