March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
β1-integrins Mediate Neutrophil Migration within the Injured Mouse Cornea
Author Affiliations & Notes
  • Samuel D. Hanlon
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Debjani Gagen
    Pathology, University of Wisconsin, Madison, Wisconsin
  • Marika N. Sauter
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Paul T. Harris
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Paul T. Landry
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Nimesh B. Patel
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Alan R. Burns
    Clinical Sciences, Univ of Houston College of Optometry, Houston, Texas
  • Footnotes
    Commercial Relationships  Samuel D. Hanlon, None; Debjani Gagen, None; Marika N. Sauter, None; Paul T. Harris, None; Paul T. Landry, None; Nimesh B. Patel, None; Alan R. Burns, None
  • Footnotes
    Support  NEI EY17120, EY001139, P30EY007551
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 3552. doi:
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      Samuel D. Hanlon, Debjani Gagen, Marika N. Sauter, Paul T. Harris, Paul T. Landry, Nimesh B. Patel, Alan R. Burns; β1-integrins Mediate Neutrophil Migration within the Injured Mouse Cornea. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3552.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Neutrophil migration within the inflamed corneal stroma involves contact with extracellular matrix molecules and keratocytes. Cell surface integrin receptors have been implicated in these interactions. While members of β1-, β2-, and β3-integrin families are expressed on extravascular neutrophils, it is reported that in vitro migration in 3-D collagen matrices can be integrin-independent. The purpose of the present study was to use, for the first time, in vivo confocal microscopy for time-lapse recordings to quantify the effect of blocking integrin function on neutrophil motility following corneal epithelial abrasion.

Methods: : Anesthetized adult C57BL/6 mice received corneal epithelial abrasions using an Alger brush. Immediately after wounding, blocking antibody (anti-β1-, β2-, or β3-integrin) or IgG control was applied to the cornea. Eight hours later, the injured mice were imaged with an HRTIII-RCM for 10 minute at 1 frame per second. Image stabilization, cell tracking and movement analysis were accomplished with a custom MatLab program.

Results: : Control IgG antibody had no effect on neutrophil motility within the corneal stroma. Neutrophils moved with an average cell speed of 6.93±1.01(SD) µm/minute. Average straight-line index (SI) of the neutrophil population was 0.60±0.07, where a value of 1 indicates a perfectly straight path. While anti-β2- or β3- integrin antibodies had no effect on cell speed or SI, β1-integrin antibody resulted in a 28 % reduction in speed (p<0.05) and a 33% reduction in SI (p<0.05). The resultant vector for average neutrophil movement within a given cornea was toward the wound in 65.5% of the corneas, parallel to the wound in 24.1% and away from the wound in 10.4%, with no difference among experimental groups.

Conclusions: : β1-integrin, but not β2- or β3-integrin, appears to play a role in neutrophil trafficking within the corneal stroma. Our results showing that β1-integrin blockade only partially reduces neutrophil migration velocity and SI (~30%, respectively), suggest neutrophils are capable of migration through the physically confined environment of the corneal stroma without the benefit of integrin adhesion.

Keywords: cornea: basic science • inflammation • extracellular matrix 
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