Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression

J. Yannariello-Brown, C. K. Hallberg, M. Nakajima, M. C. Trocme, M. Brysk, Janak Patel, S. D. Trocme

Research output: Contribution to journalArticle

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Abstract

Purpose. To determine if Intercellular Adhesion Molecule-1 (ICAM-1; CD54) plays a role in the attachment of eosinophils to the cornea during inflammation associated with severe ocular allergy, we investigated whether proinflammatory cytokines could regulate ICAM-1 protein expression on cultured primary human corneal epithelial cells (HCEs). Methods. HCEs were obtained by trypsin/pronase digestion of human corneas (Lions Eye Bank, Houston & San Antonio, TX) and cultured in keratinocyte growth medium. HCEs were grown to confluency in either culture flasks or 96-well plates, then treated with various concentrations of Interferon-γ (IFN-γ 1-500U/ml) or Interleukin-1α (IL-1α; 0.001-10ng/ml) for various times. The cells were then washed in PBS and fixed in 1% paraformaldehyde in PBS. ICAM-1 expression was measured using FACS analysis and a cell-based ELISA assay using a monoclonal mouse anti-human ICAM-1 antibody. Results. IFN-γ induced a dose and time dependent increase in ICAM-1 expression. Maximal expression was seen at 50U/ml using both FACS analysis and the ELISA. ICAM-1 expression increased 20-fold over control values. No change in ICAM-1 expression could be detected after IL-1α treatment with either technique. Conclusions. We demonstrate that ICAM-1 can be up-regulated by the cytokine IFN-γ on cultured primary human corneal epithelial cells in a dose and time dependent fashion. The expression of corneal epithelial ICAM-1 during inflammation associated with a severe allergic response could contribute to corneal damage by aiding in the attachment of eosinophils.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996

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Intercellular Adhesion Molecule-1
Epithelial Cells
Cytokines
Interleukin-1
Eosinophils
Cornea
Enzyme-Linked Immunosorbent Assay
Eye Banks
Lions
Inflammation
Pronase
Keratinocytes
Trypsin
Interferons
Digestion
Hypersensitivity
Antibodies

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Yannariello-Brown, J., Hallberg, C. K., Nakajima, M., Trocme, M. C., Brysk, M., Patel, J., & Trocme, S. D. (1996). Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression. Investigative Ophthalmology and Visual Science, 37(3).

Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression. / Yannariello-Brown, J.; Hallberg, C. K.; Nakajima, M.; Trocme, M. C.; Brysk, M.; Patel, Janak; Trocme, S. D.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 3, 15.02.1996.

Research output: Contribution to journalArticle

Yannariello-Brown, J, Hallberg, CK, Nakajima, M, Trocme, MC, Brysk, M, Patel, J & Trocme, SD 1996, 'Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression', Investigative Ophthalmology and Visual Science, vol. 37, no. 3.
Yannariello-Brown J, Hallberg CK, Nakajima M, Trocme MC, Brysk M, Patel J et al. Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression. Investigative Ophthalmology and Visual Science. 1996 Feb 15;37(3).
Yannariello-Brown, J. ; Hallberg, C. K. ; Nakajima, M. ; Trocme, M. C. ; Brysk, M. ; Patel, Janak ; Trocme, S. D. / Cytokine regulation of human corneal epithelial cell ICAM-1 (CD54) expression. In: Investigative Ophthalmology and Visual Science. 1996 ; Vol. 37, No. 3.
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abstract = "Purpose. To determine if Intercellular Adhesion Molecule-1 (ICAM-1; CD54) plays a role in the attachment of eosinophils to the cornea during inflammation associated with severe ocular allergy, we investigated whether proinflammatory cytokines could regulate ICAM-1 protein expression on cultured primary human corneal epithelial cells (HCEs). Methods. HCEs were obtained by trypsin/pronase digestion of human corneas (Lions Eye Bank, Houston & San Antonio, TX) and cultured in keratinocyte growth medium. HCEs were grown to confluency in either culture flasks or 96-well plates, then treated with various concentrations of Interferon-γ (IFN-γ 1-500U/ml) or Interleukin-1α (IL-1α; 0.001-10ng/ml) for various times. The cells were then washed in PBS and fixed in 1{\%} paraformaldehyde in PBS. ICAM-1 expression was measured using FACS analysis and a cell-based ELISA assay using a monoclonal mouse anti-human ICAM-1 antibody. Results. IFN-γ induced a dose and time dependent increase in ICAM-1 expression. Maximal expression was seen at 50U/ml using both FACS analysis and the ELISA. ICAM-1 expression increased 20-fold over control values. No change in ICAM-1 expression could be detected after IL-1α treatment with either technique. Conclusions. We demonstrate that ICAM-1 can be up-regulated by the cytokine IFN-γ on cultured primary human corneal epithelial cells in a dose and time dependent fashion. The expression of corneal epithelial ICAM-1 during inflammation associated with a severe allergic response could contribute to corneal damage by aiding in the attachment of eosinophils.",
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N2 - Purpose. To determine if Intercellular Adhesion Molecule-1 (ICAM-1; CD54) plays a role in the attachment of eosinophils to the cornea during inflammation associated with severe ocular allergy, we investigated whether proinflammatory cytokines could regulate ICAM-1 protein expression on cultured primary human corneal epithelial cells (HCEs). Methods. HCEs were obtained by trypsin/pronase digestion of human corneas (Lions Eye Bank, Houston & San Antonio, TX) and cultured in keratinocyte growth medium. HCEs were grown to confluency in either culture flasks or 96-well plates, then treated with various concentrations of Interferon-γ (IFN-γ 1-500U/ml) or Interleukin-1α (IL-1α; 0.001-10ng/ml) for various times. The cells were then washed in PBS and fixed in 1% paraformaldehyde in PBS. ICAM-1 expression was measured using FACS analysis and a cell-based ELISA assay using a monoclonal mouse anti-human ICAM-1 antibody. Results. IFN-γ induced a dose and time dependent increase in ICAM-1 expression. Maximal expression was seen at 50U/ml using both FACS analysis and the ELISA. ICAM-1 expression increased 20-fold over control values. No change in ICAM-1 expression could be detected after IL-1α treatment with either technique. Conclusions. We demonstrate that ICAM-1 can be up-regulated by the cytokine IFN-γ on cultured primary human corneal epithelial cells in a dose and time dependent fashion. The expression of corneal epithelial ICAM-1 during inflammation associated with a severe allergic response could contribute to corneal damage by aiding in the attachment of eosinophils.

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