May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Tumor Necrosis Factor- (TNF-) and TNF- Receptor R1 in Peripheral Ulcerative Keratitis (PUK)
Author Affiliations & Notes
  • C.V. Chandrupatla
    Department of Ophthalmology and Visual Sciences, University of Illinois, Chicago, IL, United States
  • S. Grover
    Department of Ophthalmology and Visual Sciences, University of Illinois, Chicago, IL, United States
  • D.P. Edward
    Department of Ophthalmology and Visual Sciences, University of Illinois, Chicago, IL, United States
  • Footnotes
    Commercial Relationships  C.V. Chandrupatla, None; S. Grover, None; D.P. Edward, None.
  • Footnotes
    Support  Illinois Society of Prevention of Blindness
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1397. doi:
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      C.V. Chandrupatla, S. Grover, D.P. Edward; Tumor Necrosis Factor- (TNF-) and TNF- Receptor R1 in Peripheral Ulcerative Keratitis (PUK) . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1397.

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

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Abstract

Abstract: : Purpose: TNF-α is a cytokine that is an important mediator of inflammation. Its presence and its role in PUK have not yet been investigated. It is hypothesized that TNF-α and its receptor, R1 might be upregulated in PUK, and play a role in corneal ulceration and melt. This experiment seeks to determine if TNF-α and TNF-α R1 can be immunolocalized in normal human corneas, and if their expression was increased in corneas with PUK and bullous keratopathy (BK). Methods: Thirteen corneas each with PUK (ages, 21-71 years) and BK (ages, 32-91 years) were compared to fourteen normal human corneas (ages, 45-84 years). Indirect immunohistochemistry was performed on deparaffinized slides using antibodies against TNF-α and TNF-α R1. The corneal epithelium, keratocytes, and inflammatory cells, when present, were examined for immunoreactivity and the intensity graded by two independent observers. Results: In normal corneas, anti-TNF-α immunostaining was absent in all layers in a majority of specimens. 3/14 normal corneas showed weak staining in the basal epithelium. In PUK, 4/13 specimens with epithelium present showed moderate to intense anti-TNF-α staining. In addition, 12/13 PUK specimens showed mild to moderate staining of anti-TNF-α in keratocytes mainly localized to the area of ulceration. Also, 12/13 specimens showed mild to moderate staining of the inflammatory cells in the cornea. In BK, 5/13 specimens showed mild anti-TNF-α immunostaining in the basal epithelium and mild labeling in the keratocytes in 8/13 specimens. Anti-TNF-α staining was negative in the corneal endothelium in all sections examined. Anti-TNF-α R1 immunostaining was mildly positive in focal inflammatory cells in 4/12 PUK specimens, whereas immunolabeling was absent in the epithelium, keratocytes and endothelium in PUK, BK and normal corneas. Conclusions: In PUK, increased intensity of TNF-α immunoreactivity was observed not only in the inflammatory cells but also in the keratocytes and basal epithelium when compared to normal and BK corneas. This could imply the upregulation of TNF-α in PUK and a possible role in the mechanism of corneal melt; however, the absence of TNF-α R1 immunoreactivity suggests that this receptor is unlikely to play a role in the pathogenesis of PUK. TNF-α may represent a target for therapy against the inflammatory reaction induced in autoimmune corneal degenerative diseases.

Keywords: cytokines/chemokines • cornea: stroma and keratocytes • keratitis 
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