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Br J Ophthalmol 2000;84:85-91 doi:10.1136/bjo.84.1.85
  • Original Article
    • Laboratory science

Expression of gelatinase B in trachomatous conjunctivitis

  1. Ahmed M Abu El-Asrara,
  2. Karel Geboesb,
  3. Soliman A Al-Kharashia,
  4. Abdulrahman A Al-Mosallama,
  5. Luc Missottenc,
  6. Liesbet Paemend,
  7. Ghislain Opdenakkerd
  1. aDepartment of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia, bLaboratory of Histochemistry and Cytochemistry, University Hospital St Rafael, Leuven, Belgium, cDepartment of Ophthalmology, dRega Institute for Medical Research, Laboratory of Molecular Immunology, University of Leuven, Leuven, Belgium
  1. Dr Ahmed M Abu El-Asrar, Department of Ophthalmology, King Abdulaziz University Hospital, Airport Road, PO Box 245, Riyadh 11411, Saudi Arabia
  • Accepted 6 September 1999

Abstract

BACKGROUND/AIMS Gelatinase B is a matrix metalloproteinase involved in extracellular matrix (ECM) breakdown often associated with scarring and other pathological disorders. It was investigated whether gelatinase B is involved in the pathogenesis of ECM degradation associated with trachomatous conjunctivitis.

METHODS Conjunctival biopsy specimens obtained from six patients with active trachoma, six patients with active vernal keratoconjunctivitis (VKC), and seven control subjects were studied. Immunohistochemical techniques and a specific monoclonal antibody against human gelatinase B were used, and a monoclonal antibody against macrophage CD68 to identify mononuclear cells with gelatinase B immunoreactivity. In addition, quantitative zymography was used to compare the activity of gelatinase B in conjunctival biopsy specimens from seven patients with active trachoma and seven control subjects.

RESULTS Gelatinase B was detected by immunohistochemistry only in polymorphonuclear cells located in the vascular lumens in three normal conjunctival biopsy specimens. In all trachoma specimens and in five VKC specimens, gelatinase B was localised in monocyte/macrophage cells, positive for the CD68 marker, and in polymorphonuclear cells. The majority of the latter cell type was located in intravascular spaces. Compared with VKC specimens, trachoma specimens showed significantly more immunoreactive gelatinase B monocyte/macrophage cells (52.3 (21.9)v 8.2 (6.4); p <0.001) and polymorphonuclear cells (23.2 (14.2) v 6.3 (5.4); p = 0.013). Activated macrophages with giant cell morphology clearly stained with the gelatinase B specific monoclonal antibody were observed in trachoma specimens. Zymography revealed that gelatinase B levels in trachoma specimens were significantly higher than the levels found in normal conjunctiva (1739.6 (1078.3)v 609.3 (395.9) scanning units; p = 0.0127).

CONCLUSIONS The increased activity of gelatinase B and numbers of inflammatory cells containing gelatinase B in trachoma specimens suggest that this enzyme plays a part in the pathogenesis of conjunctival scarring in trachoma.

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