title: [Fibrocyte reaction to interleukin 1 stimulation in keratoconus. Original title: Fibrocyte response to interleukin 1 stimulation in keratoconus].
abstract: BACKGROUND
  The reduced mechanical strength of the tissues around a keratoconus and the ultrastructural disorganization of its matrix components are caused by proteolytic breakdown and incomplete repair. In most biochemical studies on this subject, reduced collagen content and increased collagenase and gelatinase activity have been reported.
  
  
  METHODS
  Since interleukin-1 (IL-1) promotes secretion of prostaglandin E-2 (PG-E2 and collagenase, we were interested in the number of membrane receptors for these cytokines on keratoconus fibroblasts and determined the corresponding dissociation constant (kD). We also studied the kinetics of cyclo-oxygenase and the synthesis of PG-E2, IL-1 and collagen. We compared the data with data from normal human corneas.
  
  
  RESULTS
  1) There was a significant difference (P < 0.05) between the specific binding of [125I]-IL-1 in keratoconic and normal corneal cells. In keratoconus, the number of receptors was four times higher (7000 +/- 100 binding sites per cell) than in normal corneas (1540 +/- 100 binding sites per cell). However, there was little difference between the dissociation constants for keratoconic ([6.21 +/- 0.5] x 10(-11) and normal ([6.27 +/- 0.5] x 10(-11) corneal cells. 2) Under the study conditions, interleukin-1 was found neither in normal nor in keratoconic cornea. 3) Synthesis of PG-E2 without stimulation of cells by IL-1, which was observed in 8 corneas with and 8 without keratoconus, showed that keratoconus cells secrete ten times more PG-E2 than normal corneals cells. If IL-1 is added to the incubation medium, which contains [3H]-labeled arachidonic acid, PG-E2 synthesis increases more than in normal corneal cells. 4) After adding IL-1, the collagen concentration in keratoconus cells in culture was more pronounced than in normal corneal cells.
  
  
  CONCLUSIONS
  It is still not known why the anomalies discussed above occur in keratoconus. The increase in IL-1 receptor expression and the high level of cyclooxygenase activity are very probably due to genetic causes, because they are observed even after 40 generations of cell cultures.
authors.affiliation: Laboratoire de Recherche Ophthalmologique, Hôtel Dieu, Paris.
authors.forename: J
authors.initials: J
authors.lastname: Bureau
authors.forename: Y
authors.initials: Y
authors.lastname: Pouliquen
authors.forename: G
authors.initials: G
authors.lastname: Lorans
mesh_terms: D002478:Cells, Cultured; D017364:Collagenases / Q000502:physiology; D015232:Dinoprostone / Q000096:biosynthesis; D005347:Fibroblasts / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism / Q000494:pharmacology*; D007640:Keratoconus / Q000503:physiopathology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D017472:Receptors, Interleukin-1 / Q000187:drug effects* / Q000502:physiology
chemical_list: D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D011451:Prostaglandin-Endoperoxide Synthases; D017364:Collagenases; D015232:Dinoprostone
vernacular_title: Fibrozytenreaktion auf Interleukin-1-stimulation bei Keratokonus. Originaltitel: Fibrocyte response to interleukin 1 stimulation in keratoconus.