title: Analysis of corneal inflammation induced by cauterisation in CCR2 and MCP-1 knockout mice.
abstract: OBJECTIVE
  To elucidate the role of CCR2/MCP-1 in corneal inflammation.
  
  
  METHODS
  A cauterisation induced corneal inflammation model was used. The corneas were cauterised with silver nitrate in CCR2 knockout (KO) mice, MCP-1 KO mice, and control mice. Clinical signs such as corneal oedema and opacity were examined 96 hours after cauterisation and the phenotypes of the cells infiltrating the cornea were analysed by flow cytometry. Corneal inflammation in neutrophil depleted mice was also analysed.
  
  
  RESULTS
  After cauterisation both CCR2 KO and MCP-1 KO mice showed the same levels of corneal oedema and opacity as control mice. Flow cytometry revealed that in control mice most of the infiltrating cells were neutrophils and macrophages, whereas in both CCR2 KO mice and MCP-1 KO mice, the number of macrophages infiltrating the cornea were markedly reduced. However, prominent infiltrates of neutrophils were still observed in the cornea in CCR2 KO mice and MCP-1 KO mice. The depletion of neutrophils significantly reduced the oedema and opacity induced in the cornea by cauterisation.
  
  
  CONCLUSIONS
  The CCR2 and MCP-1 molecules are not essential for cauterisation induced corneal inflammation. Neutrophils, rather than migrated macrophages, are the final effector cells involved in inducing inflammation in this model.
authors.affiliation: Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Oshima
authors.forename: K-H
authors.initials: KH
authors.lastname: Sonoda
authors.forename: C
authors.initials: C
authors.lastname: Tsutsumi-Miyahara
authors.forename: H
authors.initials: H
authors.lastname: Qiao
authors.forename: T
authors.initials: T
authors.lastname: Hisatomi
authors.forename: S
authors.initials: S
authors.lastname: Nakao
authors.forename: S
authors.initials: S
authors.lastname: Hamano
authors.forename: K
authors.initials: K
authors.lastname: Egashira
authors.forename: I F
authors.initials: IF
authors.lastname: Charo
authors.forename: T
authors.initials: T
authors.lastname: Ishibashi
mesh_terms: D000818:Animals; D002425:Cautery; D002452:Cell Count; D018932:Chemokine CCL2 / Q000276:immunology*; D003315:Cornea / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D003316:Corneal Diseases / Q000276:immunology* / Q000473:pathology; D015715:Corneal Edema / Q000276:immunology; D003318:Corneal Opacity / Q000276:immunology; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry / Q000379:methods; D007249:Inflammation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000276:immunology*
chemical_list: C491768:Ccl2 protein, mouse; C515335:Ccr2 protein, mouse; D018932:Chemokine CCL2; D054390:Receptors, CCR2; D019707:Receptors, Chemokine