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Macrophage inflammatory protein‐2 and vascular endothelial growth factor regulate corneal neovascularization induced by infection with Pseudomonas aeruginosa in mice
Author(s) -
Xue Meilang,
Thakur Archana,
Willcox Mark
Publication year - 2002
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.2002.01094.x
Subject(s) - corneal neovascularization , neovascularization , vascular endothelial growth factor , cornea , macrophage inflammatory protein , macrophage , immunology , angiogenesis , pseudomonas aeruginosa , immunohistochemistry , vascular endothelial growth factor a , biology , inflammation , medicine , chemokine , cancer research , vegf receptors , ophthalmology , bacteria , in vitro , biochemistry , genetics
Pseudomonas aeruginosa ocular infection causes extensive corneal neovascularization. The purpose of the present study was to investigate the role of the angiogenic factors macrophage inflammatory protein‐2 (MIP‐2) and vascular endothelial growth factor (VEGF) in the regulation of corneal neovascularization during P. aeruginosa ocular infection. After administering anti‐MIP‐2 antibody or control antibody, mouse corneas were challenged with P. aeruginosa . The expression of MIP‐2 and VEGF was detected using an ELISA from ocular homogenates. Corneal neovascularization was examined by histology. The cellular sources of MIP‐2 and VEGF were identified by immunohistochemistry. In addition, protein expression of MIP‐2 and VEGF in isolated corneas was measured to determine the ability of the cornea to produce these two mediators. Results showed that the expression of MIP‐2 and VEGF was significantly ( P < 0.05) elevated after bacterial infection, and high levels of these two mediators paralleled the extensive corneal neovascularization seen at later stages of the infection. Anti‐MIP‐2 antibody treatment resulted in a significant ( P < 0.05) reduction in VEGF expression and in corneal neovascularization. Both corneal resident cells and infiltrating neutrophils had the ability to produce MIP‐2 and VEGF after stimulation. The present study demonstrates that both MIP‐2 and VEGF are important mediators in the regulation of corneal neovascularization caused by P. aeruginosa infection, and that MIP‐2 regulates the production of VEGF.