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H. Tamura, J. Kiryu, K. Miyamoto, K. Nishijima, H. Katsuta, S. Miyahara, F. Hirose, K. Musashi, Y. Honda; Changes of inflammatory mediators and leukocyte–endothelial cell interactions in ocular inflammation of diabetic rats. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3205.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Diabetic patients may have abnormal inflammatory reactions to foreign or endogenous stimuli. This study was designed to evaluate inflammatory reactions in the diabetic eye through inflammatory mediators and retinal leukocyte dynamics in the inflamed eyes of diabetic rats. Method: Diabetes was induced in 6–week–old male Long–Evans rats by intraperitoneal injection of streptozotocin (75 mg/kg). Three weeks after diabetes induction, endotoxin–induced uveitis was produced by footpad injection of lipopolysaccharide (LPS). Eight hours after the LPS injection, the mRNA expressions of P–selectin, intercellular adhesion molecule 1 (ICAM–1) and tumor necrosis factor alpha (TNF–α) in the retina were studied. At 6, 12, 24, 48, 72 and 96 hours after LPS injection, leukocyte behavior was evaluated in vivo by aciridine orange digital fluorography. Aqueous humor was collected to count leukocyte infiltrated into the anterior chamber. Results: After injection of LPS, the levels of mRNA expression of P–selectin, ICAM–1 and TNF–α which were upregulated after LPS injection, were lower in diabetic rats than in nondiabetic rats. After injection of LPS, rolling leukocytes were observed along the walls of the major retinal veins. The number of rolling leukocytes increased in a biphasic manner, at 12 and 48 hours. The number of leukocytes accumulating in the retina reached a peak at 72 hours. The maximal numbers of rolling and accumulating leukocytes in the diabetic retina then decreased by 56.3% (p<0.01) and 46.7% (p<0.0001), respectively, as compared with the control retina. In DM rats, leukocyte count in AH were significantly lower than in non–DM rats (p<0.0001). Conclusion: This study shows that endotoxin–induced inflammation is disturbed in the diabetic eye, based on evidence that both the inflammatory mediators and the leukocyte–endothelial cell interactions stimulated by LPS were suppressed in the diabetic retina. Our findings support the theory that ocular inflammatory reactions are impaired in diabetic patients.
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