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Uveitis induction in the rabbit by muramyl dipeptides.

机译：鼠基二肽在兔中引起葡萄膜炎。

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Intraocular inflammation (uveitis) was produced in rabbits by intravenous or subcutaneous treatment with N-acetylmuramyl-L-alanyl-D-isoglutamine and several of its synthetic analogs at doses of greater than or equal to 0.2 mg/kg in saline. A dose-dependent increase in permeability of the ocular blood-aqueous barrier as measured by leakage of protein or fluoresceinated dextran from the serum into the eye was observed from 2 to 14 h after glycopeptide treatment. Peak response occurred at approximately 3 h postdose. The lowest dose found to produce maximal vascular leakage for the most active glycopeptide analogs was 1 mg/kg. The adjuvant-inactive L-L stereoisomer of N-acetylmuramyl-L-alanyl-D-isoglutamine was inactive, even at doses as high as 10 mg/kg. Analogs of N-acetylmuramyl-L-alanyl-D-isoglutamine which were homologous in the lactyl side chain were found to cause less uveitis. Chronic biweekly intravenous treatment of rabbits for 1 month with either N-acetyl-L-alpha-aminobutyryl-D-isoglutamine or its lipophilic 6-O-stearoyl derivative at 1 mg/kg, but not with murabutide, resulted in leukocytic inflammatory lesions unique to the uveal tract of the eye. The uveitis was potentially reversible and occurred with decreased severity as long as 2 months after cessation of chronic treatment. Vascular leakage but not cellular infiltrate in the choroid could be modulated by pharmacologic means. Pyrogenicity but not adjuvanticity correlated with ability of glycopeptides to induce vascular leakage. Several adjuvant-active muramyl dipeptide analogs with minimal ability to cause acute vascular leakage or chronic inflammation in the rabbit eye have been identified.
机译：眼内炎症（葡萄膜炎）是通过在生理盐水中以大于或等于0.2 mg / kg的剂量通过N-乙酰基muramyl-L-丙氨酰-D-异谷氨酰胺及其几种合成类似物进行静脉内或皮下治疗而产生的。在糖肽处理后2到14小时内，观察到眼血水屏障渗透性的剂量依赖性增加，这是通过蛋白质或荧光右旋糖酐从血清渗入眼中所测得的。用药后约3小时出现高峰反应。对于活性最高的糖肽类似物，发现产生最大血管渗漏的最低剂量为1 mg / kg。 N-乙酰基村/基-L-丙氨酰-D-异谷氨酰胺的佐剂无活性的L-L立体异构体即使在高达10 mg / kg的剂量下也无活性。发现在乳酰基侧链上同源的N-乙酰基村酰基-L-丙氨酰基-D-异谷氨酰胺的类似物引起较少的葡萄膜炎。用1 mg / kg的N-乙酰基-L-α-氨基丁酰基-D-异谷氨酰胺或其亲脂性6-O-硬脂酰衍生物对兔子进行的慢性双周静脉治疗1个月，但不使用murabutide，导致独特的白细胞炎性病变到眼睛的葡萄膜葡萄膜炎可能是可逆的，并且在停止长期治疗后的2个月内，其严重程度降低。脉络膜中的血管渗漏而不是细胞浸润可以通过药理学手段进行调节。热原性而不是佐剂性与糖肽诱导血管渗漏的能力有关。已经鉴定了几种具有最小的引起兔眼急性血管渗漏或慢性炎症的能力的佐剂活性的穆拉基二肽类似物。

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