DETOXIFICATION OF BACTERIAL LIPOPOLYSACCHARIDES (ENDOTOXINS) BY A HUMAN NEUTROPHIL ENZYME
DETOXIFICATION OF BACTERIAL LIPOPOLYSACCHARIDES (ENDOTOXINS) BY A HUMAN NEUTROPHIL ENZYME
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DOI：
10.1126/science.3529396
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发表时间：
1986-10-10
期刊：
影响因子：
56.9
通讯作者：
HALL, CL
中科院分区：
文献类型：
--
作者：
MUNFORD, RS;HALL, CL
革兰氏阴性菌细胞壁中的脂多糖在动物中引起毒性以及潜在有益的炎症反应。目前报道，脂多糖引起的组织毒性优先通过人中性粒细胞中的酶活性降低。酰氧基酰基水解除去与脂多糖的生物活性脂质A部分中的3-羟基十四酰基残基的羟基连接的脂肪酰基链。最大的酰氧酰基水解减少脂多糖的组织毒性，如在皮肤Shwartzman反应中测量的，通过100倍或更多。相反，去酰化脂多糖刺激B淋巴细胞分裂的能力仅降低了12倍。有人建议，在组织入侵革兰氏阴性菌酰氧酰基水解可能是一种防御机制，降低脂多糖的毒性，同时保留一些潜在的有益的炎症和免疫刺激。
Lipopolysaccharides in the cell walls of Gram-negative bacteria elicit toxic as well as potentially beneficial inflammatory responses in animals. It is now reported that tissue toxicity caused by lipopolysaccharides is preferentially reduced by an enzymatic activity in human neutrophils. Acyloxyacyl hydrolysis removes fatty acyl chains that are linked to the hydroxyl groups of 3-hydroxytetradecanoyl residues in the bioactive lipid A moiety of the lipopolysaccharides. Maximal acyloxyacyl hydrolysis reduced lipopolysaccharide tissue toxicity, as measured in the dermal Shwartzman reaction, by a factor of 100 or more. In contrast, the ability of the deacylated lipopolysaccharides to stimulate B lymphocytes to divide was decreased only by a factor of 12. It is suggested that during tissue invasion by Gram-negative bacteria acyloxyacyl hydrolysis may be a defense mechanism that reduces the toxicity of lipopolysaccharides while preserving some of their potentially beneficial inflammatory and immune stimuli.