Nishihara T, Koga T, Hamada S
Department of Dental Research, National Institute of Health, Tokyo, Japan.
Infect Immun. 1988 Mar;56(3):619-25. doi: 10.1128/iai.56.3.619-625.1988.
Lipopolysaccharide (LPS) was extracted from whole cells of Haemophilus actinomycetemcomitans Y4 by the hot phenol-water procedure. LPS was cleaved into its lipid A and polysaccharide moieties by hydrolysis in 1% acetic acid. The major component sugars of the polysaccharide were glucose, heptose, rhamnose, galactose, and fucose. LPS and lipid A from H. actinomycetemcomitans induced the release of interleukin-1 (IL-1) by LPS-responsive C3H/HeN murine peritoneal macrophages and cell line macrophages (P388D1 and J744.1), but not by LPS-nonresponsive C3H/HeJ peritoneal macrophages. The polysaccharide was unable to induce the release of IL-1. It suppressed the IL-1 release from LPS- and lipid A-stimulated macrophages, but not the production of cell-associated and intracellular IL-1. The addition of rhamnose, a sugar component of the polysaccharide, abrogated the inhibitory effect of the polysaccharide on IL-1 release. These results suggest the participation of a lectinlike molecule in IL-1 release.
采用热酚水法从伴放线放线杆菌Y4全细胞中提取脂多糖（LPS）。通过在1%乙酸中水解，将LPS裂解为其脂质A和多糖部分。多糖的主要组成糖为葡萄糖、庚糖、鼠李糖、半乳糖和岩藻糖。伴放线放线杆菌的LPS和脂质A可诱导LPS反应性C3H/HeN小鼠腹腔巨噬细胞和细胞系巨噬细胞（P388D1和J744.1）释放白细胞介素-1（IL-1），但不能诱导LPS无反应性C3H/HeJ腹腔巨噬细胞释放IL-1。该多糖不能诱导IL-1的释放。它抑制了LPS和脂质A刺激的巨噬细胞释放IL-1，但不抑制细胞相关和细胞内IL-1的产生。添加多糖的糖成分鼠李糖可消除多糖对IL-1释放的抑制作用。这些结果表明一种类凝集素分子参与了IL-1的释放。
