Peterson A A, Munford R S
Infect Immun. 1987 Apr;55(4):974-8. doi: 10.1128/iai.55.4.974-978.1987.
An Escherichia coli deep rough lipopolysaccharide (LPS), biosynthetically labeled with 32PO4 and [3H]glucosamine, was used to study dephosphorylation of the lipid A moiety by murine macrophages. Over a 48-h incubation period, the macrophages removed approximately two-thirds of the 32P from [3H32P]LPS that was added to the culture medium. The LPS-derived phosphate was incorporated into cell components (e.g., phospholipids), as well as released from the cells. Cell lysates were also able to remove phosphate from [3H32P]LPS. The phosphatase activity was optimal at acidic pH and was greatly reduced by 10 mM sodium fluoride or heating at 80 degrees C. There was no evident difference in the LPS-dephosphorylating ability of macrophages from LPS-responsive and -hyporesponsive mice. The results indicate that murine macrophages dephosphorylate the lipid A moiety of deep rough E. coli LPS and raise the possibility that enzymatic dephosphorylation may modify LPS bioactivity.
用经32PO4和[3H]葡糖胺进行生物合成标记的大肠杆菌深粗糙型脂多糖（LPS），研究小鼠巨噬细胞对脂质A部分的去磷酸化作用。在48小时的孵育期内，巨噬细胞从添加到培养基中的[3H32P]LPS中去除了约三分之二的32P。LPS衍生的磷酸盐被整合到细胞成分（如磷脂）中，同时也从细胞中释放出来。细胞裂解物也能够从[3H32P]LPS中去除磷酸盐。磷酸酶活性在酸性pH下最佳，10 mM氟化钠或80℃加热可使其大大降低。LPS反应性和低反应性小鼠的巨噬细胞在LPS去磷酸化能力上没有明显差异。结果表明，小鼠巨噬细胞可使深粗糙型大肠杆菌LPS的脂质A部分去磷酸化，并增加了酶促去磷酸化可能改变LPS生物活性的可能性。
