Tzianabos A O, Onderdonk A B, Smith R S, Kasper D L
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Infect Immun. 1994 Aug;62(8):3590-3. doi: 10.1128/iai.62.8.3590-3593.1994.
We have previously shown that in an animal model of sepsis positively and negatively charged groups on polysaccharide A of Bacteroides fragilis are essential for the induction of intra-abdominal abscess formation (A. O. Tzianabos, A. B. Onderdonk, B. Rosner, R. L. Cisneros, and D. L. Kasper, Science 262:416-419, 1993). By introducing chemical modifications into the structures of B. fragilis polysaccharide B as well as other abscess-inducing bacterial polysaccharides, we observed the following. (i) The presence of a nonacetylated free amino group on these polysaccharides appears to be required for abscess induction. (ii) No specific type of negatively charged group is essential to abscess induction by these polysaccharides. (iii) The density of free amino groups on these polysaccharides influences this pathobiologic host response.
我们之前已经表明,在脓毒症动物模型中,脆弱拟杆菌多糖A上的正负电荷基团对于腹腔脓肿形成的诱导至关重要(A. O. 齐亚纳博斯、A. B. 翁德东克、B. 罗斯纳、R. L. 西斯内罗斯和D. L. 卡斯珀,《科学》262:416 - 419,1993年)。通过对脆弱拟杆菌多糖B以及其他诱导脓肿的细菌多糖的结构进行化学修饰,我们观察到以下情况。(i)这些多糖上存在未乙酰化的游离氨基似乎是诱导脓肿所必需的。(ii)对于这些多糖诱导脓肿而言,不存在特定类型的负电荷基团是必不可少的。(iii)这些多糖上游离氨基的密度会影响这种病理生物学宿主反应。