Coyne M J, Tzianabos A O, Mallory B C, Carey V J, Kasper D L, Comstock L E
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Infect Immun. 2001 Jul;69(7):4342-50. doi: 10.1128/IAI.69.7.4342-4350.2001.
Bacteroides fragilis, though only a minor component of the human intestinal commensal flora, is the anaerobe most frequently isolated from intra-abdominal abscesses. B. fragilis 9343 expresses at least three capsular polysaccharides-polysaccharide A (PS A), PS B, and PS C. Purified PS A and PS B have been tested in animal models and are both able to induce the formation of intra-abdominal abscesses. Mutants unable to synthesize PS B or PS C still facilitate abscess formation at levels comparable to those of wild-type 9343. To determine the contribution of PS A to abscess formation in the context of the intact organism, the PS A biosynthesis region was cloned, sequenced, and deleted from 9343 to produce a PS A-negative mutant. Animal experiments demonstrate that the abscess-inducing capability of 9343 is severely attenuated when the organism cannot synthesize PS A, despite continued synthesis of the other capsular polysaccharides. The PS A of 9343 contains an unusual free amino sugar that is essential for abscess formation by this polymer. PCR analysis of the PS A biosynthesis loci of 50 B. fragilis isolates indicates that regions flanking each side of this locus are conserved in all strains. The downstream conserved region includes two terminal PS A biosynthesis genes that homology-based analyses predict are involved in the synthesis and transfer of the free amino sugar of PS A. Conservation of these genes suggests that this sugar is present in the PS A of all serotypes and may explain the abscessogenic nature of B. fragilis.
脆弱拟杆菌虽然只是人类肠道共生菌群的一个次要组成部分,但却是从腹腔脓肿中最常分离出的厌氧菌。脆弱拟杆菌9343表达至少三种荚膜多糖——多糖A(PSA)、PS B和PS C。纯化后的PSA和PS B已在动物模型中进行了测试,二者均能诱导腹腔脓肿的形成。无法合成PS B或PS C的突变体在促进脓肿形成方面仍与野生型9343相当。为了在完整生物体的背景下确定PSA对脓肿形成的作用,对PSA生物合成区域进行了克隆、测序,并从9343中删除以产生一个PSA阴性突变体。动物实验表明,当该生物体无法合成PSA时,尽管其他荚膜多糖仍在持续合成,9343诱导脓肿形成的能力仍会严重减弱。9343的PSA含有一种不寻常的游离氨基糖,该聚合物形成脓肿时此糖必不可少。对50株脆弱拟杆菌分离株的PSA生物合成基因座进行PCR分析表明,该基因座两侧的区域在所有菌株中均保守。下游保守区域包括两个末端PSA生物合成基因,基于同源性的分析预测它们参与PSA游离氨基糖的合成和转移。这些基因的保守性表明该糖存在于所有血清型的PSA中,这可能解释了脆弱拟杆菌的致脓肿特性。