Attachment of Fusobacterium nucleatum PK1594 to mammalian cells and its coaggregation with periodontopathogenic bacteria are mediated by the same galactose-binding adhesin.
Attachment of Fusobacterium nucleatum PK1594 to mammalian cells and its coaggregation with periodontopathogenic bacteria are mediated by the same galactose-binding adhesin.
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具核梭杆菌 PK1594 与哺乳动物细胞的附着及其与牙周病原菌的共聚集是由相同的半乳糖结合粘附素介导的。
DOI：
10.1034/j.1399-302x.2000.150606.x
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发表时间：
2000
影响因子：
--
通讯作者：
Metzger,Z
中科院分区：
文献类型：
--
作者：
Weiss,EI;Shaniztki,B;Dotan,M;Ganeshkumar,N;Kolenbrander,PE;Metzger,Z
研究表明，核梭杆菌pk1594与牙龈卟啉单胞菌pk1924通过一种半乳糖结合黏附素共同聚集。在本研究中，依恋断。对多种哺乳动物细胞的nucleatumPK1594进行了表征。nucleatumPK1594附着在所有真核细胞上，包括人颊上皮细胞、牙龈和牙周韧带成纤维细胞、HeLa细胞和小鼠淋巴细胞、巨噬细胞和多形核白细胞。这些附着物(i)被半乳糖、乳糖和n‐乙酰半乳糖胺抑制，（ii）被半乳糖结合黏附素特异性单克隆抗体抑制。nucleatumPK1594。此外，一个共聚集缺陷突变体ofF。不表现半乳糖结合活性的nucleatumPK1594 （PK2172）没有附着在哺乳动物细胞上。Coaggregation。nucleatumPK1594 withP。gingivalisPK 1924和actinobacillus放线菌comitansjp2与糖、单克隆抗体和黏附素缺陷突变体表现出相似的模式，但与其他细菌无关。结果表明，附件关闭。nucleatumPK1594向哺乳动物细胞的转移及其与牙周病原体的共聚集是由相同的半乳糖结合黏附素介导的。
It has been shown thatFusobacterium nucleatumPK1594 coaggregates withProphyromonas gingivalisPK1924 through a galactose‐binding adhesin. In the present study, attachment ofF. nucleatumPK1594 to a variety of mammalian cells was characterized.F. nucleatumPK1594 attached to all eukaryotic cells tested, including human buccal epithelial cells, gingival and periodontal ligament fibroblasts, HeLa cells and murine lymphocytes, macrophages, and polymorphonuclear leukocytes. These attachments were (i) inhibited by galactose, lactose andN‐acetylgalactosamine and (ii) inhibited by monoclonal antibody specific for the galactose‐binding adhesin ofF. nucleatumPK1594. In addition, a coaggregation‐defective mutant ofF. nucleatumPK1594 (PK2172), which does not exhibit galactose binding activity, did not attach to the mammalian cells. Coaggregation ofF. nucleatumPK1594 withP. gingivalisPK 1924 andActinobacillus actinomycetemcomitansJP2, but not with other bacteria, showed a similar pattern with sugars, monoclonal antibody, and the adhesin‐deficient mutant. The results suggest that the attachment ofF. nucleatumPK1594 to mammalian cells and its coaggregation with periodontal pathogens are mediated by the same galactose‐binding adhesin.