Local chemokine paralysis, a novel pathogenic mechanism for Porphyromonas gingivalis
Local chemokine paralysis, a novel pathogenic mechanism for Porphyromonas gingivalis
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DOI：
10.1128/iai.66.4.1660-1665.1998
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发表时间：
1998-04-01
影响因子：
3.1
通讯作者：
Lamont, RJ
中科院分区：
文献类型：
--
作者：
Darveau, RP;Belton, CM;Lamont, RJ
牙周炎是一种与牙龈卟啉单胞菌相关的持续性细菌感染，广泛存在于成人人群中。牙龈上皮细胞是牙龈假单胞菌和口腔共生细菌首先接触到的细胞之一。趋化因子白介素8(IL-8)是一种强有力的趋化因子和多形核白细胞的激活剂，由牙龈上皮细胞对正常口腔菌群组分的反应而分泌。相反，牙龈假单胞菌被发现强烈抑制牙龈上皮细胞中IL-8的积累。抑制作用与IL-8的mRNA表达减少有关。在KB细胞中没有出现IL-8积累的拮抗作用，KB细胞系是一种不支持牙龈假单胞菌高水平细胞内侵袭的上皮细胞株。此外，牙龈假单胞菌的非侵袭性突变体不能拮抗IL-8的积累。侵袭性破坏牙龈假单胞菌定植部位的IL-8趋化因子梯度(局部趋化因子麻痹)将严重损害粘膜防御，是细菌定植宿主组织的一种新机制。
Periodontitis, which is widespread in the adult population, is a persistent bacterial infection associated with Porphyromonas gingivalis. Gingival epithelial cells are among the first cells encountered by both P. gingivalis and commensal oral bacteria. The chemokine interleukin 8 (IL-8), a potent chemoattractant and activator of polymorphonuclear leukocytes, was secreted by gingival epithelial cells in response to components of the normal oral flora. In contrast, P. gingivalis was found to strongly inhibit IL-8 accumulation from gingival epithelial cells. Inhibition was associated with a decrease in mRNA for IL-8. Antagonism of IL-8 accumulation did not occur in KB cells, an epithelial cell line that does not support high levels of intracellular invasion by P. gingivalis. Furthermore, a noninvasive mutant of P. gingivalis was unable to antagonize IL-8 accumulation. Invasion-dependent destruction of the gingival IL-8 chemokine gradient at sites of P. gingivalis colonization (local chemokine paralysis) will severely impair mucosal defense and represents a novel mechanism for bacterial colonization of host tissue.