密螺旋体属的口腔细菌通常聚集起来，和其它口腔细菌混合起来产生破坏性的牙菌斑，由细菌、唾液和食物残渣组成的牙菌斑成为牙龈出血和牙周炎的主要原因，如果严重，后期会发展成严重的牙周炎，甚至牙齿掉落，造成牙周病的主要原因是口腔中各种细菌的相互作用。
来自英国的研究人员近日在密螺旋体属口腔细菌表面发现了一个CTLP分子，该分子可以识别不同的口腔细菌群落，并且吸附至其它细菌表面，一旦CTLP与其它细菌表面的分子混合，就开始在口腔中肆虐，抑制血液凝固，造成组织坏死。
Howard Jenkinson教授领导这一研究，研究论文已于近日刊登在了国际杂志Microbiology上，他表示，牙周病和牙龈出血是常见病，这种病影响很多人，包括老人，怀孕妇女和糖尿病患者，发明新的控制方法去控制口腔细菌的感染需要深入了解感染涉及的微生物，他们之间是如何进行反应的，而且还要深入了解这些口腔微生物之间是如何合作从而造成牙菌斑的。
这项研究的亮点在于发现了CTLP可以作为潜在的治疗口腔感染的新的药物靶点，CTLP分子可以让密螺旋体属的口腔细菌随意进入别的细菌构筑的社区，而且可以进行生长和繁殖，抑制了这个分子，将会阻止密螺旋体属的口腔细菌进入其它细菌的社区，进而防治了联合感染引起的牙出血，研究小组目前正在着手寻找可以抑制CTLP分子的化合物，Jenkinson教授表示，如果可以找到一种抑制CTLP分子的化合物，就可以在牙龈出血的高危病人身上进行实验。
这项最新的研究也支持了Jenkinson教授先前的关于口腔有害细菌的研究结果，Jenkinson教授最后说，保持一个有规律的刷牙习惯和保持口腔卫生对于抑制口腔有害细菌是非常重要的。（生物谷：T.Shen编译）
doi:10.1099/mic.0.055939-0
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PMID:
Treponema denticola chymotrypsin-like proteinase (CTLP) integrates spirochaetes within oral microbial communities
V. Cogoni1, A. Morgan-Smith1, J. C. Fenno2, H. F. Jenkinson1,3 and D. Dymock1
Treponema denticola is found ubiquitously in the human oral cavity and is mainly associated with bacterial communities implicated in the establishment and development of periodontal disease. The ability to become integrated within biofilm communities is crucial to the growth and survival of oral bacteria, and involves inter-bacterial coaggregation, metabolic co-operation, and synergy against host defences. In this article we show that the chymotrypsin-like proteinase (CTLP), found within a high molecular mass complex on the cell surface, mediates adherence of T. denticola to other potential periodontal pathogens Porphyromonas gingivalis, Fusobacterium nucleatum, Prevotella intermedia, and Parvimonas micra. Proteolytic activity per se did not appear to be required for the interactions, and expression of the major outer sheath protein (Msp) was not necessary, except for binding P. micra. Biofilms of densely packed cells and matrix, up to 40 µm in depth, were formed between T. denticola and P. gingivalis on salivary pellicle, with T. denticola cells enriched in the upper layers. Expression of CTLP, but not Msp, was critical for dual species biofilm formation with P. gingivalis. T. denticola did not form dual-species biofilms with any of the other three periodontal bacterial species under various conditions. Synergy between T. denticola and P. gingivalis was also shown with increased inhibition of blood clotting, which was CTLP-dependent. The results demonstrate the critical role of CTLP in interactions of T. denticola with other oral microorganisms, leading to synergy in microbial community development and host tissue pathogenesis.
