Henderson B, Wilson M
Division of Surgical Sciences, Eastman Dental Institute, University College London, United Kingdom.
J Dent Res. 1998 Sep;77(9):1674-83. doi: 10.1177/00220345980770090301.
The world we live in contains unimaginable numbers of bacteria, and these and other single-celled creatures represent the major diversity of life on our planet. During the last decade or so, the complexity and intimacy of the interactions which occur between bacteria and host eukaryotic cells during the process of infection have begun to emerge. The study of such interactions is the subject of the new discipline of cellular microbiology. This intimacy of bacteria/host interactions creates a major paradox. The average human being is 90% bacteria in terms of cell numbers. These bacteria constitute the commensal or normal microflora and populate the mucosal surfaces of the oral cavity, gastrointestinal tract, urogenital tract, and the surface of the skin. In bacterial infections, much of the pathology is due to the release of a range of bacterial components (e.g., modulins such as lipopolysaccharide, peptidoglycan, DNA, molecular chaperones), which induce the synthesis of the local hormone-like molecules known as pro-inflammatory cytokines. However, such components must also be constantly released by the vast numbers of bacteria constituting the normal microflora and, as a consequence, our mucosae should constantly be in a state of inflammation. This is patently not the case, and a hypothesis is forwarded to account for this "commensal paradox", namely, that our commensal bacteria and mucosal surfaces exist in a state of bio-communism, forming a unified "tissue" in which interactions between bacteria and epithelia are finely balanced to ensure bacterial survival and prevent the induction of damaging inflammation. Evidence is emerging that bacteria can produce a variety of proteins which can inhibit the synthesis/release of inflammatory cytokines. The authors predict that such proteins are simply one part of an extensive signaling system which occurs between bacteria and epithelial cells at mucosal surfaces such as those found in the oral cavity.
我们生活的世界中存在着数量难以想象的细菌,这些细菌以及其他单细胞生物代表了我们星球上生命的主要多样性。在过去十年左右的时间里,细菌与宿主真核细胞在感染过程中发生的相互作用的复杂性和密切程度已开始显现出来。对这种相互作用的研究是细胞微生物学这一新学科的主题。细菌与宿主相互作用的这种密切性产生了一个主要的矛盾。就细胞数量而言,普通人身体的90%是细菌。这些细菌构成了共生菌或正常微生物群,分布在口腔、胃肠道、泌尿生殖道和皮肤表面的黏膜上。在细菌感染中,许多病理情况是由于一系列细菌成分(如脂多糖、肽聚糖、DNA、分子伴侣等调节素)的释放,这些成分会诱导合成称为促炎细胞因子的局部激素样分子。然而,构成正常微生物群的大量细菌也必须不断释放这些成分,因此,我们的黏膜应该一直处于炎症状态。但显然并非如此,于是有人提出了一个假说来解释这种“共生菌矛盾”,即我们的共生菌和黏膜表面处于生物共生状态,形成一个统一的“组织”,其中细菌与上皮细胞之间的相互作用达到了精细的平衡,以确保细菌的存活并防止引发有害炎症。越来越多的证据表明,细菌可以产生多种能够抑制炎症细胞因子合成/释放的蛋白质。作者预测,这类蛋白质只是在口腔等黏膜表面的细菌与上皮细胞之间发生的广泛信号系统的一部分。