Commensal communism and the oral cavity.
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.
Henderson
B
B
Division of Surgical Sciences, Eastman Dental Institute, University College London, United Kingdom.
Wilson
M
M
D001424:Bacterial Infections / Q000276:immunology / Q000382:microbiology; D003148:Communism; D016207:Cytokines / Q000276:immunology; D004198:Disease Susceptibility; D006706:Homeostasis / Q000276:immunology; D006801:Humans; D009055:Mouth / Q000276:immunology / Q000382:microbiology* / Q000821:virology*; D009059:Mouth Diseases / Q000276:immunology / Q000382:microbiology; D012016:Reference Values; D013559:Symbiosis / Q000276:immunology
D016207:Cytokines