Commensal Communism and the Oral Cavity
- 1 September 1998
- journal article
- review article
- Published by SAGE Publications in Journal of Dental Research
- Vol. 77 (9) , 1674-1683
- https://doi.org/10.1177/00220345980770090301
Abstract
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 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 Hpopotysaccharide, 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 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.Keywords
This publication has 66 references indexed in Scilit:
- Homo bacteriens and a network of surpriseJournal of Medical Microbiology, 1996
- Platelet-Streptococcal Interactions in EndocarditisCritical Reviews in Oral Biology & Medicine, 1996
- A purified protein fromSalmonella typhimuriuminhibits proliferation of murine splenic anti-CD3 antibody-activated T-lymphocytesFEMS Immunology & Medical Microbiology, 1996
- Surface‐Associated Material from the Bacterium Actinobacillus actinomycetemcomitans Contains A Peptide Which, in Contrast to Lipopolysaccharide, Directly Stimulates Fibroblast Interleukin‐6 Gene TranscriptionEuropean Journal of Biochemistry, 1996
- Modulins: A new class of cytokine-inducing, pro-inflammatory bacterial virulence factorInflammation Research, 1995
- Peptide Antibiotics and Their Role in Innate ImmunityAnnual Review of Immunology, 1995
- Chemotactic and protease‐inhibiting activities of antibiotic peptide precursorsFEBS Letters, 1993
- A soluble receptor for interleukin-1β encoded by vaccinia virus: A novel mechanism of virus modulation of the host response to infectionCell, 1992
- Viral inhibition of inflammation: Cowpox virus encodes an inhibitor of the interleukin-1β converting enzymeCell, 1992
- Enhancement of Growth of Virulent Strains of Escherichia coli by Interleukin-1Science, 1991