| Complement and periodontitis. | |
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MedLine Citation:
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PMID: 20599785 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although the complement system is centrally involved in host defense, its overactivation or deregulation (e.g., due to inherent host genetic defects or due to pathogen subversion) may excessively amplify inflammation and contribute to immunopathology. Periodontitis is an oral infection-driven chronic inflammatory disease which exerts a systemic impact on health. This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencies in specific complement components appear to predispose to increased susceptibility to periodontitis. Animal model studies and in vitro experiments indicate that periodontal bacteria can either inhibit or activate distinct components of the complement cascade. Porphyromonas gingivalis, a keystone species in periodontitis, subverts complement receptor 3 and C5a anaphylatoxin receptor signaling in ways that promote its adaptive fitness in the presence of non-productive inflammation. Overall, available evidence suggests that complement activation or subversion contributes to periodontal pathogenesis, although not all complement pathways or functions are necessarily destructive. Effective complement-targeted therapeutic intervention in periodontitis would require determining the precise roles of the various inductive or effector complement pathways. This information is essential as it may reveal which specific pathways need to be blocked to counteract microbial evasion and inflammatory pathology or, conversely, kept intact to promote host immunity. |
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Authors:
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George Hajishengallis |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2010-06-23 |
Journal Detail:
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Title: Biochemical pharmacology Volume: 80 ISSN: 1873-2968 ISO Abbreviation: Biochem. Pharmacol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-04 Completed Date: 2010-12-15 Revised Date: 2011-12-19 |
Medline Journal Info:
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Nlm Unique ID: 0101032 Medline TA: Biochem Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 1992-2001 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Microbiology and Immunology, University of Louisville School of Dentistry, Loueisville, KY 40292, USA. g0haji01@louisville.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Complement Activation Complement C5a / physiology Complement Inactivating Agents / pharmacology, therapeutic use Complement System Proteins / genetics, physiology* Genetic Predisposition to Disease Host-Pathogen Interactions Humans Immunity, Innate Macrophage-1 Antigen / physiology Molecular Targeted Therapy Periodontitis / drug therapy, immunology*, microbiology Porphyromonas gingivalis / physiology Receptor, Anaphylatoxin C5a / antagonists & inhibitors, physiology Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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DE015254/DE/NIDCR NIH HHS; DE018292/DE/NIDCR NIH HHS; R01 DE015254-08/DE/NIDCR NIH HHS; R01 DE018292-05/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Complement Inactivating Agents; 0/Macrophage-1 Antigen; 0/Receptor, Anaphylatoxin C5a; 80295-54-1/Complement C5a; 9007-36-7/Complement System Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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