| Differential cytokine patterns in mouse macrophages and gingival fibroblasts after stimulation with porphyromonas gingivalis or Escherichia coli lipopolysaccharide. | |
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MedLine Citation:
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PMID: 20843233 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: A major cause of chronic inflammatory periodontal disease is Porphyromonas gingivalis, a non-motile, Gram-negative, rod-shaped, anaerobic bacterium. Within gingival tissue, both macrophages and fibroblasts participate in the immune response to foreign entities by releasing cytokines and expressing molecules to recruit and activate lymphocytes. However, the contribution of gingival macrophages and fibroblasts to the immune response to P. gingivalis infection is not fully known. METHODS: The AMJ2-C8 cell line (AM cells), a mouse alveolar macrophage cell line, and ESK-1 cells, a mouse gingival fibroblast cell line made in our laboratory, were treated with lipopolysaccharide (LPS) from either P. gingivalis or Escherichia coli. The expression of immune response molecules was quantified by real-time polymerase chain reaction and enzyme-linked immunoassay. RESULTS: AM and ESK-1 cells responded differently to P. gingivalis and E. coli LPS stimulation. The ESK-1 gingival fibroblast cell line was more responsive to E. coli LPS stimulation as seen by elevated levels of interleukin (IL)-6, inducible nitric oxide, and monocyte chemotactic protein-1 expression relative to stimulation by P. gingivalis LPS. Conversely, the AM macrophage cell line was more responsive to P. gingivalis LPS stimulation, particularly for interleukin IL-1β, IL-6, and monocyte chemotactic protein-1, relative to stimulation by E. coli LPS. CONCLUSION: These findings demonstrate that E. coli LPS induces a stronger cytokine and chemokine response in gingival fibroblasts, whereas P. gingivalis LPS induces a stronger response in macrophages. |
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Authors:
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Katy J Jones; Sanaz Ekhlassi; Dina Montufar-Solis; John R Klein; Jeremy S Schaefer |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2010-09-15 |
Journal Detail:
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Title: Journal of periodontology Volume: 81 ISSN: 1943-3670 ISO Abbreviation: J. Periodontol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-30 Completed Date: 2011-03-29 Revised Date: 2012-05-04 |
Medline Journal Info:
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Nlm Unique ID: 8000345 Medline TA: J Periodontol Country: United States |
Other Details:
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Languages: eng Pagination: 1850-7 Citation Subset: D; IM |
Affiliation:
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Department of Diagnostic Sciences, Dental Branch, University of Texas Health Science Center at Houston, Houston, TX 77054, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line, Transformed Chemokine CCL2 / analysis, immunology Chemokine CCL3 / analysis, immunology Chemokine CCL4 / analysis, immunology Cytokines / analysis, immunology* Enzyme-Linked Immunosorbent Assay Escherichia coli / immunology* Female Fibroblasts / immunology*, microbiology Gingiva / cytology, immunology*, microbiology Interleukin-1beta / analysis, immunology Interleukin-23 / analysis, immunology Interleukin-6 / analysis Lipopolysaccharides / immunology* Macrophages, Alveolar / immunology*, microbiology Mice Mice, Inbred C57BL Mice, Inbred Strains Nitric Oxide Synthase Type II / analysis, immunology Porphyromonas gingivalis / immunology* Reverse Transcriptase Polymerase Chain Reaction |
| Grant Support | |
ID/Acronym/Agency:
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DK035566/DK/NIDDK NIH HHS; R01 DK035566-24A1/DK/NIDDK NIH HHS; R01 DK035566-25/DK/NIDDK NIH HHS; T32DE015355/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cccl4 protein, mouse; 0/Ccl2 protein, mouse; 0/Chemokine CCL2; 0/Chemokine CCL3; 0/Chemokine CCL4; 0/Cytokines; 0/Interleukin-1beta; 0/Interleukin-23; 0/Interleukin-6; 0/Lipopolysaccharides; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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