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Ginger extract inhibits LPS induced macrophage activation and function

BACKGROUND: Macrophages play a dual role in host defence. They act as the first line of defence by mounting an inflammatory response to antigen exposure and also act as antigen presenting cells and initiate the adaptive immune response. They are also the primary infiltrating cells at the site of inf...

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Autores principales: Tripathi, Sudipta, Bruch, David, Kittur, Dilip S
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234390/
https://www.ncbi.nlm.nih.gov/pubmed/18173849
http://dx.doi.org/10.1186/1472-6882-8-1
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author Tripathi, Sudipta
Bruch, David
Kittur, Dilip S
author_facet Tripathi, Sudipta
Bruch, David
Kittur, Dilip S
author_sort Tripathi, Sudipta
collection PubMed
description BACKGROUND: Macrophages play a dual role in host defence. They act as the first line of defence by mounting an inflammatory response to antigen exposure and also act as antigen presenting cells and initiate the adaptive immune response. They are also the primary infiltrating cells at the site of inflammation. Inhibition of macrophage activation is one of the possible approaches towards modulating inflammation. Both conventional and alternative approaches are being studied in this regard. Ginger, an herbal product with broad anti inflammatory actions, is used as an alternative medicine in a number of inflammatory conditions like rheumatic disorders. In the present study we examined the effect of ginger extract on macrophage activation in the presence of LPS stimulation. METHODS: Murine peritoneal macrophages were stimulated by LPS in presence or absence of ginger extract and production of proinflammatory cytokines and chemokines were observed. We also studied the effect of ginger extract on the LPS induced expression of MHC II, B7.1, B7.2 and CD40 molecules. We also studied the antigen presenting function of ginger extract treated macrophages by primary mixed lymphocyte reaction. RESULTS: We observed that ginger extract inhibited IL-12, TNF-α, IL-1β (pro inflammatory cytokines) and RANTES, MCP-1 (pro inflammatory chemokines) production in LPS stimulated macrophages. Ginger extract also down regulated the expression of B7.1, B7.2 and MHC class II molecules. In addition ginger extract negatively affected the antigen presenting function of macrophages and we observed a significant reduction in T cell proliferation in response to allostimulation, when ginger extract treated macrophages were used as APCs. A significant decrease in IFN-γ and IL-2 production by T cells in response to allostimulation was also observed. CONCLUSION: In conclusion ginger extract inhibits macrophage activation and APC function and indirectly inhibits T cell activation.
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spelling pubmed-22343902008-02-08 Ginger extract inhibits LPS induced macrophage activation and function Tripathi, Sudipta Bruch, David Kittur, Dilip S BMC Complement Altern Med Research Article BACKGROUND: Macrophages play a dual role in host defence. They act as the first line of defence by mounting an inflammatory response to antigen exposure and also act as antigen presenting cells and initiate the adaptive immune response. They are also the primary infiltrating cells at the site of inflammation. Inhibition of macrophage activation is one of the possible approaches towards modulating inflammation. Both conventional and alternative approaches are being studied in this regard. Ginger, an herbal product with broad anti inflammatory actions, is used as an alternative medicine in a number of inflammatory conditions like rheumatic disorders. In the present study we examined the effect of ginger extract on macrophage activation in the presence of LPS stimulation. METHODS: Murine peritoneal macrophages were stimulated by LPS in presence or absence of ginger extract and production of proinflammatory cytokines and chemokines were observed. We also studied the effect of ginger extract on the LPS induced expression of MHC II, B7.1, B7.2 and CD40 molecules. We also studied the antigen presenting function of ginger extract treated macrophages by primary mixed lymphocyte reaction. RESULTS: We observed that ginger extract inhibited IL-12, TNF-α, IL-1β (pro inflammatory cytokines) and RANTES, MCP-1 (pro inflammatory chemokines) production in LPS stimulated macrophages. Ginger extract also down regulated the expression of B7.1, B7.2 and MHC class II molecules. In addition ginger extract negatively affected the antigen presenting function of macrophages and we observed a significant reduction in T cell proliferation in response to allostimulation, when ginger extract treated macrophages were used as APCs. A significant decrease in IFN-γ and IL-2 production by T cells in response to allostimulation was also observed. CONCLUSION: In conclusion ginger extract inhibits macrophage activation and APC function and indirectly inhibits T cell activation. BioMed Central 2008-01-03 /pmc/articles/PMC2234390/ /pubmed/18173849 http://dx.doi.org/10.1186/1472-6882-8-1 Text en Copyright ©2008 Tripathi et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Tripathi, Sudipta
Bruch, David
Kittur, Dilip S
Ginger extract inhibits LPS induced macrophage activation and function
title Ginger extract inhibits LPS induced macrophage activation and function
title_full Ginger extract inhibits LPS induced macrophage activation and function
title_fullStr Ginger extract inhibits LPS induced macrophage activation and function
title_full_unstemmed Ginger extract inhibits LPS induced macrophage activation and function
title_short Ginger extract inhibits LPS induced macrophage activation and function
title_sort ginger extract inhibits lps induced macrophage activation and function
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234390/
https://www.ncbi.nlm.nih.gov/pubmed/18173849
http://dx.doi.org/10.1186/1472-6882-8-1
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