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Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection

Parasitic helminthes can suppress and/or regulate the host immune response to allow long-term survival and chronic infection where toll-like receptors (TLRs) expressed on macrophages play essential roles in response to parasitic infection. Semi-quantitative PCR and flow cytometry studies about the m...

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Detalles Bibliográficos
Autores principales: Han, C., Xu, J., Liu, CH., Li, X., Zhai, P., Hashan, A., Song, M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sciendo 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6662015/
https://www.ncbi.nlm.nih.gov/pubmed/31662647
http://dx.doi.org/10.2478/helm-2018-0015
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author Han, C.
Xu, J.
Liu, CH.
Li, X.
Zhai, P.
Hashan, A.
Song, M.
author_facet Han, C.
Xu, J.
Liu, CH.
Li, X.
Zhai, P.
Hashan, A.
Song, M.
author_sort Han, C.
collection PubMed
description Parasitic helminthes can suppress and/or regulate the host immune response to allow long-term survival and chronic infection where toll-like receptors (TLRs) expressed on macrophages play essential roles in response to parasitic infection. Semi-quantitative PCR and flow cytometry studies about the modulation of TLRs and cytokine profiles in macrophages following T. spiralis infection were performed. TLRs, MyD88 and NF-κB were up-regulated by T. spiralis infection and essential to the parasite life cycles. Cytokines profiles (IL-6, IL-10, IL-12, TNF-α) were modulated during T. spiralis infection. Results suggest that T. spiralis infection may regulate the expression of TLR4 on macrophages and TLR4/MyD88/NF-κB signaling pathways. This study provides further insights into the mechanisms of TLR-mediated post-inflammatory response during T. spiralis infection.
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spelling pubmed-66620152019-10-29 Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection Han, C. Xu, J. Liu, CH. Li, X. Zhai, P. Hashan, A. Song, M. Helminthologia Research Article Parasitic helminthes can suppress and/or regulate the host immune response to allow long-term survival and chronic infection where toll-like receptors (TLRs) expressed on macrophages play essential roles in response to parasitic infection. Semi-quantitative PCR and flow cytometry studies about the modulation of TLRs and cytokine profiles in macrophages following T. spiralis infection were performed. TLRs, MyD88 and NF-κB were up-regulated by T. spiralis infection and essential to the parasite life cycles. Cytokines profiles (IL-6, IL-10, IL-12, TNF-α) were modulated during T. spiralis infection. Results suggest that T. spiralis infection may regulate the expression of TLR4 on macrophages and TLR4/MyD88/NF-κB signaling pathways. This study provides further insights into the mechanisms of TLR-mediated post-inflammatory response during T. spiralis infection. Sciendo 2018-07-28 /pmc/articles/PMC6662015/ /pubmed/31662647 http://dx.doi.org/10.2478/helm-2018-0015 Text en © 2018 C. Han, J. Xu, CH. Liu, X. Li, P. Zhai, A. Hashan, M. Song Published by Sciendo http://creativecommons.org/licenses/by-nc-nd/4.0 This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.
spellingShingle Research Article
Han, C.
Xu, J.
Liu, CH.
Li, X.
Zhai, P.
Hashan, A.
Song, M.
Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title_full Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title_fullStr Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title_full_unstemmed Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title_short Modulation of TLR2 and TLR4 in Macrophages Following Trichinella Spiralis Infection
title_sort modulation of tlr2 and tlr4 in macrophages following trichinella spiralis infection
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6662015/
https://www.ncbi.nlm.nih.gov/pubmed/31662647
http://dx.doi.org/10.2478/helm-2018-0015
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