Mechanism of the immunostimulatory activity by a polysaccharide from Dictyophora indusiata
Dictyophora indusiata, an edible mushroom, is widely used not only as health foods but also as traditional Chinese medicine. This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Resu...
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Veröffentlicht in: | International journal of biological macromolecules 2016-10, Vol.91, p.752-759 |
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description | Dictyophora indusiata, an edible mushroom, is widely used not only as health foods but also as traditional Chinese medicine. This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Results indicated that DIP induced the up-regulation of nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor (TNF-α) production as well as the mRNA expression levels of iNOS, IL-1β, IL-6 and TNF-α in macrophages. Furthermore, the functional blocking antibodies against TLR4 could markedly suppress DIP-mediated NO, IL-1β, IL-6 and TNF-α production. Flow cytometry and confocal laser-scanning microscopy analyses confirmed that DIP could bind specifically to target cells, and the binding could be inhibited by anti-TLR4 monoclonal antibodies. The expression of nuclear factor kappa B (NF-κB) p65 was significantly induced by DIP. Therefore, the DIP-induced macrophage activation may be mediated via the TLR4/NF-κB signalling pathway. |
doi_str_mv | 10.1016/j.ijbiomac.2016.06.024 |
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This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Results indicated that DIP induced the up-regulation of nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor (TNF-α) production as well as the mRNA expression levels of iNOS, IL-1β, IL-6 and TNF-α in macrophages. Furthermore, the functional blocking antibodies against TLR4 could markedly suppress DIP-mediated NO, IL-1β, IL-6 and TNF-α production. Flow cytometry and confocal laser-scanning microscopy analyses confirmed that DIP could bind specifically to target cells, and the binding could be inhibited by anti-TLR4 monoclonal antibodies. The expression of nuclear factor kappa B (NF-κB) p65 was significantly induced by DIP. Therefore, the DIP-induced macrophage activation may be mediated via the TLR4/NF-κB signalling pathway.</description><identifier>ISSN: 0141-8130</identifier><identifier>EISSN: 1879-0003</identifier><identifier>DOI: 10.1016/j.ijbiomac.2016.06.024</identifier><identifier>PMID: 27293036</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adjuvants, Immunologic - chemistry ; Adjuvants, Immunologic - pharmacology ; Agaricales - chemistry ; Animals ; Cell Line ; Dictyophora indusiata polysaccharide ; Fungal Polysaccharides - chemistry ; Fungal Polysaccharides - pharmacology ; Immunostimulatory activity ; Macrophages - metabolism ; Mechanism ; Mice ; Monokines - metabolism ; NF-kappa B - metabolism ; Nitric Oxide - metabolism ; Signal Transduction - drug effects ; Toll-Like Receptor 4 - metabolism</subject><ispartof>International journal of biological macromolecules, 2016-10, Vol.91, p.752-759</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-5220cadddcbadce7aac8c698a85d810c9f27dd131bf7a3c444f04d5b3580b6423</citedby><cites>FETCH-LOGICAL-c368t-5220cadddcbadce7aac8c698a85d810c9f27dd131bf7a3c444f04d5b3580b6423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijbiomac.2016.06.024$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27293036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Chao</creatorcontrib><creatorcontrib>Shang, Jingying</creatorcontrib><creatorcontrib>Fu, Haitian</creatorcontrib><creatorcontrib>Chen, Jingxiao</creatorcontrib><creatorcontrib>Liu, Hanying</creatorcontrib><creatorcontrib>Chen, Jinghua</creatorcontrib><title>Mechanism of the immunostimulatory activity by a polysaccharide from Dictyophora indusiata</title><title>International journal of biological macromolecules</title><addtitle>Int J Biol Macromol</addtitle><description>Dictyophora indusiata, an edible mushroom, is widely used not only as health foods but also as traditional Chinese medicine. This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Results indicated that DIP induced the up-regulation of nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor (TNF-α) production as well as the mRNA expression levels of iNOS, IL-1β, IL-6 and TNF-α in macrophages. Furthermore, the functional blocking antibodies against TLR4 could markedly suppress DIP-mediated NO, IL-1β, IL-6 and TNF-α production. Flow cytometry and confocal laser-scanning microscopy analyses confirmed that DIP could bind specifically to target cells, and the binding could be inhibited by anti-TLR4 monoclonal antibodies. The expression of nuclear factor kappa B (NF-κB) p65 was significantly induced by DIP. 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This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Results indicated that DIP induced the up-regulation of nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor (TNF-α) production as well as the mRNA expression levels of iNOS, IL-1β, IL-6 and TNF-α in macrophages. Furthermore, the functional blocking antibodies against TLR4 could markedly suppress DIP-mediated NO, IL-1β, IL-6 and TNF-α production. Flow cytometry and confocal laser-scanning microscopy analyses confirmed that DIP could bind specifically to target cells, and the binding could be inhibited by anti-TLR4 monoclonal antibodies. The expression of nuclear factor kappa B (NF-κB) p65 was significantly induced by DIP. 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subjects | Adjuvants, Immunologic - chemistry Adjuvants, Immunologic - pharmacology Agaricales - chemistry Animals Cell Line Dictyophora indusiata polysaccharide Fungal Polysaccharides - chemistry Fungal Polysaccharides - pharmacology Immunostimulatory activity Macrophages - metabolism Mechanism Mice Monokines - metabolism NF-kappa B - metabolism Nitric Oxide - metabolism Signal Transduction - drug effects Toll-Like Receptor 4 - metabolism |
title | Mechanism of the immunostimulatory activity by a polysaccharide from Dictyophora indusiata |
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