Chitosan polysaccharide suppress toll like receptor dependent immune response

Date
2015
Authors
Tincer G.
Bayyurt, B.
Arıca, Y.M.
Gürsel İ.
Advisor
Instructor
Source Title
Turkish Journal of Immunology
Print ISSN
1301109X
Electronic ISSN
Publisher
Turkish Society of Immunology
Volume
3
Issue
1
Pages
15 - 20
Language
English
Type
Article
Journal Title
Journal ISSN
Volume Title
Abstract

Objectives: Chitosan is a widely used vaccine or anti-cancer delivery vehicle. In this study, we investigated the immunomodulatory effect of chitosan/pIC nanocomplexes on mouse immune cells. Materials and methods: Proliferative and cytotoxic features of chitosan were tested via CCK-8 assay on RAW 264. 7. IL-1β production was assessed via ELISA from PEC supernatants. TNF-α, and NO induction from chitosan treated RAW cells detected by ELISA and Griess assay, respectively. mRNA message levels of TLRs and cytokines on macrophages in response to chitosan/pIC nanocomplex treatments were evaluated by RT-PCR. Results: Results revealed that chitosan is non-toxic to cells, however, proliferative capacities of macrophages were reduced by chitosan administration. Mouse PECs treated with chitosan, led to NLRP3 dependent inflammasome activation as evidenced by dose-dependent IL-1β secretion. Chitosan/pIC nanocomplexes did not improve immunostimulatory action of pIC on RAW cells, since TNF-α and NO productions remained unaltered. Expression levels of several TLRs, CXCL-16 and IFN-α messages from mouse splenocytes were down regulated in response to chitosan/pIC nanocomplex treatment. Conclusion: Our results revealed that chitosan is an anti-proliferative and inflammasome triggering macromolecule on immune cells. Utilization of chitosan as a carrier system is of concern for immunotherapeutic applications. © 2015 Turkish Journal of Immunology.

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Keywords
Biomaterial, Chitosan, Double-stranded ribonucleic acid, Innate immunity, Polysaccharide, Toll like receptor, alpha interferon, chitosan, cryopyrin, CXCL16 chemokine, gamma interferon inducible protein 10, inflammasome, interleukin 1beta, macrophage inflammatory protein 3alpha, nitric oxide, polyinosinic polycytidylic acid, polysaccharide, toll like receptor, toll like receptor 1, toll like receptor 2, toll like receptor 3, toll like receptor 4, toll like receptor 6, toll like receptor 7, toll like receptor 9, tumor necrosis factor alpha, animal cell, Article, cell proliferation, controlled study, cytokine production, cytokine release, cytotoxicity, down regulation, gene expression, immunomodulation, mouse, nonhuman, protein expression, protein induction
Citation
Published Version (Please cite this version)