Chondroitin Sulfate Intake Inhibits the IgE-Mediated Allergic Response by Down Regulating Th2 Responses in Mice
Authors
Sakai, Shinobu
Akiyama, Hiroshi
Sato, Yuji
Yoshioka, Yasuo
Linhardt, Robert J.
Goda, Yukihiro
Maitani, Tamio
Toida, Toshihiko
ORCID
https://orcid.org/0000-0003-2219-5833
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Other Contributors
Issue Date
2006-07-21
Keywords
Biology , Chemistry and chemical biology , Chemical and biological engineering , Biomedical engineering
Degree
Terms of Use
Attribution 3.0 United States
CC BY : this license allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. Credit must be given to the authors and the original work must be properly cited.
CC BY : this license allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. Credit must be given to the authors and the original work must be properly cited.
Full Citation
Chondroitin Sulfate Intake Inhibits the IgE-Mediated Allergic Response by Down Regulating Th2 Responses in Mice, S. Sakai, H. Akiyama, Y. Sato, Y. Yoshioka, R. J. Linhardt, Y. Goda, T. Maitani, T. Toida, Journal of Biological Chemistry, 281, 19872 - 19880, 2006.
Abstract
Chondroitin sulfate (CS) was administered orally to BALB/c mice immunized intraperitoneally with ovalbumin (OVA) and/or dinitrophenylated OVA. The titers of antigen-specific IgE and IgG1 in mouse sera were determined. The antigen-specific IgE production by mice fed ad libitum with CS was significantly inhibited. We also examined the effect of feeding CS on immediate-type hypersensitivity. One hour after antigen stimulation, the ears of mice fed with CS swelled less than those of the control mice. Furthermore, the rise in serum histamine in the mice fed with CS under active systemic anaphylaxis was significantly lower than that in the controls. We next examined the pattern of cytokine production by splenocytes from mice followed by re-stimulation with OVA in vitro. The splenocytes from the mice fed with CS produced less interleukin (IL)-5, IL-10, and IL-13 than those from the control group. In contrast, the production of interferon-gamma and IL-2 by the splenocytes of mice fed with CS was not significantly different from those in the control mice. In addition, the production of transforming growth factor-beta from the splenocytes of mice fed with CS was significantly higher than that of the control mice. Furthermore, we showed that the percentages of CD4(+) cells, CD8(+) cells, and CD4(+)CD25(+) cells in the splenocytes of mice fed with CS are significantly higher than those of the control. These findings suggest that oral intake of CS inhibits the specific IgE production and antigen-induced anaphylactic response by up-regulating regulatory T-cell differentiation, followed by down-regulating the Th2 response.
Description
Journal of Biological Chemistry, 281, 19872-19880
Note : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
Note : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
Department
The Linhardt Research Labs.
The Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
The Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
Publisher
Elsevier
Relationships
The Linhardt Research Labs Online Collection
Rensselaer Polytechnic Institute, Troy, NY
Journal of Biological Chemistry
https://harc.rpi.edu/
Rensselaer Polytechnic Institute, Troy, NY
Journal of Biological Chemistry
https://harc.rpi.edu/
Access
A full text version is available in DSpace@RPI
CC BY — Creative Commons Attribution
CC BY — Creative Commons Attribution