Κ-Carrageenan Enhances Lipopolysaccharide-Induced Interleukin-8 Secretion by Stimulating the Bcl10-NF-κB Pathway in HT-29 Cells and Aggravates C. freundii-Induced Inflammation in Mice. (9th January 2017)
- Record Type:
- Journal Article
- Title:
- Κ-Carrageenan Enhances Lipopolysaccharide-Induced Interleukin-8 Secretion by Stimulating the Bcl10-NF-κB Pathway in HT-29 Cells and Aggravates C. freundii-Induced Inflammation in Mice. (9th January 2017)
- Main Title:
- Κ-Carrageenan Enhances Lipopolysaccharide-Induced Interleukin-8 Secretion by Stimulating the Bcl10-NF-κB Pathway in HT-29 Cells and Aggravates C. freundii-Induced Inflammation in Mice
- Authors:
- Wu, Wei
Zhen, Zhanghe
Niu, Tingting
Zhu, Xiaojuan
Gao, Yuli
Yan, Jiangyan
Chen, Yu
Yan, Xiaojun
Chen, Haimin - Other Names:
- Zhao Dezheng Academic Editor.
- Abstract:
- Abstract : Background. The dietary usage of carrageenan as common food additive has increased observably over the last 50 years. But there is substantial controversy about its safety. Methods. We investigated whether the κ -carrageenan could enhance lipopolysaccharide-induced IL-8 expression by studying its actions on the TLR4-NF- κ B pathway. The aggravating effect of κ -carrageenan on Citrobacter freundii DBS100-induced intestinal inflammation was also investigated in a mouse model. Results. Our data show that κ -carrageenan pretreatment promoted LPS-induced IL-8 expression in HT-29 cells. Although CD14, MD-2, and TLR4 were upregulated, the binding of LPS was not enhanced. However, the pathway of Bcl10-NF- κ B was triggered. Interestingly, κ -carrageenan competitively blocked the binding of FITC-LPS. Furthermore, pretreatment with κ -carrageenan for one week previous to gavage with C. freundii DBS100 markedly aggravated weight loss, mortality, and colonic damage. The secretion of cytokines was unbalanced and the ratio of Tregs was decreased significantly. In addition, κ -carrageenan, together with C. freundii DBS100, enhanced the transcription and secretion of TLR4 and NF- κ B. Conclusions . κ -Carrageenan can synergistically activate LPS-induced inflammatory through the Bcl10-NF- κ B pathway, as indicated by its aggravation of C. freundii DBS100-induced colitis in mice. General Significance. Our results suggest that κ -carrageenan serves as a potential inflammatory agentAbstract : Background. The dietary usage of carrageenan as common food additive has increased observably over the last 50 years. But there is substantial controversy about its safety. Methods. We investigated whether the κ -carrageenan could enhance lipopolysaccharide-induced IL-8 expression by studying its actions on the TLR4-NF- κ B pathway. The aggravating effect of κ -carrageenan on Citrobacter freundii DBS100-induced intestinal inflammation was also investigated in a mouse model. Results. Our data show that κ -carrageenan pretreatment promoted LPS-induced IL-8 expression in HT-29 cells. Although CD14, MD-2, and TLR4 were upregulated, the binding of LPS was not enhanced. However, the pathway of Bcl10-NF- κ B was triggered. Interestingly, κ -carrageenan competitively blocked the binding of FITC-LPS. Furthermore, pretreatment with κ -carrageenan for one week previous to gavage with C. freundii DBS100 markedly aggravated weight loss, mortality, and colonic damage. The secretion of cytokines was unbalanced and the ratio of Tregs was decreased significantly. In addition, κ -carrageenan, together with C. freundii DBS100, enhanced the transcription and secretion of TLR4 and NF- κ B. Conclusions . κ -Carrageenan can synergistically activate LPS-induced inflammatory through the Bcl10-NF- κ B pathway, as indicated by its aggravation of C. freundii DBS100-induced colitis in mice. General Significance. Our results suggest that κ -carrageenan serves as a potential inflammatory agent that magnifies existing intestinal inflammation. … (more)
- Is Part Of:
- Mediators of inflammation. Volume 2017(2017)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 2017(2017)
- Issue Display:
- Volume 2017, Issue 2017 (2017)
- Year:
- 2017
- Volume:
- 2017
- Issue:
- 2017
- Issue Sort Value:
- 2017-2017-2017-0000
- Page Start:
- Page End:
- Publication Date:
- 2017-01-09
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1155/2017/8634865 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 23513.xml