Paclitaxel inhibits the hyper-activation of spleen cells by lipopolysaccharide and induces cell death.
10.4142/jvs.2016.17.4.453
- Author:
Hyun Ji KIM
1
;
Hong Gu JOO
Author Information
1. Laboratory of Veterinary Pharmacology, College of Veterinary Medicine, Jeju National University, Jeju 63243, Korea. jooh@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
cell death;
hyper-activation;
lipopolysaccharide;
paclitaxel;
spleen cells
- MeSH:
B-Lymphocytes;
Cell Death*;
Cell Division;
Paclitaxel*;
Phenotype;
Signal Transduction;
Spleen*;
Taxus;
Toll-Like Receptor 4
- From:Journal of Veterinary Science
2016;17(4):453-458
- CountryRepublic of Korea
- Language:English
-
Abstract:
Paclitaxel was isolated from the bark of the Pacific yew, Taxus brevifolia, and used as an anticancer agent. Paclitaxel prevents cancer cell division by inhibiting spindle fiber function, inducing cell death. A recent study demonstrated that paclitaxel binds to myeloid differentiation protein-2 of Toll-like receptor 4 and prevents the signal transduction of lipopolysaccharide (LPS). Paclitaxel converts immune cells hypo-responsive to LPS. In this study, we investigated whether paclitaxel can inhibit the phenotype and function of immune cells. To accomplish this, we used spleen cells, a major type of immune cell, LPS, a representative inflammatory agent and a mitogen for B lymphocytes. LPS profoundly increased the activation and cytokine production of spleen cells. However, paclitaxel significantly inhibited LPS-induced hyper-activation of spleen cells. Furthermore, we found that paclitaxel induced cell death of LPS-treated spleen cells. These results suggest that paclitaxel can inhibit the hyper-immune response of LPS in spleen cells via a variety of mechanisms. These findings suggest that paclitaxel can be used as a modulating agent for diseases induced by hyper-activation of B lymphocytes. Taken together, these results demonstrate that paclitaxel inhibits the function of spleen cells activated by LPS, and further induces cell death.
