Astaxanthin Protects Dendritic Cells from Lipopolysaccharide-Induced Immune Dysfunction

Astaxanthin, originating from seafood, is a naturally occurring red carotenoid pigment. Previous studies have focused on its antioxidant properties; however, whether astaxanthin possesses a desired anti-inflammatory characteristic to regulate the dendritic cells (DCs) for sepsis therapy remains unknown. Here, we explored the effects of astaxanthin on the immune functions of murine DCs. Our results showed that astaxanthin reduced the expressions of LPS-induced inflammatory cytokines (TNF-alpha, IL-6, and IL-10) and phenotypic markers (MHCII, CD40, CD80, and CD86) by DCs. Moreover, astaxanthin promoted the endocytosis levels in LPS-treated DCs, and hindered the LPS-induced migration of DCs via downregulating CCR7 expression, and then abrogated allogeneic T cell proliferation. Furthermore, we found that astaxanthin inhibited the immune dysfunction of DCs induced by LPS via the activation of the HO-1/Nrf2 axis. Finally, astaxanthin with oral administration remarkably enhanced the survival rate of LPS-challenged mice. These data showed a new approach of astaxanthin for potential sepsis treatment through avoiding the immune dysfunction of DCs.

Automated summary

Astaxanthin has anti-inflammatory effects on murine DCs by regulating cytokine and phenotype marker expression to inhibit inflammation. Additionally, it promotes endocytosis, inhibits DC migration, and reduces T cell proliferation. Finally, it inhibits immune dysfunction in DCs induced by LPS by activating the HO-1/Nrf2 axis, ultimately enhancing survival in LPS-challenged mice.