Open AccessApigenin, a potent suppressor of dendritic cell maturation and migration, protects against collagen‐induced arthritis
Author(s) -
Li Xing,
Han Yanping,
Zhou Qingyou,
Jie Hongyu,
He Yi,
Han Jiaochan,
He Juan,
Jiang Yong,
Sun Erwei
Publication year - 2016
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12717
Subject(s) - dendritic cell , arthritis , in vivo , apigenin , chemokine , immunology , cytokine , microbiology and biotechnology , chemistry , biology , inflammation , immune system , biochemistry , flavonoid , antioxidant
This study aimed to investigate whether apigenin ( API ) suppresses arthritis development through the modulation of dendritic cell functions. Bone marrow‐derived dendritic cells ( BMDC s) were stimulated in vitro with lipopolysaccharide ( LPS ) and treated with API for 24 hrs; DC functions, including phenotype expressions, cytokine secretion, phagocytosis and chemotaxis, were then investigated. The effects of API on collagen‐induced arthritis ( CIA ) were examined in vivo , and purified DC s from the lymph nodes ( LN s) of API ‐treated CIA mice were analysed for phenotypes and subsets. In in vitro , API efficiently restrained the phenotypic and functional maturation of LPS ‐stimulated BMDC s while maintaining phagocytotic capabilities. Moreover, API inhibited the chemotactic responses of LPS ‐stimulated BMDC s, which may be related to the depressive effect on chemokine receptor 4 ( CXCR 4). In in vivo , API treatment delayed the onset and reduced the severity of arthritis in CIA mice, and diminished secretion of pro‐inflammatory cytokines in the serum and supernatants from the LN cells of the CIA mice. Similar to the in vitro findings, the API ‐treated mice exhibited reduced expression of co‐stimulatory molecules and major histocompatibility complex II on DC s. Furthermore, API treatment strongly down‐regulated the number of Langerhans cells, but not plasmacytoid DC s ( pDC s) in LN s, which may be related to the depressive effect of API on the expression of CXCR 4 on DC s of peripheral blood. These data provide new insight into the mechanism of action of API on arthritis and indicate that the inhibition of maturation and migration of DC s by API may contribute to its immunosuppressive effects.