Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease

作者：Lin I Chun; Suen Jau Ling; Huang Shau Ku; Huang Shun Chen; Huang Hsin Chun; Kuo Ho Chang; Wei Chi Chen; Wang Feng Shen; Yu Hong Ren; Yang Kuender D^*

来源：Immunobiology, 2013, 218(2): 201-212.

DOI：10.1016/j.imbio.2012.04.004

• Dectin-1
• Kawasaki disease
• Macrophages
• Spleen tyrosine kinase

Kawasaki disease (KD) is not only the leading cause of childhood acquired heart diseases, but also causes profound coronary artery sequelae due to chronic vascular inflammation in adulthood. Of unknown underlying mechanism, both innate and adaptive immune responses are involved in the pathogenesis of coronary artery lesions (CALs). We investigated the role of dectin-1/spleen tyrosine kinase (Syk) pathway on macrophage in responsive to Lactobacillus casei cell wall extract (LCWE) in vitro and in vivo. We found that LCWE induced in vitro macrophage activation with increased production of IL-6, TNF-alpha, and MCP-1, concomitantly with Syk activation, and dectin-1 and TLR2 enhancement. In vivo, LCWE induced infiltration of dectin-1(+) macrophages into CALs and cardiac upregulation of IL-6 and MCP-1 on day 14 post-injection. Most importantly, Syk inhibition alleviated LCWE-induced arteritis in BALB/c mice. Blockade of either dectin-1 or Syk significantly inhibited LCWE-induced IL-6 and MCP-1 production both in vitro and in vivo. This study demonstrates that the macrophage dectin-1/Syk-mediated pathway is involved in LCWE-induced CALs and production of IL-6 and MCP-1. Given the functional equivalence of h

• 出版日期2013-2
• 单位长春大学; 河北医科大学