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

I. Chun Lin, Jau Ling Suen, Shau Ku Huang, Shun Chen Huang, Hsin Chun Huang, Ho Chang Kuo, Chi Chen Wei, Feng Shen Wang, Hong Ren Yu, Kuender D. Yang

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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-α, 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 human dectin-1 to murine, the importance of dectin-1/Syk pathway in the development of murine CALs warrants further investigation on their roles in human KD.

Original languageEnglish
Pages (from-to)201-212
Number of pages12
JournalImmunobiology
Volume218
Issue number2
DOIs
Publication statusPublished - Feb 1 2013
Externally publishedYes

Fingerprint

Lactobacillus casei
Mucocutaneous Lymph Node Syndrome
Cell Extracts
Cell Wall
Coronary Vessels
Interleukin-6
Macrophages
Arteritis
Macrophage Activation
Adaptive Immunity
Syk Kinase
dectin 1
Innate Immunity
Blood Vessels
Heart Diseases
Up-Regulation
Inflammation
Injections

Keywords

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

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology

Cite this

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

In: Immunobiology, Vol. 218, No. 2, 01.02.2013, p. 201-212.

Research output: Contribution to journalArticle

Lin, IC, Suen, JL, Huang, SK, Huang, SC, Huang, HC, Kuo, HC, Wei, CC, Wang, FS, Yu, HR & Yang, KD 2013, 'Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease', Immunobiology, vol. 218, no. 2, pp. 201-212. https://doi.org/10.1016/j.imbio.2012.04.004
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. / Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease. In: Immunobiology. 2013 ; Vol. 218, No. 2. pp. 201-212.
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AU - Kuo, Ho Chang

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AB - 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-α, 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 human dectin-1 to murine, the importance of dectin-1/Syk pathway in the development of murine CALs warrants further investigation on their roles in human KD.

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