Coxsackievirus B3 infection promotes generation of myeloid dendritic cells from bone marrow and accumulation in the myocardium

Ping Chen, Ruizhen Chen, Yingzhen Yang, Yong Yu, Yeqing Xie, Yunzeng Zou, Junbo Ge, Haozhu Chen

Research output: Contribution to journalArticle

Abstract

Myocarditis is associated with increased number of CD4+ T cells in the myocardium after coxsackievirus B3 (CVB3) infection. Previous studies show that CD11c+ myeloid dendritic cells (mDC) loaded with myosin could induce myocarditis. This study aims to investigate the generation and accumulation of mDC in CVB3-induced myocarditis. The presence of mDC in myocardium was detected by immunohistochemisty. Bone marrow-derived mDC were generated from uninfected and CVB3-infected mice. The percentage of CD11c+ mDC on cultured cells and mean fluorescence index (MFI) of double positive cells (CD11c+CD40+, CD11c+CD80+) were measured by flow cytometry. The expression of chemokine receptors (CCR5, CCR7) on mDC and chemokines (CCL4, CCL19) in the myocardium was detected. The migration of mDC in response to CCL4 or CCL19 was measured by chemotaxis assay. Mature mDC were elevated in the myocardium from CVB3-infected mice. The percentage of mDC generated from CVB3-infected group was increased. The MFI of CD11c+CD40+ and CD11c+CD80+ was increased in CVB3-infected group. The mDC showed a down-regulation of CCR5 and unaffected CCR7 mRAN levels associated with elevated CCL4 and CCL19 in the myocardium in CVB3-infected group. Numbers of migrating bone marrow-derived mDC from CVB3-infected mice were increased in vitro. We conclude that CVB3 infection induced the greater generation of mDC from bone marrow and accumulation of mature mDC in myocardial tissues. This migration was associated with increased levels of both CCL4 and CCL19 in the heart tissue. These suggest that blocking the migration of mDC may provide a novel therapy for myocarditis.

Original languageEnglish (US)
Pages (from-to)1304-1312
Number of pages9
JournalInternational Immunopharmacology
Volume9
Issue number11
DOIs
StatePublished - Oct 2009
Externally publishedYes

Fingerprint

Coxsackievirus Infections
Myeloid Cells
Dendritic Cells
Myocardium
Bone Marrow
Enterovirus
Myocarditis
Chemokine CCL19
Fluorescence
Chemokine CCL4
Chemokine Receptors
Chemotaxis
Myosins

Keywords

  • Chemokines
  • Dendritic cells
  • Inflammation
  • Viral myocarditis

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pharmacology

Cite this

Coxsackievirus B3 infection promotes generation of myeloid dendritic cells from bone marrow and accumulation in the myocardium. / Chen, Ping; Chen, Ruizhen; Yang, Yingzhen; Yu, Yong; Xie, Yeqing; Zou, Yunzeng; Ge, Junbo; Chen, Haozhu.

In: International Immunopharmacology, Vol. 9, No. 11, 10.2009, p. 1304-1312.

Research output: Contribution to journalArticle

Chen, Ping ; Chen, Ruizhen ; Yang, Yingzhen ; Yu, Yong ; Xie, Yeqing ; Zou, Yunzeng ; Ge, Junbo ; Chen, Haozhu. / Coxsackievirus B3 infection promotes generation of myeloid dendritic cells from bone marrow and accumulation in the myocardium. In: International Immunopharmacology. 2009 ; Vol. 9, No. 11. pp. 1304-1312.
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abstract = "Myocarditis is associated with increased number of CD4+ T cells in the myocardium after coxsackievirus B3 (CVB3) infection. Previous studies show that CD11c+ myeloid dendritic cells (mDC) loaded with myosin could induce myocarditis. This study aims to investigate the generation and accumulation of mDC in CVB3-induced myocarditis. The presence of mDC in myocardium was detected by immunohistochemisty. Bone marrow-derived mDC were generated from uninfected and CVB3-infected mice. The percentage of CD11c+ mDC on cultured cells and mean fluorescence index (MFI) of double positive cells (CD11c+CD40+, CD11c+CD80+) were measured by flow cytometry. The expression of chemokine receptors (CCR5, CCR7) on mDC and chemokines (CCL4, CCL19) in the myocardium was detected. The migration of mDC in response to CCL4 or CCL19 was measured by chemotaxis assay. Mature mDC were elevated in the myocardium from CVB3-infected mice. The percentage of mDC generated from CVB3-infected group was increased. The MFI of CD11c+CD40+ and CD11c+CD80+ was increased in CVB3-infected group. The mDC showed a down-regulation of CCR5 and unaffected CCR7 mRAN levels associated with elevated CCL4 and CCL19 in the myocardium in CVB3-infected group. Numbers of migrating bone marrow-derived mDC from CVB3-infected mice were increased in vitro. We conclude that CVB3 infection induced the greater generation of mDC from bone marrow and accumulation of mature mDC in myocardial tissues. This migration was associated with increased levels of both CCL4 and CCL19 in the heart tissue. These suggest that blocking the migration of mDC may provide a novel therapy for myocarditis.",
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AU - Zou, Yunzeng

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