In:
Journal of Immunology Research, Hindawi Limited, Vol. 2020 ( 2020-01-21), p. 1-9
Abstract:
Cigarette smoke is a major effector of chronic obstructive pulmonary disease (COPD), and Th17 cells and dendritic cells (DCs) involve in the pathogenesis of COPD. Previous studies have demonstrated the anti-inflammatory effects of macrolides. However, the effects of macrolides on the cigarette smoke extract- (CSE-) induced immune response are unclear. Accordingly, in this study, we evaluated the effects of erythromycin (EM) on CSE-exposed DCs polarizing naïve CD4 + T cells into Th17 cells. DCs were generated from bone marrow-derived mononuclear cells isolated from male BALB/c mice and divided into five groups: control DC group, CSE-exposed DC group, CD40-antibody-blocked CSE-exposed DC group, and EM-treated CSE-exposed DC group. The function of polarizing CD4 + T cells into Th17 cells induced by all four groups of DCs was assayed based on the mixed lymphocyte reaction (MLR) of naïve CD4 + T cells. CD40 expression in DCs in the CSE-exposed group increased significantly compared with that in the control group ( P 〈 0.05 ). The Th17 cells in the CSE-exposed DC/MLR group increased significantly compared with those in the control DC/MLR group ( P 〈 0.05 ). Moreover, Th17 cells in the CD40-blocked CSE-exposed DC/MLR group and EM-treated CSE-exposed DC/MLR group were reduced compared with those in the CSE-exposed DC/MLR group ( P 〈 0.05 ). Thus, these findings suggested that EM suppressed the CSE-exposed DC-mediated polarization of CD4 + T cells into Th17 cells and that this effect may be mediated through inhibition of the CD40/CD40L pathway.
Type of Medium:
Online Resource
ISSN:
2314-8861
,
2314-7156
DOI:
10.1155/2020/1387952
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2020
detail.hit.zdb_id:
2817541-4
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