Presence of increased inflammatory infiltrates accompanied by activated dendritic cells in the left atrium in rheumatic heart disease

Left atrial (LA) structural remodelling develops in rheumatic heart disease (RHD) according to the disease severity of the mitral valve and the presence of atrial fibrillation. Sustained active inflammation has been previously reported in the LA of patients with RHD, suggesting a direct role of cell...

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Bibliographic Details
Published in:PloS one 2018-09, Vol.13 (9), p.e0203756-e0203756
Main Authors: Shiba, Mikio, Sugano, Yasuo, Ikeda, Yoshihiko, Okada, Hideshi, Nagai, Toshiyuki, Ishibashi-Ueda, Hatsue, Yasuda, Satoshi, Ogawa, Hisao, Anzai, Toshihisa
Format: Article
Language:English
Subjects:
Adaptive immunity
Analysis
Antibodies
Antigens
Atrium
Biology and Life Sciences
Cardiac arrhythmia
Cardiomyopathy
Cardiovascular disease
CD11c antigen
CD163 antigen
CD3 antigen
CD80 antigen
Cell-mediated immunity
Coronary artery disease
Dendritic cells
Development and progression
Extracellular matrix
Fever
Fibrillation
Health aspects
Heart
Heart atrium
Heart diseases
Heart valves
Immunity
Immunoglobulins
Immunology
Immunomodulation
Inflammation
Inflammatory response
Laboratories
Lymphocytes
Lymphocytes T
Macrophages
Medicine
Medicine and Health Sciences
Mitral valve
Modulators
Pathogenesis
Patients
Proteins
Research and Analysis Methods
Rheumatic fever
Rheumatic heart disease
Risk factors
Society
Tenascin
Tenascin C
University graduates
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Description
Summary:Left atrial (LA) structural remodelling develops in rheumatic heart disease (RHD) according to the disease severity of the mitral valve and the presence of atrial fibrillation. Sustained active inflammation has been previously reported in the LA of patients with RHD, suggesting a direct role of cell-mediated immunity in the pathogenesis of LA remodelling. Dendritic cells (DCs) have a major antigen-presenting role, and are known as crucial modulators of innate and adaptive immunity. We investigated whether DCs are involved in the pathogenesis of LA remodelling in RHD. Immunohistochemical analyses were performed using antibodies to CD11c, CD209 and CD80 as markers of myeloid DCs, migratory-active DCs, mature DCs and infiltrated inflammatory cells including T lymphocytes (CD3) and M1 (CD68; pro-inflammatory profile) and M2 (CD163; pro-resolution profile) macrophages. Furthermore, tenascin-C, an extracellular matrix (ECM) protein that appears during ECM remodelling and inflammatory response, was examined. Infiltrated myeloid DCs, migratory-active DCs, mature DCs and other inflammatory infiltrates including T lymphocytes and M1 and M2 macrophages, were significantly higher in the RHD group than the non-RHD group. The positive area fraction for tenascin-C was significantly higher in the RHD group than in the non-RHD group. Our histological findings suggest that inflammation may persist long after a bout of rheumatic fever, ultimately leading to ECM remodelling. We identified and quantitatively assessed several subsets of DCs and other immunocompetent cells, and our results indicated that activation of DCs has some role in persistence of LA inflammation in patients with chronic RHD.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0203756