PMID- 30261069
OWN - NLM
STAT- MEDLINE
DCOM- 20190304
LR  - 20190304
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 13
IP  - 9
DP  - 2018
TI  - Presence of increased inflammatory infiltrates accompanied by activated dendritic 
      cells in the left atrium in rheumatic heart disease.
PG  - e0203756
LID - 10.1371/journal.pone.0203756 [doi]
LID - e0203756
AB  - AIMS: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.
FAU - Shiba, Mikio
AU  - Shiba M
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
AD  - Department of Cardiovascular Medicine, Osaka University Graduate School of 
      Medicine, Osaka, Japan.
FAU - Sugano, Yasuo
AU  - Sugano Y
AUID- ORCID: 0000-0001-6199-6030
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
AD  - Departement of Cardiovascular Medicine, Keiyu Hospital, Yokohama, Japan.
FAU - Ikeda, Yoshihiko
AU  - Ikeda Y
AD  - Department of Pathology, National Cerebral and Cardiovascular Center, Osaka, 
      Japan.
FAU - Okada, Hideshi
AU  - Okada H
AD  - Department of Emergency and Disaster Medicine, Gifu University Graduate School of 
      Medicine, Gifu, Japan.
FAU - Nagai, Toshiyuki
AU  - Nagai T
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
AD  - Department of Cardiovascular Medicine, Hokkaido University Graduate School of 
      Medicine, Sapporo, Japan.
FAU - Ishibashi-Ueda, Hatsue
AU  - Ishibashi-Ueda H
AD  - Department of Pathology, National Cerebral and Cardiovascular Center, Osaka, 
      Japan.
FAU - Yasuda, Satoshi
AU  - Yasuda S
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
FAU - Ogawa, Hisao
AU  - Ogawa H
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
FAU - Anzai, Toshihisa
AU  - Anzai T
AD  - Department of Cardiovascular Medicine, National Cerebral and Cardiovascular 
      Center, Osaka, Japan.
AD  - Department of Cardiovascular Medicine, Hokkaido University Graduate School of 
      Medicine, Sapporo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180927
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Tenascin)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Atrial Remodeling
MH  - Dendritic Cells/pathology
MH  - Female
MH  - Heart Atria/metabolism/*pathology
MH  - Humans
MH  - Immunity, Cellular
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Rheumatic Fever/complications/immunology/pathology
MH  - Rheumatic Heart Disease/immunology/metabolism/*pathology
MH  - T-Lymphocytes/pathology
MH  - Tenascin/metabolism
PMC - PMC6159861
COIS- The authors have declared that no competing interests exist.
EDAT- 2018/09/28 06:00
MHDA- 2019/03/05 06:00
PMCR- 2018/09/27
CRDT- 2018/09/28 06:00
PHST- 2017/10/26 00:00 [received]
PHST- 2018/08/27 00:00 [accepted]
PHST- 2018/09/28 06:00 [entrez]
PHST- 2018/09/28 06:00 [pubmed]
PHST- 2019/03/05 06:00 [medline]
PHST- 2018/09/27 00:00 [pmc-release]
AID - PONE-D-17-38168 [pii]
AID - 10.1371/journal.pone.0203756 [doi]
PST - epublish
SO  - PLoS One. 2018 Sep 27;13(9):e0203756. doi: 10.1371/journal.pone.0203756. 
      eCollection 2018.