Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Dendritic Cells in Subcutaneous and Epicardial Adipose Tissue of Subjects with Type 2 Diabetes, Obesity, and Coronary Artery Disease

M. Mráz, A. Cinkajzlová, J. Kloučková, Z. Lacinová, H. Kratochvílová, M. Lipš, M. Pořízka, P. Kopecký, J. Lindner, T. Kotulák, I. Netuka, M. Haluzík,

. 2019 ; 2019 (-) : 5481725. [pub] 20190509

Language English Country United States

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc20006245

Grant support
NV15-26854A MZ0 CEP Register

Dendritic cells (DCs) are professional antigen-presenting cells contributing to regulation of lymphocyte immune response. DCs are divided into two subtypes: CD11c-positive conventional or myeloid (cDCs) and CD123-positive plasmacytoid (pDCs) DCs. The aim of the study was to assess DCs (HLA-DR+ lineage-) and their subtypes by flow cytometry in peripheral blood and subcutaneous (SAT) and epicardial (EAT) adipose tissue in subjects with (T2DM, n = 12) and without (non-T2DM, n = 17) type 2 diabetes mellitus undergoing elective cardiac surgery. Subjects with T2DM had higher fasting glycemia (8.6 ± 0.7 vs. 5.8 ± 0.2 mmol/l, p < 0.001) and glycated hemoglobin (52.0 ± 3.4 vs. 36.9 ± 1.0 mmol/mol, p < 0.001) and tended to have more pronounced inflammation (hsCRP: 9.8 ± 3.1 vs. 5.1 ± 1.9 mg/ml, p = 0.177) compared with subjects without T2DM. T2DM was associated with reduced total DCs in SAT (1.57 ± 0.65 vs. 4.45 ± 1.56% for T2DM vs. non-T2DM, p = 0.041) with a similar, albeit insignificant, trend in EAT (0.996 ± 0.33 vs. 2.46 ± 0.78% for T2DM vs. non-T2DM, p = 0.171). When analyzing DC subsets, no difference in cDCs was seen between any of the studied groups or adipose tissue pools. In contrast, pDCs were increased in both SAT (13.5 ± 2.0 vs. 4.6 ± 1.9% of DC cells, p = 0.005) and EAT (29.1 ± 8.7 vs. 8.4 ± 2.4% of DC, p = 0.045) of T2DM relative to non-T2DM subjects as well as in EAT of the T2DM group compared with corresponding SAT (29.1 ± 8.7 vs. 13.5 ± 2.0% of DC, p = 0.020). Neither obesity nor coronary artery disease (CAD) significantly influenced the number of total, cDC, or pDC in SAT or EAT according to multiple regression analysis. In summary, T2DM decreased the amount of total dendritic cells in subcutaneous adipose tissue and increased plasmacytoid dendritic cells in subcutaneous and even more in epicardial adipose tissue. These findings suggest a potential role of pDCs in the development of T2DM-associated adipose tissue low-grade inflammation.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc20006245
003      
CZ-PrNML
005      
20201016140120.0
007      
ta
008      
200511s2019 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1155/2019/5481725 $2 doi
035    __
$a (PubMed)31210749
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Mráz, Miloš $u Department of Diabetes, Diabetes Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
245    10
$a Dendritic Cells in Subcutaneous and Epicardial Adipose Tissue of Subjects with Type 2 Diabetes, Obesity, and Coronary Artery Disease / $c M. Mráz, A. Cinkajzlová, J. Kloučková, Z. Lacinová, H. Kratochvílová, M. Lipš, M. Pořízka, P. Kopecký, J. Lindner, T. Kotulák, I. Netuka, M. Haluzík,
520    9_
$a Dendritic cells (DCs) are professional antigen-presenting cells contributing to regulation of lymphocyte immune response. DCs are divided into two subtypes: CD11c-positive conventional or myeloid (cDCs) and CD123-positive plasmacytoid (pDCs) DCs. The aim of the study was to assess DCs (HLA-DR+ lineage-) and their subtypes by flow cytometry in peripheral blood and subcutaneous (SAT) and epicardial (EAT) adipose tissue in subjects with (T2DM, n = 12) and without (non-T2DM, n = 17) type 2 diabetes mellitus undergoing elective cardiac surgery. Subjects with T2DM had higher fasting glycemia (8.6 ± 0.7 vs. 5.8 ± 0.2 mmol/l, p < 0.001) and glycated hemoglobin (52.0 ± 3.4 vs. 36.9 ± 1.0 mmol/mol, p < 0.001) and tended to have more pronounced inflammation (hsCRP: 9.8 ± 3.1 vs. 5.1 ± 1.9 mg/ml, p = 0.177) compared with subjects without T2DM. T2DM was associated with reduced total DCs in SAT (1.57 ± 0.65 vs. 4.45 ± 1.56% for T2DM vs. non-T2DM, p = 0.041) with a similar, albeit insignificant, trend in EAT (0.996 ± 0.33 vs. 2.46 ± 0.78% for T2DM vs. non-T2DM, p = 0.171). When analyzing DC subsets, no difference in cDCs was seen between any of the studied groups or adipose tissue pools. In contrast, pDCs were increased in both SAT (13.5 ± 2.0 vs. 4.6 ± 1.9% of DC cells, p = 0.005) and EAT (29.1 ± 8.7 vs. 8.4 ± 2.4% of DC, p = 0.045) of T2DM relative to non-T2DM subjects as well as in EAT of the T2DM group compared with corresponding SAT (29.1 ± 8.7 vs. 13.5 ± 2.0% of DC, p = 0.020). Neither obesity nor coronary artery disease (CAD) significantly influenced the number of total, cDC, or pDC in SAT or EAT according to multiple regression analysis. In summary, T2DM decreased the amount of total dendritic cells in subcutaneous adipose tissue and increased plasmacytoid dendritic cells in subcutaneous and even more in epicardial adipose tissue. These findings suggest a potential role of pDCs in the development of T2DM-associated adipose tissue low-grade inflammation.
650    _2
$a tuková tkáň $x imunologie $x metabolismus $7 D000273
650    _2
$a senioři $7 D000368
650    _2
$a nemoci koronárních tepen $x imunologie $x metabolismus $7 D003324
650    _2
$a dendritické buňky $x metabolismus $7 D003713
650    _2
$a diabetes mellitus 2. typu $x imunologie $x metabolismus $7 D003924
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a lidé $7 D006801
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a lidé středního věku $7 D008875
650    _2
$a obezita $x imunologie $x metabolismus $7 D009765
650    _2
$a perikard $x imunologie $x metabolismus $7 D010496
650    _2
$a podkožní tuk $x imunologie $x metabolismus $7 D050151
655    _2
$a časopisecké články $7 D016428
700    1_
$a Cinkajzlová, Anna $u Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Kloučková, Jana $u Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Lacinová, Zdeňka $u Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Kratochvílová, Helena $u Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Lipš, Michal $u Department of Anaesthesiology, Resuscitation and Intensive Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
700    1_
$a Pořízka, Michal $u Department of Anaesthesiology, Resuscitation and Intensive Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
700    1_
$a Kopecký, Petr $u Department of Anaesthesiology, Resuscitation and Intensive Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
700    1_
$a Lindner, Jaroslav $u 2nd Department of Surgery-Department of Cardiovascular Surgery, Charles University and General University Hospital, Prague, Czech Republic.
700    1_
$a Kotulák, Tomáš $u Anesthesiology Department, Cardiac Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Netuka, Ivan $u Cardiovascular Surgery Department, Cardiac Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Haluzík, Martin $u Department of Diabetes, Diabetes Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. Department of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
773    0_
$w MED00006378 $t Mediators of inflammation $x 1466-1861 $g Roč. 2019, č. - (2019), s. 5481725
856    41
$u https://pubmed.ncbi.nlm.nih.gov/31210749 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20200511 $b ABA008
991    __
$a 20201016140118 $b ABA008
999    __
$a ok $b bmc $g 1525103 $s 1096301
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2019 $b 2019 $c - $d 5481725 $e 20190509 $i 1466-1861 $m Mediators of inflammation $n Mediators Inflamm $x MED00006378
GRA    __
$a NV15-26854A $p MZ0
LZP    __
$a Pubmed-20200511

Find record

Citation metrics

Archiving options