Increased Number of Mast Cells in Atherosclerotic Lesions Correlates with the Presence of Myeloid but not Plasmacytoid Dendritic Cells as well as Pro-inflammatory T Cells.
BACKGROUND
Atherosclerosis is an inflammatory disease of the vessel wall promoted by different immune cells and inflammatory mediators.


METHODS
In this study, 26 human plaques and 12 control vessels without atherosclerosis were immunohistochemically stained to analyze the emergence of mast cells dependent on plaque morphology and to correlate mast cell occurrence with the emergence of myeloid as well as plasmacytoid dendritic cells. Also, mast cell emergence was correlated with the number of pro-inflammatory T cells. For this, plaques were classified as stable or unstable according to established histological criteria.


RESULTS
As expected, atherosclerotic lesions showed significantly higher numbers of tryptase+, chymase+, and cathepsin G+ mast cells compared to control vessels, particularly in lesions with unstable morphology. As a novel finding, we detected significant correlations between mast cells and myeloid dendritic cells (fascin, CD83, r > 0.3, p < 0.01), but not plasmacytoid dendritic cells (CD123, CD304). Also, we observed significant correlations of mast cells and different subgroups of pro-inflammatory T cells (CD3, CD8, CD161, CD25; r > 0.35, p < 0.05).


CONCLUSIONS
Overall, the higher number of mast cells in plaques, particularly with unstable morphology, suggests that mast cells might be involved in the progression of atherosclerosis. The correlation of mast cells with other immune cells that are pivotal in atherogenesis, e.g., myeloid dendritic cells and pro-inflammatory T cells, also suggests an interplay leading to plaque destabilization. Therefore, modulating local mast cell function and invasion into the plaque might be a therapeutic tool for plaque stabilization.
Ilonka
I
Rohm
Sandra
S
Sattler
Yevgeniya
Y
Atiskova
Daniel
D
Kretzschmar
Rudin
R
Pistulli
Marcus
M
Franz
Christian
C
Jung
Gita
G
Mall
Thomas
T
Kronert
Paul C
PC
Schulze
Atilla
A
Yilmaz
D000368:Aged; D015415:Biomarkers / Q000032:analysis; D002339:Carotid Arteries / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D016893:Carotid Stenosis / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D016022:Case-Control Studies; D003713:Dendritic Cells / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D018450:Disease Progression; D005260:Female; D005263:Femoral Artery / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D008875:Middle Aged; D022423:Myeloid Cells / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D058729:Peripheral Arterial Disease / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D058226:Plaque, Atherosclerotic; D011379:Prognosis; D012422:Rupture, Spontaneous
D015415:Biomarkers