Limits...
Adventitial inflammation and its interaction with intimal atherosclerotic lesions.

Akhavanpoor M, Wangler S, Gleissner CA, Korosoglou G, Katus HA, Erbel C - Front Physiol (2014)

Bottom Line: These ATLOs possess similarities in development, structure and function to secondary lymphoid organs.A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process.Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Heidelberg Heidelberg, Germany ; DZHK (German Centre for Cardiovascular Research) Partner Site Heidelberg/Mannheim, Germany.

ABSTRACT
The presence of adventitial inflammation in correlation with atherosclerotic lesions has been recognized for decades. In the last years, several studies have investigated the relevance and impact of adventitial inflammation on atherogenesis. In the abdominal aorta of elderly Apoe(-/-) mice, adventitial inflammatory structures were characterized as organized ectopic lymphoid tissue, and therefore termed adventitial tertiary lymphoid organs (ATLOs). These ATLOs possess similarities in development, structure and function to secondary lymphoid organs. A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process. We here review the development, phenotypic characteristics, and function of ATLOs in atherosclerosis. Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

No MeSH data available.


Related in: MedlinePlus

Adventitial inflammation in atherosclerosis. Intimal atherosclerotic lesions are frequently accompanied by an inflammatory process in the adjacent adventitia. This inflammatory process is characterized by infiltration of T cells, B cells and dendritic cells in the adventitia. In some cases T and B cell aggregations can be seen. There is a correlation between the size of the intimal lesion and the adventitial structures and a crosstalk between both compartments is suggested.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4126462&req=5

Figure 2: Adventitial inflammation in atherosclerosis. Intimal atherosclerotic lesions are frequently accompanied by an inflammatory process in the adjacent adventitia. This inflammatory process is characterized by infiltration of T cells, B cells and dendritic cells in the adventitia. In some cases T and B cell aggregations can be seen. There is a correlation between the size of the intimal lesion and the adventitial structures and a crosstalk between both compartments is suggested.

Mentions: Human adventitial inflammation was firstly described in 1962 (Schwartz and Mitchell, 1962). The frequency of the inflammatory compound next to atherosclerotic lesions varies between publications, several studies found percentages between 70 and 100% (Houtkamp et al., 2001; Watanabe et al., 2007). Within the adventitial inflammatory compounds, primarily T cells, but also some B cells and dendritic cells are present. Later-stage organized inflammatory compartments further contain lymph follicles (Watanabe et al., 2007). But whether adventitial inflammatory compounds represent ATLOs remains unknown. In addition, it can be speculated whether these adventitial compounds may transform to ATLOs, but in humans studies demonstrating ATLOs are still lacking. Figure 2 illustrates the composition of adventitial inflammation in atherosclerosis.


Adventitial inflammation and its interaction with intimal atherosclerotic lesions.

Akhavanpoor M, Wangler S, Gleissner CA, Korosoglou G, Katus HA, Erbel C - Front Physiol (2014)

Adventitial inflammation in atherosclerosis. Intimal atherosclerotic lesions are frequently accompanied by an inflammatory process in the adjacent adventitia. This inflammatory process is characterized by infiltration of T cells, B cells and dendritic cells in the adventitia. In some cases T and B cell aggregations can be seen. There is a correlation between the size of the intimal lesion and the adventitial structures and a crosstalk between both compartments is suggested.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4126462&req=5

Figure 2: Adventitial inflammation in atherosclerosis. Intimal atherosclerotic lesions are frequently accompanied by an inflammatory process in the adjacent adventitia. This inflammatory process is characterized by infiltration of T cells, B cells and dendritic cells in the adventitia. In some cases T and B cell aggregations can be seen. There is a correlation between the size of the intimal lesion and the adventitial structures and a crosstalk between both compartments is suggested.
Mentions: Human adventitial inflammation was firstly described in 1962 (Schwartz and Mitchell, 1962). The frequency of the inflammatory compound next to atherosclerotic lesions varies between publications, several studies found percentages between 70 and 100% (Houtkamp et al., 2001; Watanabe et al., 2007). Within the adventitial inflammatory compounds, primarily T cells, but also some B cells and dendritic cells are present. Later-stage organized inflammatory compartments further contain lymph follicles (Watanabe et al., 2007). But whether adventitial inflammatory compounds represent ATLOs remains unknown. In addition, it can be speculated whether these adventitial compounds may transform to ATLOs, but in humans studies demonstrating ATLOs are still lacking. Figure 2 illustrates the composition of adventitial inflammation in atherosclerosis.

Bottom Line: These ATLOs possess similarities in development, structure and function to secondary lymphoid organs.A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process.Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Heidelberg Heidelberg, Germany ; DZHK (German Centre for Cardiovascular Research) Partner Site Heidelberg/Mannheim, Germany.

ABSTRACT
The presence of adventitial inflammation in correlation with atherosclerotic lesions has been recognized for decades. In the last years, several studies have investigated the relevance and impact of adventitial inflammation on atherogenesis. In the abdominal aorta of elderly Apoe(-/-) mice, adventitial inflammatory structures were characterized as organized ectopic lymphoid tissue, and therefore termed adventitial tertiary lymphoid organs (ATLOs). These ATLOs possess similarities in development, structure and function to secondary lymphoid organs. A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process. We here review the development, phenotypic characteristics, and function of ATLOs in atherosclerosis. Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

No MeSH data available.


Related in: MedlinePlus