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Published on: July 23, 2009
Exploring antibody-dependent adaptive immunity against aortic extracellular matrix components in experimental aortic
Raphaël Coscas1, Sebastien Dupont2, Sacha Mussot3
1UMR 1148, Inserm Paris 7, Denis Diderot University, Xavier Bichat Hospital, Paris, France; UMR 1173, Inserm Paris 11, Faculty of Health Sciences Simone Veil, Versailles Saint-Quentin-en-Yvelines University, Paris-Saclay University, Montigny-le-Bretonneux, France; Department of Vascular Surgery, Ambroise Paré University Hospital, AP-HP, Boulogne-Billancourt, France; UMR 1018, Inserm Paris 11, CESP, Versailles Saint-Quentin-en-Yvelines University, Paris-Saclay University, Paul Brousse Hospital, Villejuif, France.
Adaptive immunity against aortic extracellular matrix (ECM) components, particularly structural glycoproteins and proteoglycans, significantly increases the risk of abdominal aortic aneurysm rupture in a rat model. This immune response involves immunoglobulin deposits and neutrophil activation.
Area of Science:
- Immunology
- Vascular Biology
- Extracellular Matrix Research
Background:
- Adaptive immunity is increasingly recognized in abdominal aortic aneurysm (AAA) development.
- The specific antigens driving AAA rupture remain unclear, though extracellular matrix (ECM) components are suspected.
- This study investigates the role of adaptive immunity against aortic ECM antigens in AAA rupture.
Purpose of the Study:
- To develop and characterize an experimental model of AAA rupture mediated by adaptive immunity to ECM.
- To identify specific ECM components that elicit adaptive immune responses leading to AAA rupture.
- To elucidate the immunological mechanisms underlying ECM-induced AAA rupture.
Main Methods:
- An experimental rat model using decellularized aortic xenografts (DAX) and presensitization against guinea pig aortic ECM was established.
- Rats were presensitized against specific ECM components (glycoproteins, proteoglycans, collagen, elastin) to assess their role in rupture.
- Histological, immunofluorescence, and conditioned medium analyses were performed to evaluate immune responses and tissue damage.
Main Results:
- Presensitization against aortic ECM led to 80% early rupture rate, compared to 0% in controls.
- Immunoglobulin and C3 complement deposits were observed, alongside increased matrix metalloproteinase 9 and myeloperoxidase.
- Rats presensitized against structural glycoproteins and proteoglycans showed significantly higher susceptibility to rupture.
Conclusions:
- Adaptive immunity targeting aortic ECM, especially structural glycoproteins and proteoglycans, can trigger AAA rupture.
- Neutrophil activation and extracellular trap formation are implicated in the rupture process.
- Further research is required to pinpoint the exact antigenic proteins involved in ECM-induced AAA rupture.
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