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Exploring the role of TREM-1 receptor in experimental abdominal aortic aneurysm

Vandestienne, M. (Inserm U970, Paris Cardiovascular Research Center, Université ) ; Joffre, J. (René ) ; Giraud, A. (Descartes Paris 5, Paris, France ) ; Potteaux, S. (Inserm U970, Paris Cardiovascular Research Center, Université ) ; Laurans, L. (René ) ; Tedgui, A. (Descartes Paris 5, Paris, France ) ; Derive, M. (Inserm U970, Paris Cardiovascular Research Center, Université ) ; Mallat, Z. (René ) ; Ait Oufella, H. (Descartes Paris 5, Paris, France ) ;
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    Introduction Non-syndromic Abdominal Aortic Aneurysm (AAA) is one of the leading causes of cardiovascular death in elderly men. AAA is characterized by extracellular matrix degradation, smooth muscle cell apoptosis and infiltration of inflammatory cells in the aortic wall. TREM (Triggering Receptor Expressed on Myeloid cells)-1, a receptor expressed by myeloid cells, is a key regulator of innate immune cell activity, and we hypothesized that it might be involved in AAA development. Objective We aim to decipher the role of TREM-1 in the immuno-inflammatory response associated with AAA development and rupture. Method To study the role of TREM-1 in AAA development, we used an experimental model of Angiotensin-II-induced AAA in ApoE −/− Trem-1 −/− and ApoE −/− Trem-1 +/+ mice. At day 0, 3, 7 and 28, we analyzed monocyte trafficking (flow cytometry), inflammatory cell infiltration within the aortic wall (immunostaining, qPCR), aortic wall remodeling (histology) and finally AAA development. Results Angiotensin II infusion increased TREM-1 expression on both classical and non-classical monocytes. TREM-1 deficiency limits Angiotensin II-induced monocytosis at day 3 and limits macrophage infiltration in the aorta at day 7. Trem-1 genetic deletion limits pro-inflammatory response and metalloprotease activity in the aortic wall and protects against elastin degradation. Finally, TREM-1 deficiency significantly reduced AAA rupture and severity. Conclusion We showed that TREM-1 deficiency reduced AAA development and rupture in an Angiotensin II-induced experimental mouse model.


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