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1. Harnessing intestinal tryptophan catabolism to relieve atherosclerosis in mice

Author

Chajadine, Mouna, Laurans, Ludivine, Radecke, Tobias, Mouttoulingam, Nirmala, Al-Rifai, Rida, Bacquer, Emilie, Delaroque, Clara, Rytter, Héloïse, Bredon, Marius, Knosp, Camille, Vilar, José, Fontaine, Coralie, Suffee, Nadine, Vandestienne, Marie, Esposito, Bruno, Dairou, Julien, Launay, Jean Marie, Callebert, Jacques, Tedgui, Alain, Ait-Oufella, Hafid, Sokol, Harry, Chassaing, Benoit, and Taleb, Soraya

Published
2024
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2. Genetic inhibition of CARD9 accelerates the development of atherosclerosis in mice through CD36 dependent-defective autophagy

Author

Zhang, Yujiao, Vandestienne, Marie, Lavillegrand, Jean-Rémi, Joffre, Jeremie, Santos-Zas, Icia, Lavelle, Aonghus, Zhong, Xiaodan, Le Goff, Wilfried, Guérin, Maryse, Al-Rifai, Rida, Laurans, Ludivine, Bruneval, Patrick, Guérin, Coralie, Diedisheim, Marc, Migaud, Melanie, Puel, Anne, Lanternier, Fanny, Casanova, Jean-Laurent, Cochain, Clément, Zernecke, Alma, Saliba, Antoine-Emmanuel, Mokry, Michal, Silvestre, Jean-Sebastien, Tedgui, Alain, Mallat, Ziad, Taleb, Soraya, Lenoir, Olivia, Vindis, Cécile, Camus, Stéphane M., Sokol, Harry, and Ait-Oufella, Hafid

Published
2023
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3. An obesogenic diet increases atherosclerosis through promoting microbiota dysbiosis-induced gut lymphocyte trafficking into the periphery

Author

Laurans, Ludivine, Mouttoulingam, Nirmala, Chajadine, Mouna, Lavelle, Aonghus, Diedisheim, Marc, Bacquer, Emilie, Creusot, Laura, Suffee, Nadine, Esposito, Bruno, Melhem, Nada Joe, Le Goff, Wilfried, Haddad, Yacine, Paul, Jean-Louis, Rainteau, Dominique, Tedgui, Alain, Ait-Oufella, Hafid, Zitvogel, Laurence, Sokol, Harry, and Taleb, Soraya

Published
2023
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5. Author Correction: JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

Author

Al-Rifai, Rida, Vandestienne, Marie, Lavillegrand, Jean-Rémi, Mirault, Tristan, Cornebise, Julie, Poisson, Johanne, Laurans, Ludivine, Esposito, Bruno, James, Chloé, Mansier, Olivier, Hirsch, Pierre, Favale, Fabrizia, Braik, Rayan, Knosp, Camille, Vilar, Jose, Rizzo, Giuseppe, Zernecke, Alma, Saliba, Antoine-Emmanuel, Tedgui, Alain, Lacroix, Maxime, Arrive, Lionel, Mallat, Ziad, Taleb, Soraya, Diedisheim, Marc, Cochain, Clément, Rautou, Pierre-Emmanuel, and Ait-Oufella, Hafid

Published
2022
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6. JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

Author

Al-Rifai, Rida, Vandestienne, Marie, Lavillegrand, Jean-Rémi, Mirault, Tristan, Cornebise, Julie, Poisson, Johanne, Laurans, Ludivine, Esposito, Bruno, James, Chloé, Mansier, Olivier, Hirsch, Pierre, Favale, Fabrizia, Braik, Rayan, Knosp, Camille, Vilar, Jose, Rizzo, Giuseppe, Zernecke, Alma, Saliba, Antoine-Emmanuel, Tedgui, Alain, Lacroix, Maxime, Arrive, Lionel, Mallat, Ziad, Taleb, Soraya, Diedisheim, Marc, Cochain, Clément, Rautou, Pierre-Emmanuel, and Ait-Oufella, Hafid

Published
2022
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7. L-Wnk1 Deletion in Smooth Muscle Cells Causes Aortitis and Inflammatory Shift.

Author

Quelquejay, Helene, Al-Rifai, Rida, Silvestro, Michele, Vandestienne, Marie, Ferreira, Irmine, Mirault, Tristan, Henrion, Daniel, Xiaodan Zhong, Santos-Zas, Icia, Goudot, Guillaume, Alayrac, Paul, Robidel, Estelle, Autret, Gwennhael, Balvay, Daniel, Taleb, Soraya, Tedgui, Alain, Boulanger, Chantal M., Zernecke, Alma, Saliba, Antoine-Emmanuel, and Hadchouel, Juliette

Published
2024
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10. Role of MAIT cells in atherosclerosis

Author

Radecke, Tobias, Chajadine, Mouna, Charles, Caër, Al-Rifai, Rida, Mouttoulingam, Nirmala, Bacquer, Emilie, Esposito, Bruno, Wang, Louise, Mallat, Ziad, Mirault, Tritan, Ait-Oufella, Hafid, Lotersztajn, Sophie, Tedgui, Alain, and Taleb, Soraya

Published
2024
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12. Alternating high-fat diet enhances atherosclerosis by neutrophil reprogramming

Author

Lavillegrand, Jean-Rémi, Al-Rifai, Rida, Thietart, Sara, Guyon, Théo, Vandestienne, Marie, Cohen, Raphael, Duval, Vincent, Zhong, Xiaodan, Yen, Daniel, Ozturk, Mumin, Negishi, Yutaka, Konkel, Joanne, Pinteaux, Emmanuel, Lenoir, Olivia, Vilar, Jose, Laurans, Ludivine, Esposito, Bruno, Bredon, Marius, Sokol, Harry, Diedisheim, Marc, Saliba, Antoine-Emmanuel, Zernecke, Alma, Cochain, Clément, Haub, Jessica, Tedgui, Alain, Speck, Nancy A., Taleb, Soraya, Mhlanga, Musa M., Schlitzer, Andreas, Riksen, Niels P., and Ait-Oufella, Hafid

Abstract

Systemic immune responses caused by chronic hypercholesterolaemia contribute to atherosclerosis initiation, progression and complications1. However, individuals often change their dietary habits over time2, and the effects of an alternating high-fat diet (HFD) on atherosclerosis remain unclear. Here, to address this relevant issue, we developed a protocol using atherosclerosis-prone mice to compare an alternating versus continuous HFD while maintaining similar overall exposure periods. We found that an alternating HFD accelerated atherosclerosis in Ldlr−/−and Apoe−/−mice compared with a continuous HFD. This pro-atherogenic effect of the alternating HFD was also observed in Apoe−/−Rag2−/−mice lacking T, B and natural killer T cells, ruling out the role of the adaptive immune system in the observed phenotype. Discontinuing the HFD in the alternating HFD group downregulated RUNX13, promoting inflammatory signalling in bone marrow myeloid progenitors. After re-exposure to an HFD, these cells produced IL-1β, leading to emergency myelopoiesis and increased neutrophil levels in blood. Neutrophils infiltrated plaques and released neutrophil extracellular traps, exacerbating atherosclerosis. Specific depletion of neutrophils or inhibition of IL-1β pathways abolished emergency myelopoiesis and reversed the pro-atherogenic effects of the alternating HFD. This study highlights the role of IL-1β-dependent neutrophil progenitor reprogramming in accelerated atherosclerosis induced by alternating HFD.

Published
2024
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14. Genetic deficiency of indoleamine 2,3-dioxygenase promotes gut microbiota-mediated metabolic health

Author

Laurans, Ludivine, Venteclef, Nicolas, Haddad, Yacine, Chajadine, Mouna, Alzaid, Fawaz, Metghalchi, Sarvenaz, Sovran, Bruno, Denis, Raphael G. P., Dairou, Julien, Cardellini, Marina, Moreno-Navarrete, Jose-Maria, Straub, Marjolene, Jegou, Sarah, McQuitty, Claire, Viel, Thomas, Esposito, Bruno, Tavitian, Bertrand, Callebert, Jacques, Luquet, Serge H., Federici, Massimo, Fernandez-Real, José Manuel, Burcelin, Remy, Launay, Jean-Marie, Tedgui, Alain, Mallat, Ziad, Sokol, Harry, and Taleb, Soraya

Published
2018
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15. TREM-1 orchestrates angiotensin II-induced monocyte trafficking and promotes experimental abdominal aortic aneurysm

Author

Vandestienne, Marie, Zhang, Yujiao, Santos-Zas, Icia, Al-Rifai, Rida, Joffre, Jeremie, Giraud, Andreas, Laurans, Ludivine, Esposito, Bruno, Pinet, Florence, Bruneval, Patrick, Raffort, Juliette, Lareyre, Fabien, Vilar, Jose, Boufenzer, Amir, Guyonnet, Lea, Guerin, Coralie, Clauser, Eric, Silvestre, Jean-Sebastien, Lang, Sylvie, Soulat-Dufour, Laurie, Tedgui, Alain, Mallat, Ziad, Taleb, Soraya, Boissonnas, Alexandre, Derive, Marc, Chinetti, Giulia, and Ait-Oufella, Hafid

Subjects
Monocytes -- Physiological aspects -- Health aspects, Abdominal aneurysm -- Development and progression -- Models, Membrane proteins -- Physiological aspects -- Health aspects, Health care industry
Abstract

The triggering receptor expressed on myeloid cells 1 (TREM-1) drives inflammatory responses in several cardiovascular diseases but its role in abdominal aortic aneurysm (AAA) remains unknown. Our objective was to explore the role of TREM-1 in a mouse model of angiotensin Il-induced (AngII-induced) AAA. TREM-1 expression was detected in mouse aortic aneurysm and colocalized with macrophages. Treml gene deletion ([Apoe.sup.-/-] [Trem1.sup.-/-]), as well as TREM-1 pharmacological blockade with LR-12 peptide, limited both AAA development and severity. Treml gene deletion attenuated the inflammatory response in the aorta, with a reduction of Il1b, Tnfa, Mmp2, and Mmp9 mRNA expression, and led to a decreased macrophage content due to a reduction of [Ly6C.sup.hi] classical monocyte trafficking. Conversely, antibody-mediated TREM-1 stimulation exacerbated [Ly6C.sup.hi] monocyte aorta infiltration after AngII infusion through CD62L upregulation and promoted proinflammatory signature in the aorta, resulting in worsening AAA severity. AngII infusion stimulated TREM-1 expression and activation on [Ly6C.sup.hi] monocytes through AngII receptor type I ([AT.sub.1]R). In human AAA, TREM-1 was detected and TREM1 mRNA expression correlated with SELL mRNA expression. Finally, circulating levels of sTREM-1 were increased in patients with AAA when compared with patients without AAA. In conclusion, TREM-1 is involved in AAA pathophysiology and may represent a promising therapeutic target in humans., Introduction Nonsyndromic abdominal aortic aneurysm (AAA) is one of the leading causes of cardiovascular death, particularly in men and women over 60 years of age (1). Other defined risk factors [...]

Published
2021
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17. Indoleamine 2,3-Dioxygenase Fine-Tunes Immune Homeostasis in Atherosclerosis and Colitis through Repression of Interleukin-10 Production

Author

Metghalchi, Sarvenaz, Ponnuswamy, Padmapriya, Simon, Tabassome, Haddad, Yacine, Laurans, Ludivine, Clément, Marc, Dalloz, Marion, Romain, Mélissa, Esposito, Bruno, Koropoulis, Vincent, Lamas, Bruno, Paul, Jean-Louis, Cottin, Yves, Kotti, Salma, Bruneval, Patrick, Callebert, Jacques, den Ruijter, Hester, Launay, Jean-Marie, Danchin, Nicolas, Sokol, Harry, Tedgui, Alain, Taleb, Soraya, and Mallat, Ziad

Published
2015
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18. Genetic inhibition of CARD9 accelerates the development of experimental atherosclerosis through CD36 dependent-defective autophagy

Author

ZHANG, Yujiao, primary, Vandestienne, Marie, additional, Lavillegrand, Jean-Rémi, additional, Joffre, Jeremie, additional, Santos-Zas, Icia, additional, Lavelle, Aonghus, additional, Zhong, Xiadan, additional, Goff, Wilfried Le, additional, Guerin, Maryse, additional, Lenoir, Olivia, additional, Laurans, Ludivine, additional, Bruneval, Patrick, additional, Guérin, Coralie, additional, Diedisheim, Marc, additional, Migaud, Melanie, additional, Puel, Anne, additional, Lanternier, Fanny, additional, Casanova, Jean-Laurent, additional, Cochain, Clement, additional, Zernecke, Alma, additional, Saliba, Antoine-Emmanuel, additional, Silvestre, Jean-sébastien, additional, Tedgui, Alain, additional, Mallat, Ziad, additional, Taleb, Soraya, additional, Vindis, Cecile, additional, Camus, Stephane, additional, Sokol, Harry, additional, and Ait-Oufella, Hafid, additional

Published
2022
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23. CARD9 impacts colitis by altering gut microbiota metabolism of tryptophan into aryl hydrocarbon receptor ligands

Author

Lamas, Bruno, Richard, Mathias L, Leducq, Valentin, Pham, Hang-Phuong, Michel, Marie-Laure, Da Costa, Gregory, Bridonneau, Chantal, Jegou, Sarah, Hoffmann, Thomas W, Natividad, Jane M, Brot, Loic, Taleb, Soraya, Couturier-Maillard, Aurélie, Nion-Larmurier, Isabelle, Merabtene, Fatiha, Seksik, Philippe, Bourrier, Anne, Cosnes, Jacques, Ryffel, Bernhard, Beaugerie, Laurent, Launay, Jean-Marie, Langella, Philippe, Xavier, Ramnik J, and Sokol, Harry

Subjects
Inflammatory bowel diseases -- Risk factors -- Care and treatment, Microbiota (Symbiotic organisms) -- Physiological aspects -- Research, Tryptophan -- Physiological aspects -- Dosage and administration, Immune response -- Analysis -- Physiological aspects, Colitis -- Physiological aspects -- Health aspects, Caspases -- Research, Biological sciences, Health
Abstract

Complex interactions between the host and the gut microbiota govern intestinal homeostasis but remain poorly understood. Here we reveal a relationship between gut microbiota and caspase recruitment domain family member 9 (CARD9), a susceptibility gene for inflammatory bowel disease (IBD) that functions in the immune response against microorganisms. CARD9 promotes recovery from colitis by promoting interleukin (IL)-22 production, and Card9[sup.-/-] mice are more susceptible to colitis. The microbiota is altered in Card9[sup.-/-] mice, and transfer of the microbiota from Card9[sup.-/-] to wild-type, germ-free recipients increases their susceptibility to colitis. The microbiota from Card9[sup.-/-] mice fails to metabolize tryptophan into metabolites that act as aryl hydrocarbon receptor (AHR) ligands. Intestinal inflammation is attenuated after inoculation of mice with three Lactobacillus strains capable of metabolizing tryptophan or by treatment with an AHR agonist. Reduced production of AHR ligands is also observed in the microbiota from individuals with IBD, particularly in those with CARD9 risk alleles associated with IBD. Our findings reveal that host genes affect the composition and function of the gut microbiota, altering the production of microbial metabolites and intestinal inflammation., Author(s): Bruno Lamas [1, 2, 3, 4, 5, 6]; Mathias L Richard [5, 6]; Valentin Leducq [1, 2, 3, 4, 6]; Hang-Phuong Pham [7]; Marie-Laure Michel [5, 6]; Gregory Da [...]

Published
2016
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25. Tryptophan: From Diet to Cardiovascular Diseases

Author

Melhem, Nada Joe and Taleb, Soraya

Subjects
QH301-705.5, Review, Models, Biological, Diet, kynurenine, IDO, Chemistry, myocardial infarction, Cardiovascular Diseases, cardiovascular disease, Metabolome, tryptophan catabolism, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase, tryptophan, atherosclerosis, Biology (General), cardiometabolic diseases, QD1-999
Abstract

Cardiovascular disease (CVD) is one of the major causes of mortality worldwide. Inflammation is the underlying common mechanism involved in CVD. It has been recently related to amino acid metabolism, which acts as a critical regulator of innate and adaptive immune responses. Among different metabolites that have emerged as important regulators of immune and inflammatory responses, tryptophan (Trp) metabolites have been shown to play a pivotal role in CVD. Here, we provide an overview of the fundamental aspects of Trp metabolism and the interplay between the dysregulation of the main actors involved in Trp metabolism such as indoleamine 2, 3-dioxygenase 1 (IDO) and CVD, including atherosclerosis and myocardial infarction. IDO has a prominent and complex role. Its activity, impacting on several biological pathways, complicates our understanding of its function, particularly in CVD, where it is still under debate. The discrepancy of the observed IDO effects could be potentially explained by its specific cell and tissue contribution, encouraging further investigations regarding the role of this enzyme. Thus, improving our understanding of the function of Trp as well as its derived metabolites will help to move one step closer towards tailored therapies aiming to treat CVD.

Published
2021

28. TGF-β activity protects against inflammatory aortic aneurysm progression and complications in angiotensin II-infused mice

Author

Wang, Yu, Ait-Oufella, Hafid, Herbin, Olivier, Bonnin, Philippe, Ramkhelawon, Bhama, Taleb, Soraya, Huang, Jin, Offenstadt, Georges, Combadiere, Christophe, Renia, Laurent, Johnson, Jason L., Tharaux, Pierre-Louis, Tedgui, Alain, and Mallat, Ziad

Subjects
Immune response -- Physiological aspects -- Health aspects, Aortic aneurysms -- Complications and side effects -- Development and progression -- Patient outcomes, Transforming growth factors -- Health aspects -- Physiological aspects, Angiotensin -- Complications and side effects -- Dosage and administration -- Health aspects -- Physiological aspects, Health care industry
Abstract

Complicated abdominal aortic aneurysm (AAA) is a major cause of mortality in elderly men. Ang II-dependent TGF-β activity promotes aortic aneurysm progression in experimental Marfan syndrome. However, the role of TGF-β in experimental models of AAA has not been comprehensively assessed. Here, we show that systemic neutralization of TGF-β activity breaks the resistance of normocholesterolemic C57BL/6 mice to Ang II-induced AAA formation and markedly increases their susceptibility to the disease. These aneurysms displayed a large spectrum of complications on echography, including fissuration, double channel formation, and rupture, leading to death from aneurysm complications. The disease was refractory to inhibition of IFN-γ, IL-4, IL-6, or TNF-α signaling. Genetic deletion of T and B cells or inhibition of the CX3CR1 pathway resulted in partial protection. Interestingly, neutralization of TGF-β activity enhanced monocyte invasiveness, and monocyte depletion markedly inhibited aneurysm progression and complications. Finally, TGF-β neutralization increased MMP-12 activity, and MMP-12 deficiency prevented aneurysm rupture. These results clearly identify a critical role for TGF-β in the taming of the innate immune response and the preservation of vessel integrity in C57BL/6 mice, which contrasts with its reported pathogenic role in Marfan syndrome., Introduction Abdominal aortic aneurysm (AAA) is an age-associated disease that affects approximately 5% of elderly men and is responsible for a significant number of deaths in Western countries (1). At [...]

Published
2010
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30. Endothelial Cell Indoleamine 2, 3-Dioxygenase 1 Alters Cardiac Function After Myocardial Infarction Through Kynurenine

Author

Melhem, Nada Joe, primary, Chajadine, Mouna, additional, Gomez, Ingrid, additional, Howangyin, Kiave-Yune, additional, Bouvet, Marion, additional, Knosp, Camille, additional, Sun, Yanyi, additional, Rouanet, Marie, additional, Laurans, Ludivine, additional, Cazorla, Olivier, additional, Lemitre, Mathilde, additional, Vilar, José, additional, Mallat, Ziad, additional, Tedgui, Alain, additional, Ait-Oufella, Hafid, additional, Hulot, Jean-Sébastien, additional, Callebert, Jacques, additional, Launay, Jean-Marie, additional, Fauconnier, Jeremy, additional, Silvestre, Jean-Sébastien, additional, and Taleb, Soraya, additional

Published
2021
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40. Reduction of Macrophage Infiltration and Chemoattractant Gene Expression Changes in White Adipose Tissue of Morbidly Obese Subjects After Surgery-Induced Weight Loss

Author

Cancello, Raffaella, Henegar, Corneliu, Viguerie, Nathalie, Taleb, Soraya, Poitou, Christine, Rouault, Christine, Coupaye, Muriel, Pelloux, Veronique, Hugol, Danielle, Bouillot, Jean-Luc, Bouloumié, Anne, Barbatelli, Giorgio, Cinti, Saverio, Svensson, Per-Arne, Barsh, Gregory S., Zucker, Jean-Daniel, Basdevant, Arnaud, Langin, Dominique, and Clément, Karine

Published
2005

47. The Dendritic Cell Receptor DNGR-1 Promotes the Development of Atherosclerosis in Mice

Author

Haddad, Yacine, primary, Lahoute, Charlotte, additional, Clément, Marc, additional, Laurans, Ludivine, additional, Metghalchi, Sarvenaz, additional, Zeboudj, Lynda, additional, Giraud, Andreas, additional, Loyer, Xavier, additional, Vandestienne, Marie, additional, Wain-Hobson, Julien, additional, Esposito, Bruno, additional, Potteaux, Stephane, additional, Ait-Oufella, Hafid, additional, Tedgui, Alain, additional, Mallat, Ziad, additional, and Taleb, Soraya, additional

Published
2017
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48. Type-2 innate lymphoid cells control the development of atherosclerosis in mice

Author

Newland, Stephen A., primary, Mohanta, Sarajo, additional, Clément, Marc, additional, Taleb, Soraya, additional, Walker, Jennifer A., additional, Nus, Meritxell, additional, Sage, Andrew P., additional, Yin, Changjun, additional, Hu, Desheng, additional, Kitt, Lauren L., additional, Finigan, Alison J., additional, Rodewald, Hans-Reimer, additional, Binder, Christoph J., additional, McKenzie, Andrew N. J., additional, Habenicht, Andreas J., additional, and Mallat, Ziad, additional

Published
2017
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49. Abstract 226: C-type Lectin Receptor Clec9a on Cd8a+ Dendritic Cells Promotes the Development of Atherosclerosis in Mice

Author

Yacine, Haddad, primary, Lahoutte, Charlotte, additional, Clément, Marc, additional, Laurans, Ludivine, additional, Sarvenaz.Metghalchi, Sarvenaz.Metghalchi, additional, Zeboudj, Lynda, additional, Giraud, Andreas, additional, Loyer, Xavier, additional, Vandestienne, Marie, additional, Wain-Hobson, Julien, additional, Esposito, Bruno, additional, Potteaux, Stephane, additional, Ait-Oufella, Hafid, additional, Reis e Sousa, Caetano, additional, Tedgui, Alain, additional, Mallat, Ziad, additional, and Taleb, Soraya, additional

Published
2017
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50. Abstract 309: Blockade of Transforming Growth Factor Beta Activity in Elastase-Induced Aortic Injury in Mice Induces a Human-Like Abdominal Aneurysm

Author

Clement, Marc, primary, Lareyre, Fabien, additional, Raffort, Juliette, additional, Pohlod, Stefanie, additional, Patel, Meghana, additional, Esposito, Bruno, additional, Master, Leanne, additional, Finigan, Alison, additional, Villabuena, Pablo, additional, Stamponi, Marco, additional, Taleb, Soraya, additional, Trashet, Bram, additional, and Mallat, Ziad, additional

Published
2017
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