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51. Transcriptomic-based clustering of human atherosclerotic plaques identifies subgroups with different underlying biology and clinical presentation

Author

CDL Onderzoek Pasterkamp, Experimentele Afd. Cardiologie 1, Child Health, Circulatory Health, CDL Cluster Onderzoek en Onderwijs, Onderzoek Precision medicine, Zorgeenheid Vaatchirurgie Medisch, Cancer, Regenerative Medicine and Stem Cells, Infection & Immunity, Onderzoek Vrouw Hart & Vaatziekten, Team Medisch, Centraal Diagnostisch Laboratorium, Mokry, Michal, Boltjes, Arjan, Slenders, Lotte, Bel-Bordes, Gemma, Cui, Kai, Brouwer, Eli, Mekke, Joost M., Depuydt, Marie A. C., Timmerman, Nathalie, Waissi, Farahnaz, Verwer, Maarten C., Turner, Adam W., Khan, Mohammad Daud, Hodonsky, Chani J., Diez Benavente, Ernest, Hartman, Robin J. G., van den Dungen, Noortje A. M., Lansu, Nico, Nagyova, Emilia, Prange, Koen H. M., Kovacic, Jason C., Björkegren, Johan L. M., Pavlos, Eleftherios, Andreakos, Evangelos, Schunkert, Heribert, Owens, Gary K., Monaco, Claudia, Finn, Aloke V., Virmani, Renu, Leeper, Nicholas J., de Winther, Menno P. J., Kuiper, Johan, de Borst, Gert J., Stroes, Erik S. G., Civelek, Mete, de Kleijn, Dominique P. V., den Ruijter, Hester M., Asselbergs, Folkert W., van der Laan, Sander W., Miller, Clint L., Pasterkamp, Gerard, CDL Onderzoek Pasterkamp, Experimentele Afd. Cardiologie 1, Child Health, Circulatory Health, CDL Cluster Onderzoek en Onderwijs, Onderzoek Precision medicine, Zorgeenheid Vaatchirurgie Medisch, Cancer, Regenerative Medicine and Stem Cells, Infection & Immunity, Onderzoek Vrouw Hart & Vaatziekten, Team Medisch, Centraal Diagnostisch Laboratorium, Mokry, Michal, Boltjes, Arjan, Slenders, Lotte, Bel-Bordes, Gemma, Cui, Kai, Brouwer, Eli, Mekke, Joost M., Depuydt, Marie A. C., Timmerman, Nathalie, Waissi, Farahnaz, Verwer, Maarten C., Turner, Adam W., Khan, Mohammad Daud, Hodonsky, Chani J., Diez Benavente, Ernest, Hartman, Robin J. G., van den Dungen, Noortje A. M., Lansu, Nico, Nagyova, Emilia, Prange, Koen H. M., Kovacic, Jason C., Björkegren, Johan L. M., Pavlos, Eleftherios, Andreakos, Evangelos, Schunkert, Heribert, Owens, Gary K., Monaco, Claudia, Finn, Aloke V., Virmani, Renu, Leeper, Nicholas J., de Winther, Menno P. J., Kuiper, Johan, de Borst, Gert J., Stroes, Erik S. G., Civelek, Mete, de Kleijn, Dominique P. V., den Ruijter, Hester M., Asselbergs, Folkert W., van der Laan, Sander W., Miller, Clint L., and Pasterkamp, Gerard

Published
2022

52. Preclinical Aortic Atherosclerosis in Adolescents With Chronic Disease

Author

CTI Boes, Onderzoek Vrouw Hart & Vaatziekten, Circulatory Health, Experimentele Afd. Cardiologie 1, Genetica Oper.Mang. Clinical Genetics, Cancer, Cluster B, Immuno/reuma ERN, Child Health, Infection & Immunity, Regenerative Medicine and Stem Cells, Longziekten patientenzorg, Speerpunt Child Health, Onderzoek, MS Radiologie, Cardiologie patientenzorg, Ververs, Francesca A, Eikendal, Anouk L M, Kofink, Daniel, Nuboer, Roos, Westenberg, Jos J M, Hovenkamp, Gijs T, Kemps, Jitske J A, Coenen, Iris C J, Daems, Joëlle J N, Claus, Laura R, Ju, Yillie, Wulffraat, Nico M, van der Ent, Cornelis K, Monaco, Claudia, Boes, Marianne, Leiner, Tim, Grotenhuis, Heynric B, Schipper, Henk S, CTI Boes, Onderzoek Vrouw Hart & Vaatziekten, Circulatory Health, Experimentele Afd. Cardiologie 1, Genetica Oper.Mang. Clinical Genetics, Cancer, Cluster B, Immuno/reuma ERN, Child Health, Infection & Immunity, Regenerative Medicine and Stem Cells, Longziekten patientenzorg, Speerpunt Child Health, Onderzoek, MS Radiologie, Cardiologie patientenzorg, Ververs, Francesca A, Eikendal, Anouk L M, Kofink, Daniel, Nuboer, Roos, Westenberg, Jos J M, Hovenkamp, Gijs T, Kemps, Jitske J A, Coenen, Iris C J, Daems, Joëlle J N, Claus, Laura R, Ju, Yillie, Wulffraat, Nico M, van der Ent, Cornelis K, Monaco, Claudia, Boes, Marianne, Leiner, Tim, Grotenhuis, Heynric B, and Schipper, Henk S

Published
2022

54. Translational opportunities of single-cell biology in atherosclerosis.

Author

Winther, Menno P J de, Bäck, Magnus, Evans, Paul, Gomez, Delphine, Goncalves, Isabel, Jørgensen, Helle F, Koenen, Rory R, Lutgens, Esther, Norata, Giuseppe Danilo, Osto, Elena, Dib, Lea, Simons, Michael, Stellos, Konstantinos, Ylä-Herttuala, Seppo, Winkels, Holger, Bochaton-Piallat, Marie-Luce, and Monaco, Claudia

Subjects
BIOLOGY, CARDIOVASCULAR diseases, INTERNATIONAL relations, MUSCLE cells, PATIENT care
Abstract

The advent of single-cell biology opens a new chapter for understanding human biological processes and for diagnosing, monitoring, and treating disease. This revolution now reaches the field of cardiovascular disease (CVD). New technologies to interrogate CVD samples at single-cell resolution are allowing the identification of novel cell communities that are important in shaping disease development and direct towards new therapeutic strategies. These approaches have begun to revolutionize atherosclerosis pathology and redraw our understanding of disease development. This review discusses the state-of-the-art of single-cell analysis of atherosclerotic plaques, with a particular focus on human lesions, and presents the current resolution of cellular subpopulations and their heterogeneity and plasticity in relation to clinically relevant features. Opportunities and pitfalls of current technologies as well as the clinical impact of single-cell technologies in CVD patient care are highlighted, advocating for multidisciplinary and international collaborative efforts to join the cellular dots of CVD. [ABSTRACT FROM AUTHOR]

Published
2023
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57. A blood atlas of COVID-19 defines hallmarks of disease severity and specificity

Author

Ahern, David J., primary, Ai, Zhichao, additional, Ainsworth, Mark, additional, Allan, Chris, additional, Allcock, Alice, additional, Angus, Brian, additional, Ansari, M. Azim, additional, Arancibia-Cárcamo, Carolina V., additional, Aschenbrenner, Dominik, additional, Attar, Moustafa, additional, Baillie, J. Kenneth, additional, Barnes, Eleanor, additional, Bashford-Rogers, Rachael, additional, Bashyal, Archana, additional, Beer, Sally, additional, Berridge, Georgina, additional, Beveridge, Amy, additional, Bibi, Sagida, additional, Bicanic, Tihana, additional, Blackwell, Luke, additional, Bowness, Paul, additional, Brent, Andrew, additional, Brown, Andrew, additional, Broxholme, John, additional, Buck, David, additional, Burnham, Katie L., additional, Byrne, Helen, additional, Camara, Susana, additional, Candido Ferreira, Ivan, additional, Charles, Philip, additional, Chen, Wentao, additional, Chen, Yi-Ling, additional, Chong, Amanda, additional, Clutterbuck, Elizabeth A., additional, Coles, Mark, additional, Conlon, Christopher P., additional, Cornall, Richard, additional, Cribbs, Adam P., additional, Curion, Fabiola, additional, Davenport, Emma E., additional, Davidson, Neil, additional, Davis, Simon, additional, Dendrou, Calliope A., additional, Dequaire, Julie, additional, Dib, Lea, additional, Docker, James, additional, Dold, Christina, additional, Dong, Tao, additional, Downes, Damien, additional, Drakesmith, Hal, additional, Dunachie, Susanna J., additional, Duncan, David A., additional, Eijsbouts, Chris, additional, Esnouf, Robert, additional, Espinosa, Alexis, additional, Etherington, Rachel, additional, Fairfax, Benjamin, additional, Fairhead, Rory, additional, Fang, Hai, additional, Fassih, Shayan, additional, Felle, Sally, additional, Fernandez Mendoza, Maria, additional, Ferreira, Ricardo, additional, Fischer, Roman, additional, Foord, Thomas, additional, Forrow, Aden, additional, Frater, John, additional, Fries, Anastasia, additional, Gallardo Sanchez, Veronica, additional, Garner, Lucy C., additional, Geeves, Clementine, additional, Georgiou, Dominique, additional, Godfrey, Leila, additional, Golubchik, Tanya, additional, Gomez Vazquez, Maria, additional, Green, Angie, additional, Harper, Hong, additional, Harrington, Heather A., additional, Heilig, Raphael, additional, Hester, Svenja, additional, Hill, Jennifer, additional, Hinds, Charles, additional, Hird, Clare, additional, Ho, Ling-Pei, additional, Hoekzema, Renee, additional, Hollis, Benjamin, additional, Hughes, Jim, additional, Hutton, Paula, additional, Jackson-Wood, Matthew A., additional, Jainarayanan, Ashwin, additional, James-Bott, Anna, additional, Jansen, Kathrin, additional, Jeffery, Katie, additional, Jones, Elizabeth, additional, Jostins, Luke, additional, Kerr, Georgina, additional, Kim, David, additional, Klenerman, Paul, additional, Knight, Julian C., additional, Kumar, Vinod, additional, Kumar Sharma, Piyush, additional, Kurupati, Prathiba, additional, Kwok, Andrew, additional, Lee, Angela, additional, Linder, Aline, additional, Lockett, Teresa, additional, Lonie, Lorne, additional, Lopopolo, Maria, additional, Lukoseviciute, Martyna, additional, Luo, Jian, additional, Marinou, Spyridoula, additional, Marsden, Brian, additional, Martinez, Jose, additional, Matthews, Philippa C., additional, Mazurczyk, Michalina, additional, McGowan, Simon, additional, McKechnie, Stuart, additional, Mead, Adam, additional, Mentzer, Alexander J., additional, Mi, Yuxin, additional, Monaco, Claudia, additional, Montadon, Ruddy, additional, Napolitani, Giorgio, additional, Nassiri, Isar, additional, Novak, Alex, additional, O'Brien, Darragh P., additional, O'Connor, Daniel, additional, O'Donnell, Denise, additional, Ogg, Graham, additional, Overend, Lauren, additional, Park, Inhye, additional, Pavord, Ian, additional, Peng, Yanchun, additional, Penkava, Frank, additional, Pereira Pinho, Mariana, additional, Perez, Elena, additional, Pollard, Andrew J., additional, Powrie, Fiona, additional, Psaila, Bethan, additional, Quan, T. Phuong, additional, Repapi, Emmanouela, additional, Revale, Santiago, additional, Silva-Reyes, Laura, additional, Richard, Jean-Baptiste, additional, Rich-Griffin, Charlotte, additional, Ritter, Thomas, additional, Rollier, Christine S., additional, Rowland, Matthew, additional, Ruehle, Fabian, additional, Salio, Mariolina, additional, Sansom, Stephen Nicholas, additional, Sanches Peres, Raphael, additional, Santos Delgado, Alberto, additional, Sauka-Spengler, Tatjana, additional, Schwessinger, Ron, additional, Scozzafava, Giuseppe, additional, Screaton, Gavin, additional, Seigal, Anna, additional, Semple, Malcolm G., additional, Sergeant, Martin, additional, Simoglou Karali, Christina, additional, Sims, David, additional, Skelly, Donal, additional, Slawinski, Hubert, additional, Sobrinodiaz, Alberto, additional, Sousos, Nikolaos, additional, Stafford, Lizzie, additional, Stockdale, Lisa, additional, Strickland, Marie, additional, Sumray, Otto, additional, Sun, Bo, additional, Taylor, Chelsea, additional, Taylor, Stephen, additional, Taylor, Adan, additional, Thongjuea, Supat, additional, Thraves, Hannah, additional, Todd, John A., additional, Tomic, Adriana, additional, Tong, Orion, additional, Trebes, Amy, additional, Trzupek, Dominik, additional, Tucci, Felicia Anna, additional, Turtle, Lance, additional, Udalova, Irina, additional, Uhlig, Holm, additional, van Grinsven, Erinke, additional, Vendrell, Iolanda, additional, Verheul, Marije, additional, Voda, Alexandru, additional, Wang, Guanlin, additional, Wang, Lihui, additional, Wang, Dapeng, additional, Watkinson, Peter, additional, Watson, Robert, additional, Weinberger, Michael, additional, Whalley, Justin, additional, Witty, Lorna, additional, Wray, Katherine, additional, Xue, Luzheng, additional, Yeung, Hing Yuen, additional, Yin, Zixi, additional, Young, Rebecca K., additional, Youngs, Jonathan, additional, Zhang, Ping, additional, and Zurke, Yasemin-Xiomara, additional

Published
2022
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58. Interferon regulatory factor-5-dependent CD11c+ macrophages contribute to the formation of rupture–prone atherosclerotic plaques

Author

Edsfeldt, Andreas, primary, Swart, Maarten, additional, Singh, Pratibha, additional, Dib, Lea, additional, Sun, Jiangming, additional, Cole, Jennifer E, additional, Park, Inhye, additional, Al-Sharify, Dania, additional, Persson, Ana, additional, Nitulescu, Mihaela, additional, Borges, Patricia Das Neves, additional, Kassiteridi, Christina, additional, Goddard, Michael E, additional, Lee, Regent, additional, Volkov, Petr, additional, Orho-Melander, Marju, additional, Maegdefessel, Lars, additional, Nilsson, Jan, additional, Udalova, Irina, additional, Goncalves, Isabel, additional, and Monaco, Claudia, additional

Published
2022
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61. Transcriptomic-based clustering of advanced atherosclerotic plaques identifies subgroups of plaques with differential underlying biology that associate with clinical presentation

Author

Mokry, Michal, primary, Boltjes, Arjan, additional, Cui, Kai, additional, Slenders, Lotte, additional, Mekke, Joost M., additional, depuydt, Marie A.C., additional, Timmerman, Nathalie M., additional, Waissi, Farahnaz, additional, Verwer, Maarten C., additional, Turner, Adam W., additional, Khan, Mohammad D., additional, Hodonsky, Chani J., additional, Diez Benavente, Ernest, additional, Hartman, Robin J. G., additional, van den Dungen, Noortje A. M., additional, Lansu, Nico, additional, Nagyova, Emilia, additional, Prange, Koen H. M., additional, Pavlos, Eleftherios, additional, Andreakos, Evangelos, additional, Schunkert, Heribert, additional, Owens, Gary K., additional, Monaco, Claudia, additional, Finn, Aloke V., additional, Virmani, Renu, additional, Leeper, Nicholas J., additional, de Winther, Menno P. J., additional, Kuiper, Johan, additional, de Borst, Gert J., additional, Stroes, Erik S. G., additional, Civelek, Mete, additional, de Kleijn, Dominique P. V., additional, den Ruijter, Hester M., additional, Asselbergs, Folkert W., additional, van der Laan, Sander W., additional, Miller, Clint L., additional, and Pasterkamp, Gerard, additional

Published
2021
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64. The aorta can act as a site of naïve CD4+ T-cell priming

Author

Macritchie N., Grassia G., Noonan J., Cole J. E., Hughes C. E., Schroeder J., Benson R. A., Cochain C., Zernecke A., Guzik T. J., Garside P., Monaco Claudia, Maffia P., Macritchie, N., Grassia, G., Noonan, J., Cole, J. E., Hughes, C. E., Schroeder, J., Benson, R. A., Cochain, C., Zernecke, A., Guzik, T. J., Garside, P., Monaco, Claudia, and Maffia, P.

Subjects
Kinetic, Animal, Mice, Knockout, ApoE, T cell, Adaptive Immunity, Aortic Disease, Lymphocyte Activation, T-Lymphocytes, Regulatory, Plaque, Atherosclerotic, Mice, Inbred C57BL, Disease Models, Animal, Genes, T-Cell Receptor, Phenotype, Th1 Cell, Priming, Atherosclerosi, Disease Progression, Membrane Glycoprotein, Cytokine, Aorta, Cells, Cultured, Cell Proliferation
Abstract

Aims: Aortic adaptive immunity plays a role in atherosclerosis; however, the precise mechanisms leading to T-cell activation in the arterial wall remain poorly understood. Methods and results: Here, we have identified naïve T cells in the aorta of wild-Type and T-cell receptor transgenic mice and we demonstrate that naïve T cells can be primed directly in the vessel wall with both kinetics and frequency of T-cell activation found to be similar to splenic and lymphoid T cells. Aortic homing of naïve T cells is regulated at least in part by the P-selectin glycosylated ligand-1 receptor. In experimental atherosclerosis the aorta supports CD4+ T-cell activation selectively driving Th1 polarization. By contrast, secondary lymphoid organs display Treg expansion. Conclusion: Our results demonstrate that the aorta can support T-cell priming and that naïve T cells traffic between the circulation and vessel wall. These data underpin the paradigm that local priming of T cells specific for plaque antigens contributes to atherosclerosis progression.

Published
2020

65. Study of the Myocardial Contraction and Relaxation Velocities through Doppler Tissue Imaging Echocardiography: A New Alternative in the Assessment of the Segmental Ventricular Function

Author

Silva Carlos Eduardo Suaide, Ferreira Luiz Darcy Cortez, Peixoto Luciana Braz, Monaco Claudia Gianini, Gil Manuel Adán, and Ortiz Juarez

Subjects
Doppler tissue imaging, ventricular function, echocardiography, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

OBJECTIVE: Doppler tissue imaging (DTI) enables the study of the velocity of contraction and relaxation of myocardial segments. We established standards for the peak velocity of the different myocardial segments of the left ventricle in systole and diastole, and correlated them with the electrocardiogram. METHODS: We studied 35 healthy individuals (27 were male) with ages ranging from 12 to 59 years (32.9 ± 10.6). Systolic and diastolic peak velocities were assessed by Doppler tissue imaging in 12 segments of the left ventricle, establishing their mean values and the temporal correlation with the cardiac cycle. RESULTS: The means (and standard deviation) of the peak velocities in the basal, medial, and apical regions (of the septal, anterior, lateral, and posterior left ventricle walls) were respectively, in cm/s, 7.35(1.64), 5.26(1.88), and 3.33(1.58) in systole and 10.56(2.34), 7.92(2.37), and 3.98(1.64) in diastole. The mean time in which systolic peak velocity was recorded was 131.59ms (±19.12ms), and diastolic was 459.18ms (±18.13ms) based on the peak of the R wave of the electrocardiogram. CONCLUSION: In healthy individuals, maximum left ventricle segment velocities decreased from the bases to the ventricular apex, with certain proportionality between contraction and relaxation (P

Published
2002

66. Novel methodologies for biomarker discovery in atherosclerosis

Author

Hoefer, Imo E., Steffens, Sabine, Ala-Korpela, Mika, Bäck, Magnus, Badimon, Lina, Bochaton-Piallat, Marie-Luce, Boulanger, Chantal M., Caligiuri, Giuseppina, Dimmeler, Stefanie, Egido, Jesus, Evans, Paul C., Guzik, Tomasz, Kwak, Brenda R., Landmesser, Ulf, Mayr, Manuel, Monaco, Claudia, Pasterkamp, Gerard, Tuñón, Jose, and Weber, Christian

Published
2015
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69. CD200 Limits Monopoiesis and Monocyte Recruitment in Atherosclerosis

Author

Kassiteridi, Christina, primary, Cole, Jennifer E., additional, Griseri, Thibault, additional, Falck-Hansen, Mika, additional, Goddard, Michael E., additional, Seneviratne, Anusha N., additional, Green, Patricia A., additional, Park, Inhye, additional, Shami, Annelie G., additional, Pattarabanjird, Tanyaporn, additional, Upadhye, Aditi, additional, Taylor, Angela M., additional, Handa, Ashok, additional, Channon, Keith M., additional, Lutgens, Esther, additional, McNamara, Coleen A., additional, Williams, Richard O., additional, and Monaco, Claudia, additional

Published
2021
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70. COVID-19 and myocarditis: a systematic review and overview of current challenges

Author

Monaco Claudia, Teresa Castiello, Sanjay K Prasad, Georgios Georgiopoulos, Alberto Aimo, Gherardo Finocchiaro, Andrea Gianatti, and Dimitrios Delialis

Subjects
Male, medicine.medical_specialty, 2019nCoV, Myocarditis, Cardiovascular Complication, MEDLINE, 030204 cardiovascular system & hematology, Cochrane Library, Article, Pathogenesis, 03 medical and health sciences, Cardiac damage, 0302 clinical medicine, Internal medicine, Biopsy, Humans, Medicine, Myocytes, Cardiac, Registries, 030212 general & internal medicine, medicine.diagnostic_test, business.industry, SARS-CoV-2, COVID-19, medicine.disease, Cardiac injury, Coronavirus, Myocardial damage, Pathophysiology, Heart failure, Cardiology and Cardiovascular Medicine, business
Abstract

Myocardial inflammation in COVID-19 has been documented. Its pathogenesis is not fully elucidated, but the two main theories foresee a direct role of ACE2 receptor and a hyperimmune response, which may also lead to isolated presentation of COVID-19-mediated myocarditis. The frequency and prognostic impact of COVID-19-mediated myocarditis is unknown. This review aims to summarise current evidence on this topic. We performed a systematic review of MEDLINE and Cochrane Library (1/12/19–30/09/20). We also searched clinicaltrials.gov for unpublished studies testing therapies with potential implication for COVID-19-mediated cardiovascular complication. Eligible studies had laboratory confirmed COVID-19 and a clinical and/or histological diagnosis of myocarditis by ESC or WHO/ISFC criteria. Reports of 38 cases were included (26 male patients, 24 aged

Published
2021

71. Immunometabolic factors in adolescent chronic disease are associated with Th1 skewing of invariant Natural Killer T cells

Author

Afd Pharmacology, Pharmacology, Ververs, Francesca A, Engelen, Suzanne E, Nuboer, Roos, Vastert, Bas, van der Ent, Cornelis K, Van't Land, Belinda, Garssen, Johan, Monaco, Claudia, Boes, Marianne, Schipper, Henk S, Afd Pharmacology, Pharmacology, Ververs, Francesca A, Engelen, Suzanne E, Nuboer, Roos, Vastert, Bas, van der Ent, Cornelis K, Van't Land, Belinda, Garssen, Johan, Monaco, Claudia, Boes, Marianne, and Schipper, Henk S

Published
2021

72. The changing landscape of the vulnerable plaque: a call for fine-tuning of preclinical models

Author

Experimentele Afd. Cardiologie 1, CDL Onderzoek Pasterkamp, Circulatory Health, Onderzoek Vrouw Hart & Vaatziekten, Centraal Diagnostisch Laboratorium, Child Health, Buono, Michele F, Slenders, Lotte, Wesseling, Marian, Hartman, Robin J G, Monaco, Claudia, den Ruijter, Hester M, Pasterkamp, Gerard, Mokry, Michal, Experimentele Afd. Cardiologie 1, CDL Onderzoek Pasterkamp, Circulatory Health, Onderzoek Vrouw Hart & Vaatziekten, Centraal Diagnostisch Laboratorium, Child Health, Buono, Michele F, Slenders, Lotte, Wesseling, Marian, Hartman, Robin J G, Monaco, Claudia, den Ruijter, Hester M, Pasterkamp, Gerard, and Mokry, Michal

Published
2021

73. Immunometabolic factors in adolescent chronic disease are associated with Th1 skewing of invariant Natural Killer T cells

Author

CTI Boes, Child Health, Immuno/reuma onderzoek 5 (Vastert2), CTI Van Loosdregt, Infection & Immunity, Speerpunt Child Health, Longziekten patientenzorg, CTI Research, Immuno/reuma onderzoek 2 (Boes), Onderzoek, Circulatory Health, Cardiologie patientenzorg, Ververs, Francesca, Engelen, Suzanne, Nuboer, Roos, Vastert, SJ, van der Ent, Kors, van 't Land, Belinda, Garssen, Johan, Monaco, Claudia, Boes, Marianne, Schipper, Henk, CTI Boes, Child Health, Immuno/reuma onderzoek 5 (Vastert2), CTI Van Loosdregt, Infection & Immunity, Speerpunt Child Health, Longziekten patientenzorg, CTI Research, Immuno/reuma onderzoek 2 (Boes), Onderzoek, Circulatory Health, Cardiologie patientenzorg, Ververs, Francesca, Engelen, Suzanne, Nuboer, Roos, Vastert, SJ, van der Ent, Kors, van 't Land, Belinda, Garssen, Johan, Monaco, Claudia, Boes, Marianne, and Schipper, Henk

Published
2021

75. Tumor necrosis factor-[alpha] triggers a cytokine cascade yielding postoperative cognitive decline

Author

Terrando, Niccolo, Monaco, Claudia, Ma, Daqing, Foxwell, Brian M.J., Feldmann, Marc, and Maze, Mervyn

Subjects
Cognition disorders -- Development and progression, Tumor necrosis factor -- Properties, Cytokines -- Properties, Natural immunity -- Physiological aspects, Surgery -- Complications, Surgery -- Diagnosis, Surgery -- Care and treatment, Science and technology
Abstract

Cognitive decline following surgery in older individuals is a major clinical problem of uncertain mechanism; a similar cognitive decline also follows severe infection, chemotherapy, or trauma and is currently without effective therapy. A variety of mechanisms have been proposed, and exploring the role of inflammation, we recently reported the role of IL-1[beta] in the hippocampus after surgery in mice with postoperative cognitive dysfunction. Here, we show that TNF-[alpha] is upstream of IL-1 and provokes its production in the brain. Peripheral blockade of TNF-[alpha] is able to limit the release of IL-1 and prevent neuroinflammation and cognitive decline in a mouse model of surgery-induced cognitive decline. TNF-[alpha] appears to synergize with MyD88, the IL-1/TLR superfamily common signaling pathway, to sustain postoperative cognitive decline. Taken together, our results suggest a unique therapeutic potential for preemptive treatment with anti-TNF antibody to prevent surgery-induced cognitive decline. innate immunity | surgical complications | delirium | dementia doi/ 10.1073/pnas.1014557107

Published
2010

77. The aorta can act as site of naïve CD4+ T cell priming

Author

MacRitchie, Neil, Grassia, Gianluca, Noonan, Jonathan, Cole, Jennifer E., Hughes, Catherine E., Schroeder, Juliane, Benson, Robert A., Cochain, Clement, Zernecke, Alma, Guzik, Tomasz J., Garside, Paul, Monaco, Claudia, and Maffia, Pasquale

Subjects
cardiovascular system
Abstract

Aims:\ud \ud Aortic adaptive immunity plays a role in atherosclerosis; however, the precise mechanisms leading to T-cell activation in the arterial wall remain poorly understood.\ud Methods and results:\ud \ud Here, we have identified naïve T cells in the aorta of wild-type and T-cell receptor transgenic mice and we demonstrate that naïve T cells can be primed directly in the vessel wall with both kinetics and frequency of T-cell activation found to be similar to splenic and lymphoid T cells. Aortic homing of naïve T cells is regulated at least in part by the P-selectin glycosylated ligand-1 receptor. In experimental atherosclerosis the aorta supports CD4+ T-cell activation selectively driving Th1 polarization. By contrast, secondary lymphoid organs display Treg expansion.\ud Conclusion:\ud \ud Our results demonstrate that the aorta can support T-cell priming and that naïve T cells traffic between the circulation and vessel wall. These data underpin the paradigm that local priming of T cells specific for plaque antigens contributes to atherosclerosis progression.

Published
2020

78. Meta-Analysis of Leukocyte Diversity in Atherosclerotic Mouse Aortas

Author

Zernecke, Alma, Winkels, Holger, Cochain, Clement, Williams, Jesse W., Wolf, Dennis, Soehnlein, Oliver, Robbins, Clint S., Monaco, Claudia, Park, Inhye, McNamara, Coleen A., Binder, Christoph J., Cybulsky, Myron I., Scipione, Corey A., Hedrick, Catherine C., Galkina, Elena V., Kyaw, Tin, Ghosheh, Yanal, Dinh, Huy Q., Ley, Klaus, Zernecke, Alma, Winkels, Holger, Cochain, Clement, Williams, Jesse W., Wolf, Dennis, Soehnlein, Oliver, Robbins, Clint S., Monaco, Claudia, Park, Inhye, McNamara, Coleen A., Binder, Christoph J., Cybulsky, Myron I., Scipione, Corey A., Hedrick, Catherine C., Galkina, Elena V., Kyaw, Tin, Ghosheh, Yanal, Dinh, Huy Q., and Ley, Klaus

Abstract

The diverse leukocyte infiltrate in atherosclerotic mouse aortas was recently analyzed in 9 single-cell RNA sequencing and 2 mass cytometry studies. In a comprehensive meta-analysis, we confirm 4 known macrophage subsets-resident, inflammatory, interferon-inducible cell, and Trem2 (triggering receptor expressed on myeloid cells-2) foamy macrophages-and identify a new macrophage subset resembling cavity macrophages. We also find that monocytes, neutrophils, dendritic cells, natural killer cells, innate lymphoid cells-2, and CD (cluster of differentiation)-8 T cells form prominent and separate immune cell populations in atherosclerotic aortas. Many CD4 T cells express IL (interleukin)-17 and the chemokine receptor CXCR (C-X-C chemokine receptor)-6. A small number of regulatory T cells and T helper 1 cells is also identified. Immature and naive T cells are present in both healthy and atherosclerotic aortas. Our meta-analysis overcomes limitations of individual studies that, because of their experimental approach, over- or underrepresent certain cell populations. Mass cytometry studies demonstrate that cell surface phenotype provides valuable information beyond the cell transcriptomes. The present analysis helps resolve some long-standing controversies in the field. First, Trem2(+)foamy macrophages are not proinflammatory but interferon-inducible cell and inflammatory macrophages are. Second, about half of all foam cells are smooth muscle cell-derived, retaining smooth muscle cell transcripts rather than transdifferentiating to macrophages. Third,Pf4, which had been considered specific for platelets and megakaryocytes, is also prominently expressed in the main population of resident vascular macrophages. Fourth, a new type of resident macrophage shares transcripts with cavity macrophages. Finally, the discovery of a prominent innate lymphoid cell-2 cluster links the single-cell RNA sequencing work to recent flow cytometry data suggesting a strong atheroprotective role o

Published
2020

81. Canonical pathway of nuclear factor [kappa]B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis

Author

Monaco, Claudia, Andreakos, Evangelos, Kiriakidis, Serafim, Maurit, Claudia, Bicknell, Colin, Foxwell, Brian, Cheshire, Nicholas, Paleolog, Ewa, and Feldmann, Marc

Subjects
Cells -- Research, Science and technology
Abstract

Nuclear factor KB (NF-[kappa]B) activation has been observed in human atherosclerotic plaques and is enhanced in unstable coronary plaques, but whether such activation has a protective or pathophysiological role remains to be determined. We addressed this question by developing a short-term culture system of cells isolated from human atherosclerotic tissue, allowing efficient gene transfer to directly investigate signaling pathways in human atherosclerosis. We found that NF-[kappa]B is activated in these cells and that this activity involves p65, p50, and c-Rel but not p52 or RelB. This NF-[kappa]B activation can be blocked by overexpression of I[kappa]B[alpha] or dominant-negative I[kappa]B kinase (IKK)-2 but not dominant-negative IKK-1 or NF-[kappa]B-inducing kinase, resulting in selective inhibition of inflammatory cytokines (tumor necrosis factor [alpha], IL-6, and IL-8) tissue factor, and matrix metalloproteinases without affecting the antiinflammatory cytokine IL-10 or tissue inhibitor of matrix me talloproteinases. Our results demonstrate that the canonical pathway of NF-[kappa]B activation that involves p65, p50, c-Rel, and IKK-2 is activated in human atherosclerosis and results in selective up regulation of major proinflammatory and prothrombotic mediators of the disease.

Published
2004

91. ROS-producing immature neutrophils in giant cell arteritis are linked to vascular pathologies

Author

Wang, Lihui, primary, Ai, Zhichao, additional, Khoyratty, Tariq, additional, Zec, Kristina, additional, Eames, Hayley L., additional, van Grinsven, Erinke, additional, Hudak, Alison, additional, Morris, Susan, additional, Ahern, David, additional, Monaco, Claudia, additional, Eruslanov, Evgeniy B., additional, Luqmani, Raashid, additional, and Udalova, Irina A., additional

Published
2020
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92. Glucocorticoid-induced tumour necrosis factor receptor family-related protein (GITR) drives atherosclerosis in mice and is associated with an unstable plaque phenotype and cerebrovascular events in humans

Author

Shami, Annelie, primary, Atzler, Dorothee, additional, Bosmans, Laura A, additional, Winkels, Holger, additional, Meiler, Svenja, additional, Lacy, Michael, additional, van Tiel, Claudia, additional, Ta Megens, Remco, additional, Nitz, Katrin, additional, Baardman, Jeroen, additional, Kusters, Pascal, additional, Seijkens, Tom, additional, Buerger, Christina, additional, Janjic, Aleksandar, additional, Riccardi, Carlo, additional, Edsfeldt, Andreas, additional, Monaco, Claudia, additional, Daemen, Mat, additional, de Winther, Menno P J, additional, Nilsson, Jan, additional, Weber, Christian, additional, Gerdes, Norbert, additional, Gonçalves, Isabel, additional, and Lutgens, Esther, additional

Published
2020
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93. Meta-Analysis of Leukocyte Diversity in Atherosclerotic Mouse Aortas

Author

Zernecke, Alma, primary, Winkels, Holger, additional, Cochain, Clément, additional, Williams, Jesse W., additional, Wolf, Dennis, additional, Soehnlein, Oliver, additional, Robbins, Clint S., additional, Monaco, Claudia, additional, Park, Inhye, additional, McNamara, Coleen A., additional, Binder, Christoph J., additional, Cybulsky, Myron I., additional, Scipione, Corey A., additional, Hedrick, Catherine C., additional, Galkina, Elena V., additional, Kyaw, Tin, additional, Ghosheh, Yanal, additional, Dinh, Huy Q., additional, and Ley, Klaus, additional

Published
2020
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95. Immune cell census in murine atherosclerosis: cytometry by time of flight illuminates vascular myeloid cell diversity

Author

Cole, Jennifer E., Park, Inhye, Ahern, David, Kassiteridi, Christina, Danso Abeam, Dina, Goddard, Michael, Green, Patricia, Maffia, Pasquale, Monaco, Claudia, Cole, Jennifer E., Park, Inhye, Ahern, David J., Kassiteridi, Christina, Abeam, Dina Danso, Goddard, Michael E., Green, Patricia, Maffia, Pasquale, and Monaco, Claudia

Subjects
Mice, Knockout, ApoE, Macrophage, Physiology, Aortic Diseases, Cell Separation, Antigen-Antibody Complex, Diet, High-Fat, Immunophenotyping, Mice, Vascular, Physiology (medical), Animals, Myeloid Cells, Aorta, Immunity and Inflammation, Immune cell, Spectrophotometry, Atomic, Macrophages, Immune cells, Censuses, Original Articles, Cytometry by time of flight, Flow Cytometry, Atherosclerosis, Plaque, Atherosclerotic, Disease Models, Animal, Editor's Choice, Phenotype, Atherosclerosi, Cardiology and Cardiovascular Medicine, Biomarkers
Abstract

Aims: \ud Atherosclerosis is characterised by the abundant infiltration of myeloid cells starting at early stages of disease. Myeloid cells are key players in vascular immunity during atherogenesis. However, the subsets of vascular myeloid cells have eluded resolution due to shared marker expression and atypical heterogeneity in vascular tissues. We applied the high-dimensionality of mass cytometry to the study of myeloid cell subsets in atherosclerosis.\ud \ud Methods and Results: \ud Apolipoprotein E-deficient (ApoE-/-) mice were fed a chow or a high fat (western) diet for 12 weeks. Single cell aortic preparations were probed with a panel of 35 metal-conjugated antibodies using Cytometry by time of flight (CyTOF). Clustering of marker expression on live CD45+ cells from the aortas of ApoE-/- mice identified 13 broad populations of leucocytes. Monocyte, macrophage, type 1 and type 2 conventional dendritic cell (cDC1 and cDC2), plasmacytoid dendritic cell (pDC), neutrophil, eosinophil, B cell, CD4+ and CD8+ T cell, γδ T cell, natural killer (NK) cell and innate lymphoid (ILC) cell populations accounted for approximately 95% of the live CD45+ aortic cells. Automated clustering algorithms applied to the Lin-CD11blo-hi cells revealed 20 clusters of myeloid cells. Comparison between chow and high fat fed animals revealed increases in monocytes (both Ly6C+ and Ly6C-), pDC and a CD11c+ macrophage subset with high fat feeding. Concomitantly, the proportions of CD206+ CD169+ subsets of macrophages were significantly reduced as were cDC2.\ud \ud Conclusions: \ud A CyTOF-based comprehensive mapping of the immune cell subsets within atherosclerotic aortas from ApoE-/- mice offers tools for myeloid cell discrimination within the vascular compartment and it reveals that high fat feeding skews the myeloid cell repertoire towards inflammatory monocyte-macrophage populations rather than resident macrophage phenotypes and cDC2 during atherogenesis.

Published
2018

98. Identifying the anti-inflammatory response to lipid lowering therapy: a position paper from the working group on atherosclerosis and vascular biology of the European Society of Cardiology

Author

Tuñón, José, Badimón, Lina, Bochaton-Piallat, Marie-Luce, Cariou, Bertrand, Daemen, Mat J, Egido, Jesus, Evans, Paul C, Hoefer, Imo E, Ketelhuth, Daniel F J, Lutgens, Esther, Matter, Christian M, Monaco, Claudia, Steffens, Sabine, Stroes, Erik, Vindis, Cécile, Weber, Christian, Bäck, Magnus, Tuñón, José, Badimón, Lina, Bochaton-Piallat, Marie-Luce, Cariou, Bertrand, Daemen, Mat J, Egido, Jesus, Evans, Paul C, Hoefer, Imo E, Ketelhuth, Daniel F J, Lutgens, Esther, Matter, Christian M, Monaco, Claudia, Steffens, Sabine, Stroes, Erik, Vindis, Cécile, Weber, Christian, and Bäck, Magnus

Abstract

Dysregulated lipid metabolism induces an inflammatory and immune response leading to atherosclerosis. Conversely, inflammation may alter lipid metabolism. Recent treatment strategies in secondary prevention of atherosclerosis support beneficial effects of both anti-inflammatory and lipid-lowering therapies beyond current targets. There is a controversy about the possibility that anti-inflammatory effects of lipid-lowering therapy may be either independent or not of a decrease in low-density lipoprotein cholesterol. In this Position Paper, we critically interpret and integrate the results obtained in both experimental and clinical studies on anti-inflammatory actions of lipid-lowering therapy and the mechanisms involved. We highlight that: (i) besides decreasing cholesterol through different mechanisms, most lipid-lowering therapies share anti-inflammatory and immunomodulatory properties, and the anti-inflammatory response to lipid-lowering may be relevant to predict the effect of treatment, (ii) using surrogates for both lipid metabolism and inflammation as biomarkers or vascular inflammation imaging in future studies may contribute to a better understanding of the relative importance of different mechanisms of action, and (iii) comparative studies of further lipid lowering, anti-inflammation and a combination of both are crucial to identify effects that are specific or shared for each treatment strategy.

Published
2019

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