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11 results on '"Guan Ng, Lai"'

2. Notch-dependent cooperativity between myeloid lineages promotes Langerhans cell histiocytosis pathology

Author

Kvedaraite, Egle, primary, Milne, Paul, additional, Khalilnezhad, Ahad, additional, Chevrier, Marion, additional, Sethi, Raman, additional, Lee, Hong Kai, additional, Hagey, Daniel W., additional, von Bahr Greenwood, Tatiana, additional, Mouratidou, Natalia, additional, Jädersten, Martin, additional, Lee, Nicole Yee Shin, additional, Minnerup, Lara, additional, Tan, Yingrou, additional, Dutertre, Charles-Antoine, additional, Benac, Nathan, additional, Hwang, You Yi, additional, Lum, Josephine, additional, Loh, Amos Hong Pheng, additional, Jansson, Jessica, additional, Teng, Karen Wei Weng, additional, Khalilnezhad, Shabnam, additional, Xu, Weili, additional, Resteu, Anastasia, additional, Tey, Hong Liang, additional, Guan, Ng Lai, additional, Larbi, Anis, additional, Howland, Shanshan Wu, additional, Arnell, Henrik, additional, Andaloussi, Samir E. L., additional, Braier, Jorge, additional, Rassidakis, Georgios, additional, Galluzzo, Laura, additional, Dzionek, Andrzej, additional, Henter, Jan-Inge, additional, Chen, Jinmiao, additional, Collin, Matthew, additional, and Ginhoux, Florent, additional

Published
2022
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3. High-fat diet induces a predisposition to follicular hyperkeratosis and neutrophilic folliculitis in mice

Author

Nakamizo, Satoshi, primary, Honda, Tetsuya, additional, Sato, Tomohito, additional, Al Mamun, Md., additional, Chow, Zachary, additional, Duan, Kaibo, additional, Lum, Josephine, additional, Tan, Kahbing Jasmine, additional, Tomari, Kaori, additional, Sato, Reiko, additional, Kitoh, Akihiko, additional, Tay, Angeline S.L., additional, Common, John E.A., additional, Guan, Ng Lai, additional, Setou, Mitsutoshi, additional, Ginhoux, Florent, additional, and Kabashima, Kenji, additional

Published
2021
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4. A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart

Author

Ministerio de Economía y Competitividad (España), European Research Council, European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Fondation Leducq, Comunidad de Madrid, La Caixa, Fundació La Marató de TV3, Fundación la Caixa, Howard Hughes Medical Institute, Centro Nacional de Investigaciones Cardiovasculares (España), Nicolás-Ávila, José A., Lechuga, Ana, Sanchez-Díaz, María, Díaz-García, Elena, Santiago, Demetrio J., Rubio-Ponce, Andrea, LiangYao Li, Jackson, Balachander, Akhila, Quintana, Juan A., Martínez de Mena, Raquel, Castejón-Vega, Beatriz, Pun-García, Andrés, Través, Paqui G., Bonzón-Kulichenko, Elena, García-Marqués, Fernando, Cussó, Lorena, González, Noelia A., González-Guerra, Andrés, Roche-Molina, Marta, Martin-Salamanca, Sandra, Crainiciuc, Georgiana, Guzmán, Gabriela, Larrazabal, Jagoba, Herrero-Galán, Elías, Alegre-Cebollada, Jorge, Lemke, Greg, Rothlin, Carla V., Jiménez-Borreguero, Luis J., Reyes, Guillermo, Castrillo, Antonio, Desco, Manuel, Muñoz-Cánoves, Pura, Ibáñez, Borja, Torres, Miguel, Guan Ng, Lai, Priori, Silvia G., Bueno, Héctor, Vázquez, Jesús, Cordero, Mario D., Bernal, Juan, Enríquez, José Antonio, Hidalgo, Andrés, Ministerio de Economía y Competitividad (España), European Research Council, European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Fondation Leducq, Comunidad de Madrid, La Caixa, Fundació La Marató de TV3, Fundación la Caixa, Howard Hughes Medical Institute, Centro Nacional de Investigaciones Cardiovasculares (España), Nicolás-Ávila, José A., Lechuga, Ana, Sanchez-Díaz, María, Díaz-García, Elena, Santiago, Demetrio J., Rubio-Ponce, Andrea, LiangYao Li, Jackson, Balachander, Akhila, Quintana, Juan A., Martínez de Mena, Raquel, Castejón-Vega, Beatriz, Pun-García, Andrés, Través, Paqui G., Bonzón-Kulichenko, Elena, García-Marqués, Fernando, Cussó, Lorena, González, Noelia A., González-Guerra, Andrés, Roche-Molina, Marta, Martin-Salamanca, Sandra, Crainiciuc, Georgiana, Guzmán, Gabriela, Larrazabal, Jagoba, Herrero-Galán, Elías, Alegre-Cebollada, Jorge, Lemke, Greg, Rothlin, Carla V., Jiménez-Borreguero, Luis J., Reyes, Guillermo, Castrillo, Antonio, Desco, Manuel, Muñoz-Cánoves, Pura, Ibáñez, Borja, Torres, Miguel, Guan Ng, Lai, Priori, Silvia G., Bueno, Héctor, Vázquez, Jesús, Cordero, Mario D., Bernal, Juan, Enríquez, José Antonio, and Hidalgo, Andrés

Abstract

Cardiomyocytes are subjected to the intense mechanical stress and metabolic demands of the beating heart. It is unclear whether these cells, which are long-lived and rarely renew, manage to preserve homeostasis on their own. While analyzing macrophages lodged within the healthy myocardium, we discovered that they actively took up material, including mitochondria, derived from cardiomyocytes. Cardiomyocytes ejected dysfunctional mitochondria and other cargo in dedicated membranous particles reminiscent of neural exophers, through a process driven by the cardiomyocyte's autophagy machinery that was enhanced during cardiac stress. Depletion of cardiac macrophages or deficiency in the phagocytic receptor Mertk resulted in defective elimination of mitochondria from the myocardial tissue, activation of the inflammasome, impaired autophagy, accumulation of anomalous mitochondria in cardiomyocytes, metabolic alterations, and ventricular dysfunction. Thus, we identify an immune-parenchymal pair in the murine heart that enables transfer of unfit material to preserve metabolic stability and organ function. Video Abstract: [Figure presented] A system of macrophages in the heart supports cardiomyocyte health by phagocytosing exopher particles ejected from cardiomyocytes that contain defective mitochondria, among other cellular contents.

Published
2020

6. A Neutrophil Timer Coordinates Immune Defense and Vascular Protection

Author

Ministerio de Economía, Industria y Competitividad (España), Ministerio de Economía y Competitividad (España), European Commission, European Research Council, German Research Foundation, German Centre for Cardiovascular Research, Adrover, José M., Fresno, Carlos del, Crainiciuc, Georgiana, Cuartero, María Isabel, Casanova-Acebes, María, Weiss, L.A., Huerga Encabo, Héctor, Silvestre-Roig, C., Rossaint, Jan, Cossío, Itziar, Lechuga-Vieco, Ana V., García-Prieto, Jaime, Gómez-Parrizas, Mónica, Quintana, Juan A., Ballesteros, Iván, Martin-Salamanca, Sandra, Aroca-Crevillen, Alejandra, Zhen Chong, Shu, Evrard, Maximilien, Balabanian, Karl, López, Jorge, Bidzhekov, Kiril, Bachelerie, Françoise, Abad-Santos, Francisco, Muñoz-Calleja, Cecilia, Zarbock, Alexander, Soehnlein, Oliver, Weber, C., Guan Ng, Lai, López-Rodríguez, Cristina, Sancho, David, Moro, María A., Ibáñez, Borja, Hidalgo, Andrés, Ministerio de Economía, Industria y Competitividad (España), Ministerio de Economía y Competitividad (España), European Commission, European Research Council, German Research Foundation, German Centre for Cardiovascular Research, Adrover, José M., Fresno, Carlos del, Crainiciuc, Georgiana, Cuartero, María Isabel, Casanova-Acebes, María, Weiss, L.A., Huerga Encabo, Héctor, Silvestre-Roig, C., Rossaint, Jan, Cossío, Itziar, Lechuga-Vieco, Ana V., García-Prieto, Jaime, Gómez-Parrizas, Mónica, Quintana, Juan A., Ballesteros, Iván, Martin-Salamanca, Sandra, Aroca-Crevillen, Alejandra, Zhen Chong, Shu, Evrard, Maximilien, Balabanian, Karl, López, Jorge, Bidzhekov, Kiril, Bachelerie, Françoise, Abad-Santos, Francisco, Muñoz-Calleja, Cecilia, Zarbock, Alexander, Soehnlein, Oliver, Weber, C., Guan Ng, Lai, López-Rodríguez, Cristina, Sancho, David, Moro, María A., Ibáñez, Borja, and Hidalgo, Andrés

Abstract

Neutrophils eliminate pathogens efficiently but can inflict severe damage to the host if they over-activate within blood vessels. It is unclear how immunity solves the dilemma of mounting an efficient anti-microbial defense while preserving vascular health. Here, we identify a neutrophil-intrinsic program that enabled both. The gene Bmal1 regulated expression of the chemokine CXCL2 to induce chemokine receptor CXCR2-dependent diurnal changes in the transcriptional and migratory properties of circulating neutrophils. These diurnal alterations, referred to as neutrophil aging, were antagonized by CXCR4 (C-X-C chemokine receptor type 4) and regulated the outer topology of neutrophils to favor homeostatic egress from blood vessels at night, resulting in boosted anti-microbial activity in tissues. Mice engineered for constitutive neutrophil aging became resistant to infection, but the persistence of intravascular aged neutrophils predisposed them to thrombo-inflammation and death. Thus, diurnal compartmentalization of neutrophils, driven by an internal timer, coordinates immune defense and vascular protection. Neutrophils display circadian oscillations in numbers and phenotype in the circulation. Adrover and colleagues now identify the molecular regulators of neutrophil aging and show that genetic disruption of this process has major consequences in immune cell trafficking, anti-microbial defense, and vascular health.

Published
2019

7. The gut microbiota influences blood-brain barrier permeability in mice

Author

Braniste, Viorica, Al-Asmakh, Maha, Kowal, Czeslawa, Anuar, Farhana, Abbaspour, Afrouz, Toth, Miklos, Korecka, Agata, Bakocevic, Nadja, Guan, Ng Lai, Kundu, Parag, Gulyas, Balazs, Halldin, Christer, Hultenby, Kjell, Nilsson, Harriet, Hebert, Hans, Volpe, Bruce T., Diamond, Betty, Pettersson, Sven, Braniste, Viorica, Al-Asmakh, Maha, Kowal, Czeslawa, Anuar, Farhana, Abbaspour, Afrouz, Toth, Miklos, Korecka, Agata, Bakocevic, Nadja, Guan, Ng Lai, Kundu, Parag, Gulyas, Balazs, Halldin, Christer, Hultenby, Kjell, Nilsson, Harriet, Hebert, Hans, Volpe, Bruce T., Diamond, Betty, and Pettersson, Sven

Abstract

Pivotal to brain development and function is an intact blood-brain barrier (BBB), which acts as a gatekeeper to control the passage and exchange of molecules and nutrients between the circulatory system and the brain parenchyma. The BBB also ensures homeostasis of the central nervous system (CNS). We report that germ-free mice, beginning with intrauterine life, displayed increased BBB permeability compared to pathogen-free mice with a normal gut flora. The increased BBB permeability was maintained in germ-free mice after birth and during adulthood and was associated with reduced expression of the tight junction proteins occludin and claudin-5, which are known to regulate barrier function in endothelial tissues. Exposure of germ-free adult mice to a pathogen-free gut microbiota decreased BBB permeability and up-regulated the expression of tight junction proteins. Our results suggest that gut microbiota-BBB communication is initiated during gestation and propagated throughout life., QC 20150127. Correction in: Science Translational Medicine, vol. 6, issue 266, page 266er7. Doi: 10.1126/scitranslmed.aaa4288, ScopusID: 2-s2.0-84916939455

Published
2014
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8. ISDN2012_0182: The indigenous gut microbiota modulates the blood–brain barrier in mice

Author

Anuar, Farhana, primary, Al‐Asmakh, Maha, additional, Miklos, Toth, additional, Kwak, Young‐Keun, additional, Möllby, Roland, additional, Bakocevic, Nadja, additional, Guan, Ng Lai, additional, Hibberd, Martin L., additional, Gulyas, Balazs, additional, Halldin, Christer, additional, Volpe, Bruce T., additional, Diamond, Betty, additional, and Pettersson, Sven, additional

Published
2012
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9. Lung endothelial cell antigen cross-presentation to CD8+T cells drives malaria-associated lung injury.

Author

Claser, Carla, Nguee, Samantha Yee Teng, Balachander, Akhila, Wu Howland, Shanshan, Becht, Etienne, Gunasegaran, Bavani, Hartimath, Siddesh V., Lee, Audrey W. Q., Theng Theng Ho, Jacqueline, Bing Ong, Chee, Newell, Evan W., Goggi, Julian, Guan Ng, Lai, and Renia, Laurent

Subjects
ENDOTHELIAL cells, ERYTHROCYTES, PARASITE antigens, ADULT respiratory distress syndrome, LUNG injuries, LUNGS
Abstract

Malaria-associated acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are life-threatening manifestations of severe malaria infections. The pathogenic mechanisms that lead to respiratory complications, such as vascular leakage, remain unclear. Here, we confirm that depleting CD8+T cells with anti-CD8β antibodies in C57BL/6 mice infected with P. berghei ANKA (PbA) prevent pulmonary vascular leakage. When we transfer activated parasite-specific CD8+T cells into PbA-infected TCRβ−/− mice (devoid of all T-cell populations), pulmonary vascular leakage recapitulates. Additionally, we demonstrate that PbA-infected erythrocyte accumulation leads to lung endothelial cell cross-presentation of parasite antigen to CD8+T cells in an IFNγ−dependent manner. In conclusion, pulmonary vascular damage in ALI is a consequence of IFNγ-activated lung endothelial cells capturing, processing, and cross-presenting malaria parasite antigen to specific CD8+T cells induced during infection. The mechanistic understanding of the immunopathogenesis in malaria-associated ARDS and ALI provide the basis for development of adjunct treatments. Severe malaria can be associated with respiratory complications. Here, the authors show that malaria-associated pulmonary vascular damage is a consequence of IFNγ-activated lung endothelial cells capturing, processing, and cross-presenting malaria parasite antigen to specific CD8+ T cells induced during infection. [ABSTRACT FROM AUTHOR]

Published
2019
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11. The gut microbiota influences blood-brain barrier permeability in mice.

Author

Braniste V, Al-Asmakh M, Kowal C, Anuar F, Abbaspour A, Tóth M, Korecka A, Bakocevic N, Ng LG, Kundu P, Gulyás B, Halldin C, Hultenby K, Nilsson H, Hebert H, Volpe BT, Diamond B, and Pettersson S

Subjects
Animals, Female, Mice, Permeability, Pregnancy, Tight Junctions metabolism, Blood-Brain Barrier, Intestines microbiology, Microbiota
Abstract

Pivotal to brain development and function is an intact blood-brain barrier (BBB), which acts as a gatekeeper to control the passage and exchange of molecules and nutrients between the circulatory system and the brain parenchyma. The BBB also ensures homeostasis of the central nervous system (CNS). We report that germ-free mice, beginning with intrauterine life, displayed increased BBB permeability compared to pathogen-free mice with a normal gut flora. The increased BBB permeability was maintained in germ-free mice after birth and during adulthood and was associated with reduced expression of the tight junction proteins occludin and claudin-5, which are known to regulate barrier function in endothelial tissues. Exposure of germ-free adult mice to a pathogen-free gut microbiota decreased BBB permeability and up-regulated the expression of tight junction proteins. Our results suggest that gut microbiota-BBB communication is initiated during gestation and propagated throughout life., (Copyright © 2014, American Association for the Advancement of Science.)

Published
2014
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