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19 results on '"Nguyen, Quang Tam"'

1. Stricturing Crohn’s Disease Single-Cell RNA Sequencing Reveals Fibroblast Heterogeneity and Intercellular Interactions

Author

Mukherjee, Pranab K., Nguyen, Quang Tam, Li, Jiannan, Zhao, Shuai, Christensen, Stephen M., West, Gail A., Chandra, Jyotsna, Gordon, Ilyssa O., Lin, Sinan, Wang, Jie, Mao, Ren, Czarnecki, Douglas, Rayan, Carla, Goren, Idan, Banerjee, Suhanti, Kotak, Prerna, Plesec, Thomas, Lal, Samir, Fabre, Thomas, Asano, Shoh, Bound, Kathryn, Hart, Kevin, Park, Chanyoung, Martinez, Robert, Dower, Ken, Wynn, Thomas A., Hu, Shaomin, Naydenov, Nayden, Decaris, Martin, Turner, Scott, Holubar, Stefan D., Steele, Scott R., Fiocchi, Claudio, Ivanov, Andrei I., Kravarik, Kellie M., and Rieder, Florian

Published
2023
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2. Development of highly potent glucocorticoids for steroid-resistant severe asthma

Author

He, Yuanzheng, Shi, Jingjing, Nguyen, Quang Tam, You, Erli, Liu, Hongbo, Ren, Xin, Wu, Zhongshan, Li, Jianshuang, Qiu, Wenli, Khoo, Sok Kean, Yang, Tao, Yi, Wei, Sun, Feng, Xi, Zhijian, Huang, Xiaozhu, Melcher, Karsten, Min, Booki, and Xu, H Eric

Subjects
Lung, Asthma, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Respiratory, Animals, Anti-Asthmatic Agents, Disease Models, Animal, Drug Development, Female, Glucocorticoids, Male, Mice, Receptors, Glucocorticoid, Severity of Illness Index, steroid resistant asthma, glucocorticoid, high potency, VSG158, VSG159, steroid-resistant asthma
Abstract

Clinical application of inhaled glucocorticoids (GCs) has been hampered in the case of steroid-resistant severe asthma. To overcome this limitation, we have developed a series of highly potent GCs, including VSGC12, VSG158, and VSG159 based on the structural insight into the glucocorticoid receptor (GR). Particularly, VSG158 exhibits a maximal repression of lung inflammation and is 10 times more potent than the currently most potent clinical GC, Fluticasone Furoate (FF), in a murine model of asthma. More importantly, VSG158 displays a unique property to reduce neutrophilic inflammation in a steroid-resistant airway inflammation model, which is refractory to clinically available GCs, including dexamethasone and FF. VSG158 and VSG159 are able to deliver effective treatments with reduced off-target and side effects. In addition, these GCs also display pharmacokinetic properties that are suitable for the inhalation delivery method for asthma treatment. Taken together, the excellent therapeutic and side-effect profile of these highly potent GCs holds promise for treating steroid-resistant severe asthma.

Published
2019

8. Tu1246 CROHN'S DISEASE STRICTURE MATRISOME ANALYSIS REVEALS THE ANTI-FIBROTIC ACTIVITY OF MILK-FAT GLOBULE-EPIDERMAL GROWTH FACTOR 8 (MFGE8)

Author

Lin, Sinan, Wang, Jie, Mukherjee, Pranab, Mao, Ren, West, Gail A., Czarnecki, Doug, Zhao, Shuai, Nguyen, Quang Tam, Chandra, Jyotsna, Le, Thi Hong Nga, Dejanovic, Dina, Chen, Minhu, Holubar, Stefan D., Olman, Mitch, Southern, Brian D., Hu, Shaomin, Gordon, Ilyssa O., Atabai, Kamran, Fiocchi, Claudio, and Rieder, Florian

Published
2023
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9. Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3+ Regulatory T Cells via a miR-342-Dependent Mechanism

Author

Kim, Dongkyun, primary, Nguyen, Quang Tam, additional, Lee, Juyeun, additional, Lee, Sung Hwan, additional, Janocha, Allison, additional, Kim, Sohee, additional, Le, Hongnga T., additional, Dvorina, Nina, additional, Weiss, Kelly, additional, Cameron, Mark J., additional, Asosingh, Kewal, additional, Erzurum, Serpil C., additional, Baldwin, William M., additional, Lee, Ju-Seog, additional, and Min, Booki, additional

Published
2020
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16. Stimulation of the Molecule 4-1BB Enhances Host Defense against Listeria monocytogenes Infection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes

Author

Lee, Sang-Chul, primary, Ju, Seong-A, additional, Sung, Boo-Hee, additional, Heo, Sook-Kyoung, additional, Cho, Hong Rae, additional, Lee, Eun A., additional, Kim, Jung Dae, additional, Lee, In Hee, additional, Park, Sang-Min, additional, Nguyen, Quang Tam, additional, Suh, Jae-Hee, additional, and Kim, Byung-Sam, additional

Published
2009
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17. Stimulation of the Molecule 4-1BB Enhances Host Defense against Listeria monocytogenesInfection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes

Author

Lee, Sang-Chul, Ju, Seong-A, Sung, Boo-Hee, Heo, Sook-Kyoung, Cho, Hong Rae, Lee, Eun A., Kim, Jung Dae, Lee, In Hee, Park, Sang-Min, Nguyen, Quang Tam, Suh, Jae-Hee, and Kim, Byung-Sam

Abstract

ABSTRACTThe tumor necrosis factor receptor family molecule 4-1BB (CD137) has diverse roles in adaptive and innate immune responses. However, little is known of its role in bacterial infections. Previously, we showed that 4-1BB-deficient mice have enhanced susceptibility to Listeria monocytogenesinfection, and mice pretreated with agonistic anti-4-1BB antibody (3E1) were much more resistant to L. monocytogenesinfection than mice treated with control antibody. In this study, we report that stimulating 4-1BB by administering 3E1 in the early phase of L. monocytogenesinfection is critical for promoting the survival of mice by inducing rapid infiltration of neutrophils and monocytes into L. monocytogenes-infected livers. The levels of tumor necrosis factor alpha, interleukin 6, and monocyte chemoattractant protein 1 in the livers of 3E1-treated mice increased as early as 30 min postinfection and peaked by 1 to 2 h, while those in mice treated with control antibody started to increase only at 16 h postinfection. Monocytes and neutrophils from the 3E1-treated mice had higher levels of activation markers, phagocytic activity, and reactive oxygen species than those from control mice. In vitro stimulation of 4-1BB induced the production of the inflammatory cytokines/chemokines of neutrophils, but not those of monocytes. These results suggest that 4-1BB stimulation of neutrophils in the early phase of L. monocytogenesinfection causes rapid production of inflammatory cytokines/chemokines and that the subsequent infiltration of neutrophils and monocytes is crucial for eliminating the infecting L. monocytogenes.

Published
2009
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19. Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3 + Regulatory T Cells via a miR-342-Dependent Mechanism.

Author

Kim D, Nguyen QT, Lee J, Lee SH, Janocha A, Kim S, Le HT, Dvorina N, Weiss K, Cameron MJ, Asosingh K, Erzurum SC, Baldwin WM 3rd, Lee JS, and Min B

Subjects
Animals, Anti-Inflammatory Agents pharmacology, Forkhead Transcription Factors metabolism, Mechanistic Target of Rapamycin Complex 2 metabolism, Mice, Mice, Inbred C57BL, MicroRNAs biosynthesis, Receptors, Glucocorticoid genetics, T-Lymphocytes, Regulatory metabolism, Dexamethasone pharmacology, Glucocorticoids pharmacology, Inflammation drug therapy, MicroRNAs genetics, Rapamycin-Insensitive Companion of mTOR Protein metabolism, T-Lymphocytes, Regulatory immunology
Abstract

Glucocorticoids (GC) are the mainstay treatment option for inflammatory conditions. Despite the broad usage of GC, the mechanisms by which GC exerts its effects remain elusive. Here, utilizing murine autoimmune and allergic inflammation models, we report that Foxp3 + regulatory T (Treg) cells are irreplaceable GC target cells in vivo. Dexamethasone (Dex) administered in the absence of Treg cells completely lost its ability to control inflammation, and the lack of glucocorticoid receptor in Treg cells alone resulted in the loss of therapeutic ability of Dex. Mechanistically, Dex induced miR-342-3p specifically in Treg cells and miR-342-3p directly targeted the mTORC2 component, Rictor. Altering miRNA-342-3p or Rictor expression in Treg cells dysregulated metabolic programming in Treg cells, controlling their regulatory functions in vivo. Our results uncover a previously unknown contribution of Treg cells during glucocorticoid-mediated treatment of inflammation and the underlying mechanisms operated via the Dex-miR-342-Rictor axis., Competing Interests: Declaration of Interests Authors declare that they have no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Published
2020
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