2025 CALA Friday seminar series
Ke Yuan
CALA Happy Friday Seminar
January 10th, 2025
Time: EST 9:00 pm; PST: 6:00 pm; Beijing time: January 11th, 10:00 am
Zoom: 849 9682 9273 (Password: 654321)
Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae
Xiaoqing Wei, PhD
Research Scientist, University of Virginia
Bio: Dr. Xiaoqin Wei earned her PhD from Wuhan University, where she focused on understanding the cellular mechanisms of Kaposi’s sarcoma-associated herpesvirus (KSHV) pathogenesis. In 2021, she began her postdoctoral training with Dr. Jie Sun at the Carter Immunology Center, University of Virginia. Her research focuses on respiratory innate immunity in the context of viral infections, particularly SARS-CoV-2 and influenza. Dr. Wei is particularly interested in macrophage biology and macrophage immunometabolism, investigating how these processes contribute to acute disease during respiratory virus infection and the chronic sequelae of viral infections. Her recent studies have identified critical pathways, such as the role of the mitochondrial pyruvate carrier and peroxisome dysfunction in lung macrophages, in mitigating hyperinflammation and promoting tissue regeneration. Through these insights, she hopes to contribute to a deeper understanding of and novel approaches for treating severe respiratory infections and their chronic sequelae.
Abstract: Peroxisomes are vital but often overlooked metabolic organelles. Here we found that excessive interferon signaling remodelled macrophage peroxisomes. This loss of peroxisomes impaired inflammation resolution and lung repair during severe respiratory viral infections. Peroxisomes were found to modulate lipid metabolism and mitochondrial health in a macrophage type-specific manner and enhanced alveolar macrophage-mediated tissue repair and alveolar regeneration after viral infection. Peroxisomes also prevented excessive macrophage inflammasome activation and IL-1β release, limiting accumulation of KRT8high dysplastic epithelial progenitors post viral injury. Pharmacologically enhancing peroxisome biogenesis mitigated both acute symptoms and post-acute sequelae of COVID-19 (PASC) in animal models. Thus, macrophage peroxisome dysfunction contributes to chronic lung pathology and fibrosis after SARS-CoV-2 infection.
Ke Yuan
CALA Happy Friday Seminar
January 10th, 2025
Time: EST 9:00 pm; PST: 6:00 pm; Beijing time: January 11th, 10:00 am
Zoom: 849 9682 9273 (Password: 654321)
Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae
Xiaoqin Wei, PhD
Research Scientist, University of Virginia
Bio: Dr. Xiaoqin Wei earned her PhD from Wuhan University, where she focused on understanding the cellular mechanisms of Kaposi’s sarcoma-associated herpesvirus (KSHV) pathogenesis. In 2021, she began her postdoctoral training with Dr. Jie Sun at the Carter Immunology Center, University of Virginia. Her research focuses on respiratory innate immunity in the context of viral infections, particularly SARS-CoV-2 and influenza. Dr. Wei is particularly interested in macrophage biology and macrophage immunometabolism, investigating how these processes contribute to acute disease during respiratory virus infection and the chronic sequelae of viral infections. Her recent studies have identified critical pathways, such as the role of the mitochondrial pyruvate carrier and peroxisome dysfunction in lung macrophages, in mitigating hyperinflammation and promoting tissue regeneration. Through these insights, she hopes to contribute to a deeper understanding of and novel approaches for treating severe respiratory infections and their chronic sequelae.
Abstract: Peroxisomes are vital but often overlooked metabolic organelles. Here we found that excessive interferon signaling remodelled macrophage peroxisomes. This loss of peroxisomes impaired inflammation resolution and lung repair during severe respiratory viral infections. Peroxisomes were found to modulate lipid metabolism and mitochondrial health in a macrophage type-specific manner and enhanced alveolar macrophage-mediated tissue repair and alveolar regeneration after viral infection. Peroxisomes also prevented excessive macrophage inflammasome activation and IL-1β release, limiting accumulation of KRT8high dysplastic epithelial progenitors post viral injury. Pharmacologically enhancing peroxisome biogenesis mitigated both acute symptoms and post-acute sequelae of COVID-19 (PASC) in animal models. Thus, macrophage peroxisome dysfunction contributes to chronic lung pathology and fibrosis after SARS-CoV-2 infection.
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
April 4th
, 2025
Time: EST 9:00 pm; PST: 6:00 pm; Beijing time: April 5th
, 10:00 am
Zoom: 849 9682 9273 (Password: 654321)
Vascular Niche in Lung Injury, Repair, and Regeneration
Bisheng Zhou, PhD
Assistant Professor, Department of Pharmacology and Regenerative Medicine,
College of Medicine, University of Illinois at Chicago
Bio:
Dr. Bisheng Zhou is an Assistant Professor in the Department of Pharmacology and Regenerative
Medicine at the University of Illinois at Chicago (UIC). He earned his PhD in Biochemistry and
Molecular Biology from Huazhong University of Science and Technology in China and completed
postdoctoral training in vascular biology and immunology at Northwestern University and UIC. Before
establishing his independent laboratory, he served as a Research Assistant Professor at UIC.
Dr. Zhou’s research focuses on the complex interactions between the vasculature and immune system
in the lungs, particularly their roles in lung injury, repair, and regeneration. His work has been published
in leading peer-reviewed journals, including Nature Immunology and Arteriosclerosis, Thrombosis, and
Vascular Biology (ATVB). Recently, he secured two NIH R01 grants as the sole Principal Investigator
to support his research.
In this seminar, Dr. Zhou will present his lab’s latest findings on the vascular niche’s role in lung injury,
repair, and regeneration
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
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