Qi Chen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Qi Chen has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Deshi Shi
College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
1 shared publication - Huiwen Zhu
State Key Laboratory of Agriculture Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
1 shared publication - Qiling Xiao
State Key Laboratory of Agriculture Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
1 shared publication - Qiongqiong Zhou
State Key Laboratory of Veterinary Public Health and Safety, China Agricultural University
1 shared publication - Xiliang Wang
State Key Laboratory of Agriculture Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
1 shared publication - Yuelin Fu
State Key Laboratory of Agriculture Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
1 shared publication
Latest Publications
- Open Access
Pig Liver Esterase Hydrolysis of 2-Arachidonoglycerol Exacerbates PRRSV-Induced Inflammation via PI3K-Akt-NF-κB Pathway
Inflammation is essential for host defense but requires strict regulation to prevent immunopathology. This study reveals how pig liver esterase (PLE) in alveolar macrophages (PAMs) modulates PRRSV-induced inflammation through endocannabinoid metabolism. We identified PLE6 as the dominant hydrolytically active subtype in PAMs. Functional studies demonstrated that PLE promotes pro-inflammatory cytokine expression during PRRSV infection, while its substrate 2-arachidonoylglycerol (2-AG) exerts anti-inflammatory effects. Animal experiments confirmed that PLE inhibition reduces pulmonary inflammation and tissue damage in PRRSV-infected piglets. Transcriptomic and mechanistic analyses revealed that PLE hydrolyzes 2-AG to activate the PI3K-Akt-NF-κB pathway, particularly through enhanced phosphorylation of Akt and p65. These findings establish a novel pathological mechanism where PLE-mediated 2-AG degradation disrupts endocannabinoid homeostasis, amplifying PRRSV-induced inflammation. The study provides therapeutic insights for targeting endocannabinoid hydrolysis to control inflammatory diseases.
Open AccessPig Liver Esterase Hydrolysis of 2-Arachidonoglycerol Exacerbates PRRSV-Induced Inflammation via PI3K-Akt-NF-κB Pathway
Inflammation is essential for host defense but requires strict regulation to prevent immunopathology. This study reveals how pig liver esterase (PLE) in alveolar macrophages (PAMs) modulates PRRSV-induced inflammation through endocannabinoid metabolism. We identified PLE6 as the dominant hydrolytically active subtype in PAMs. Functional studies demonstrated that PLE promotes pro-inflammatory cytokine expression during PRRSV infection, while its substrate 2-arachidonoylglycerol (2-AG) exerts anti-inflammatory effects. Animal experiments confirmed that PLE inhibition reduces pulmonary inflammation and tissue damage in PRRSV-infected piglets. Transcriptomic and mechanistic analyses revealed that PLE hydrolyzes 2-AG to activate the PI3K-Akt-NF-κB pathway, particularly through enhanced phosphorylation of Akt and p65. These findings establish a novel pathological mechanism where PLE-mediated 2-AG degradation disrupts endocannabinoid homeostasis, amplifying PRRSV-induced inflammation. The study provides therapeutic insights for targeting endocannabinoid hydrolysis to control inflammatory diseases.