Dingjun Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Dingjun Wang has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Biying Zhong
School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China
1 shared publication - Huiying Zheng
School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China
1 shared publication - Jiehan Chen
School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China
1 shared publication - Li Liu
School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China
1 shared publication - Qiaowen Wang
School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China
1 shared publication - Tiantian Liu
School of public health, Guangdong Pharmaceutical University
1 shared publication
Latest Publications
- Open Access
- 10 April 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (8) , 4178
Activation of the RIG-I/MAVS Signaling Pathway during Human Adenovirus Type 3 Infection Impairs the Pro-Inflammatory Response Induced by Secondary Infection with Staphylococcus aureus
The exacerbation of pneumonia in children with human adenovirus type 3 (HAdV-3E) is secondary to a Staphylococcus aureus (S. aureus) infection. The influence of host–pathogen interactions on disease progression remains unclear. It is important to note that S. aureus infections following an HAdV-3E infection are frequently observed in clinical settings, yet the underlying susceptibility mechanisms are not fully understood. This study utilized an A549 cell model to investigate secondary infection with S. aureus following an HAdV-3E infection. The findings suggest that HAdV-3E exacerbates the S. aureus infection by intensifying lung epithelial cell damage. The results highlight the role of HAdV-3E in enhancing the interferon signaling pathway through RIG-I (DDX58), resulting in the increased expression of interferon-stimulating factors like MX1, RSAD2, and USP18. The increase in interferon-stimulating factors inhibits the NF-κB and MAPK/P38 pro-inflammatory signaling pathways. These findings reveal new mechanisms of action for HAdV-3E and S. aureus in secondary infections, enhancing our comprehension of pathogenesis.
- 10 April 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (8) , 4178
Open AccessActivation of the RIG-I/MAVS Signaling Pathway during Human Adenovirus Type 3 Infection Impairs the Pro-Inflammatory Response Induced by Secondary Infection with Staphylococcus aureus
The exacerbation of pneumonia in children with human adenovirus type 3 (HAdV-3E) is secondary to a Staphylococcus aureus (S. aureus) infection. The influence of host–pathogen interactions on disease progression remains unclear. It is important to note that S. aureus infections following an HAdV-3E infection are frequently observed in clinical settings, yet the underlying susceptibility mechanisms are not fully understood. This study utilized an A549 cell model to investigate secondary infection with S. aureus following an HAdV-3E infection. The findings suggest that HAdV-3E exacerbates the S. aureus infection by intensifying lung epithelial cell damage. The results highlight the role of HAdV-3E in enhancing the interferon signaling pathway through RIG-I (DDX58), resulting in the increased expression of interferon-stimulating factors like MX1, RSAD2, and USP18. The increase in interferon-stimulating factors inhibits the NF-κB and MAPK/P38 pro-inflammatory signaling pathways. These findings reveal new mechanisms of action for HAdV-3E and S. aureus in secondary infections, enhancing our comprehension of pathogenesis.