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Updated: Sep 24, 2025
Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages
Published on: November 3, 2014
Gene expression profiling of RIP2-knockdown in HD11 macrophages - elucidation of potential pathways (gene network)
Hongyan Sun1,2, Yexin Yang3, Yuxuan Cao3
1College of Animal Science and Technology, Yangzhou University, Yangzhou, 225009, China. sunhy@yzu.edu.cn.
Background:
Receptor interacting serine/threonine kinase 2 (RIP2), ubiquitous in many tissue/cell types, is the key regulator of immune and inflammatory responses for many diseases, including avian pathogenic E. coli (APEC), which causes a wide variety of localized or systemic infections. However, the molecular mechanisms by which RIP2 drives its transcriptional program to affect immune and inflammatory response upon APEC infection remains poorly understood.
Results:
In this study, RNA-seq and bioinformatics analyses were used to detect gene expression and new direct/indirect RIP2 targets in the treatments of wild type HD11 cells (WT), RIP2 knockdown cells (shRIP2), APEC stimulation cells (APEC), and RIP2 knockdown cells combined with APEC infection (shRIP2 + APEC). The results revealed that a total of 4691 and 2605 differentially expressed genes (DEGs) were screened in shRIP2 + APEC vs. APEC and shRIP2 vs. WT, respectively. Functional annotation analysis showed that apoptosis, MAPK, p53, Toll-like receptor, and Nod-like receptor signaling pathways were involved in APEC-induced RIP2 knockdown HD11 cells. By analyzing the enriched pathway and gene networks, we identified that several DEGs, including HSP90AB1, BID, and CASP9 were targeted by RIP2 upon APEC infection.
Conclusion:
As a whole, this study can not only provide data support for constructing gene networks of RIP2 knockdown with APEC challenge but also provide new ideas for improving the immune and inflammatory response.
Insights
Receptor interacting serine/threonine kinase 2 (RIP2) regulates immune responses to avian pathogenic E. coli (APEC). This study identified RIP2 targets and pathways involved in APEC infection, offering insights into immune modulation.
Area of Science:
- Immunology
- Molecular Biology
- Genomics
Background:
- Receptor interacting serine/threonine kinase 2 (RIP2) is crucial for immune and inflammatory responses.
- Its role in avian pathogenic E. coli (APEC) infection mechanisms is not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms of RIP2 in regulating immune and inflammatory responses during APEC infection.
- To identify direct and indirect RIP2 targets and associated signaling pathways.
Main Methods:
- RNA sequencing (RNA-seq) and bioinformatics analyses were employed.
- Gene expression profiling was performed on wild type HD11 cells, RIP2 knockdown cells, APEC-infected cells, and combined treatments.
Main Results:
- A significant number of differentially expressed genes (DEGs) were identified between treatment groups.
- Key pathways including apoptosis, MAPK, p53, Toll-like receptor, and Nod-like receptor signaling were implicated.
- RIP2 was found to target DEGs such as HSP90AB1, BID, and CASP9 during APEC infection.
Conclusions:
- This study provides data for constructing gene networks related to RIP2 knockdown and APEC challenge.
- Findings offer novel strategies for enhancing immune and inflammatory responses.
