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Updated: Jun 20, 2026
An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Comparative transcriptome analysis of PBMCs in cats diagnosed with and recovered from FIPV
Ju Young Lee1, Hyeong Ryeol Cho1, Hong-Geun Oh2,3
1Center for Large Animals Convergence Research, Korea Institue of Toxicology, 30 Baekhak1- gil, Jeongeup, Jellabuk-do, 56212, Republic of Korea.
Background:
Feline infectious peritonitis is a viral disease caused by feline coronavirus an enveloped virus with a single-stranded RNA genome that is approximately 30 kb long. Although FCoV generally causes mild symptoms, approximately 5% of cases progress to death in cats worldwide. FCoV shares certain virological features with severe acute respiratory syndrome coronavirus 2 that causes COVID-19, indicating that common therapeutic strategies may be applicable. GS-441524 the parent drug of remdesivir and a competitive inhibitor of nucleoside triphosphates in viral RNA synthesis is a well-known treatment for FIP. However, comparative transcriptome and gene ontology analyses of normal (Normal), FIP-diseased (FIPD), and FIP-recovered (FIPR) cats have not yet been conducted.
Results:
In this study, we compared the mRNA expression profiles of peripheral blood mononuclear cells from Normal, FIPD, and FIPR cats to identify immunological alterations. We identified 677 (FIPD/Normal) and 431 (FIPR/FIPD) differentially expressed genes with statistical significance. These data were input into the bioinformatics program. As a result, the analysis revealed statistically significant and contrasting patterns of canonical pathways of neutrophil degranulation and interleukin-8 (IL-8) signaling pathways. Additionally, we observed that kruppel-like factor 6 (KLF6) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were upstream molecules of IL-8, promoting neutrophil activation and function.
Conclusions:
This study identified immunological alterations in PBMCs of Normal, FIPD, and FIPR cats. KLF-6 and NF-κB were found to regulate IL-8-mediated neutrophil activation.
Insights
This study reveals key immunological changes in cats with feline infectious peritonitis (FIP). It identifies Kruppel-like factor 6 (KLF6) and NF-κB as regulators of IL-8, crucial for neutrophil activation in FIP.
Area of Science:
- Veterinary Immunology
- Molecular Virology
- Comparative Genomics
Background:
- Feline infectious peritonitis (FIP) is a severe disease caused by feline coronavirus (FCoV).
- FCoV shares similarities with SARS-CoV-2, suggesting potential shared therapeutic targets.
- GS-441524, a precursor to remdesivir, is an established FIP treatment.
Purpose of the Study:
- To investigate immunological alterations in cats with FIP.
- To compare gene expression profiles in normal, FIP-diseased, and FIP-recovered cats.
- To identify key molecular pathways and regulators involved in FIP pathogenesis.
Main Methods:
- Comparative transcriptome analysis of peripheral blood mononuclear cells (PBMCs).
- Bioinformatic analysis of differentially expressed genes.
- Gene ontology analysis to identify affected canonical pathways.
Main Results:
- Identified 677 differentially expressed genes between FIP-diseased and normal cats.
- Identified 431 differentially expressed genes between FIP-recovered and FIP-diseased cats.
- Revealed significant alterations in neutrophil degranulation and IL-8 signaling pathways, with KLF6 and NF-κB identified as upstream regulators of IL-8.
Conclusions:
- Significant immunological alterations occur in feline infectious peritonitis.
- KLF6 and NF-κB play critical roles in regulating IL-8-mediated neutrophil activation in FIP.
- These findings provide insights into the molecular mechanisms of FIP and potential therapeutic targets.
