Comparative transcriptome analysis of equine alveolar macrophages
A E Karagianni1, R Kapetanovic1, K M Summers1
1Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, UK.
Equine Veterinary Journal
|April 21, 2016
Summary
Equine alveolar macrophages (AMs) show distinct gene expression compared to peritoneal macrophages (PMs). Their response to lipopolysaccharide (LPS) resembles human macrophages, suggesting horses as a model for lung inflammation studies.
Area of Science:
- Comparative immunology
- Equine respiratory health
- Macrophage biology
Background:
- Alveolar macrophages (AMs) are crucial for lung defense against pathogens.
- Understanding equine macrophage biology is vital for treating airway infections in horses.
- AMs are potential therapeutic targets for opportunistic lung infections.
Purpose of the Study:
- To compare the gene expression profiles of equine alveolar macrophages (AMs) and peritoneal macrophages (PMs).
- To investigate the impact of lipopolysaccharide (LPS) stimulation on equine AMs.
Main Methods:
- Gene expression analysis using microarrays on equine AMs and PMs.
- Isolation of cells from bronchoalveolar and peritoneal lavage fluid of euthanized horses.
- Comparison of equine AM gene expression with human and murine macrophage data, focusing on LPS-induced inflammatory responses.
Main Results:
- A significant differential basal expression of 451 genes was observed between equine AMs and PMs.
- Equine AMs exhibited an alternative (M2) polarization profile, while PMs showed a hybrid activation profile, possibly due to endotoxin tolerance.
- LPS stimulation altered the expression of 240 genes in equine AMs, including key inflammatory genes, with a profile more similar to human than murine macrophages.
Conclusions:
- This study enhances the understanding of equine macrophage biology.
- Equine AMs share similarities with human macrophages, particularly in LPS-induced inflammatory responses.
- The horse may serve as a valuable animal model for studying human macrophage-associated lung inflammation.


