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Updated: Jun 22, 2026
Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow
Published on: August 14, 2014
PECAM-1 is involved in neutrophil transmigration across Histophilus somni treated bovine brain endothelial cells
Raksha Tiwari1, J Sullivan, C J Czuprynski
1Department of Pathobiological Sciences, University of Wisconsin-Madison, 53706, USA.
Abstract:
Histophilus somni (H. somni) is a gram-negative bacterial pathogen that causes respiratory, reproductive, and central nervous system disease in cattle. The hallmark of systemic H. somni infection is diffused vasculitis that can lead to an acute central nervous system disease known as thrombotic meningoencephalitis (TME). Because platelet endothelial cell adhesion molecule-1 (PECAM-1) and endothelial nitric oxide synthase (eNOS) play fundamental roles in maintaining homeostasis in blood vessels, we sought to determine if PECAM-1 and eNOS expression play a role in events related to the pathogenesis of TME. Our findings demonstrate that neutrophil transmigration across H. somni-treated TBBEC (SV-40 transformed bovine brain endothelial cell line) was reduced by treatment with anti-PECAM-1 antibodies. Confocal microscopy indicated that H. somni treatment leads to redistribution of PECAM-1 and eNOS on the surface of TBBEC. These findings suggest that PECAM-1 and eNOS may play a role in the early pathogenesis of TME.
Insights
Histophilus somni causes thrombotic meningoencephalitis (TME) in cattle. This study shows platelet endothelial cell adhesion molecule-1 (PECAM-1) and endothelial nitric oxide synthase (eNOS) are involved in TME pathogenesis.
Area of Science:
- Veterinary Pathology
- Bacterial Pathogenesis
- Immunology
Background:
- Histophilus somni (H. somni) is a significant bacterial pathogen in cattle, responsible for respiratory, reproductive, and central nervous system diseases.
- Systemic H. somni infections are characterized by vasculitis, which can progress to thrombotic meningoencephalitis (TME), an acute neurological condition.
- Platelet endothelial cell adhesion molecule-1 (PECAM-1) and endothelial nitric oxide synthase (eNOS) are crucial for maintaining vascular homeostasis.
Purpose of the Study:
- To investigate the potential role of PECAM-1 and eNOS expression in the pathogenesis of TME caused by H. somni.
- To understand the molecular mechanisms underlying H. somni-induced vascular damage and neurological disease.
Main Methods:
- Utilized bovine brain endothelial cells (TBBEC) treated with H. somni.
- Assessed neutrophil transmigration across endothelial cell monolayers.
- Employed confocal microscopy to visualize the expression and distribution of PECAM-1 and eNOS.
Main Results:
- Neutrophil transmigration across H. somni-treated TBBEC was significantly reduced by anti-PECAM-1 antibody treatment.
- Confocal microscopy revealed that H. somni infection induced a redistribution of PECAM-1 and eNOS on the surface of TBBEC.
- These molecular changes suggest an interaction between H. somni and endothelial cell surface molecules.
Conclusions:
- PECAM-1 and eNOS are implicated in the early stages of TME pathogenesis.
- Targeting PECAM-1 may offer a therapeutic strategy to mitigate H. somni-induced vascular damage.
- Further research is warranted to elucidate the precise mechanisms of PECAM-1 and eNOS involvement in TME.
