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Effects of BHV-1 on PMN adhesion to bovine lung endothelial cells
L M Warren1, L A Babiuk, M Campos
1Veterinary Infectious Disease Organization, Saskatoon, Canada.
Abstract:
Bovine herpes virus-1 (BHV-1) infection appears to decrease the rate of polymorphonuclear leukocyte (PMN) influx into the lung in response to the secondary invader, Pasteurella haemolytica. It was postulated that BHV-1 may affect the rate of cellular infiltration by altering the function of the endothelium, thereby preventing PMN movement across the blood-tissue barrier. Therefore, we decided to investigate the effect of BHV-1 on the ability of PMN to adhere to lung endothelial cells (LEC). LEC were isolated from fetal bovine fetal tissue and were shown to function in PMN adhesion assays. Furthermore, enhanced PMN adhesion was observed after exposure of LEC to recombinant bovine TNF-alpha (rBoTNF-alpha) for 4, 8, 12, and 24 h. LEC infected with BHV-1 were shown to be less responsive to rBoTNF-alpha. However, infection of LEC with BHV-1 at an multiplicity of infection (MOI) of 1.0 or 10 did not affect basal levels of PMN adhesion to these cells. Decreased PMN binding to BHV-1-infected LEC, simultaneously treated with rBoTNF-alpha, was observed at 10-12 h post-infection. The data suggest that BHV-1 may prevent cytokine-induced PMN infiltration of the lung through the modification of EC responses to cytokines.
Insights
Bovine herpes virus-1 (BHV-1) infection reduces polymorphonuclear leukocyte (PMN) lung infiltration. BHV-1-infected lung endothelial cells show decreased PMN adhesion, potentially by altering responses to inflammatory signals.
Area of Science:
- Veterinary Virology
- Immunology
- Cellular Biology
Background:
- Bovine herpes virus-1 (BHV-1) infection is linked to reduced polymorphonuclear leukocyte (PMN) lung influx.
- This phenomenon may involve altered endothelial cell function, impeding PMN transmigration across the blood-tissue barrier.
Purpose of the Study:
- To investigate the impact of BHV-1 infection on the adhesion of PMN to lung endothelial cells (LEC).
- To determine if BHV-1 affects LEC responsiveness to inflammatory stimuli like TNF-alpha.
Main Methods:
- Isolation of bovine LEC from fetal tissue for PMN adhesion assays.
- Exposure of LEC to recombinant bovine TNF-alpha (rBoTNF-alpha) to induce PMN adhesion.
- Infection of LEC with BHV-1 at varying multiplicities of infection (MOI) and assessment of PMN adhesion.
Main Results:
- BHV-1 infection did not alter basal PMN adhesion to LEC.
- Exposure to rBoTNF-alpha enhanced PMN adhesion to LEC.
- BHV-1-infected LEC exhibited reduced responsiveness to rBoTNF-alpha, with decreased PMN binding observed 10-12 hours post-infection.
Conclusions:
- BHV-1 infection may impede PMN infiltration into the lung by modulating endothelial cell responses to cytokines.
- This mechanism could contribute to the observed decrease in PMN influx during secondary lung infections.