ABSTRACT
Title
Chronic stress affects lung sphingosine kinase isoenzymes and increases the risk of lung bacterial infections
Authors
V.Lucini, M.Pannacci, S.Dugnani, F.Scaglione
Dept. of Pharmacology,Chemotherapy and Toxicology; University of Milan, Italy
Abstract
It is well known that stress can affect the immune system and may increase the risk of respiratory infections (RTI). Sphingosine-1-phosphate (S1P) is a biologically active metabolite of plasma-membrane sphingolipids that is essential for immune-cell trafficking and vascular integrity. the quantification of S1P in different tissues showed that the lung contained the highest amount of S1P, suggesting its possible involvement in the induction of innate antimicrobial immune response at the interface with external airway environment.
This study explored the hypothesis that S1P may involved in the mechanisms of stress related lung infections.
Gene expression of sphingosine kinase isoenzymes (SphK1, SphK2) and S1P receptors (S1PR1and S1PR2) were detected in lung of chronic stressed male BALB/cJ mice and in controls.
Stressed an control mice were underwent to inhalations of a virulent strain of S. pneumoniae and rate of lung infections were detected.
Controls and chronic stressed mice resulted infected. However, the pneumonia was more extended in the stressed group than in controls. The bacterial size was significantly higher (p< 0.001) in the stressed animals vs controls (5x10^6 ± 2,9 CFU/lung vs 3x10^4 ± 2.3 CFU/lung). SphK1 and SphK2 expression significantly increased in control infected mice (p<0.01) while was unchanged in mice undergo to chronic exercise. No significant variations were observed in the S1PR1 and S1PR2 expression.
Thesedata confirmed that a prolonged exercise increased susceptibility to RTI; S1P could play a protective role in the bacterial diffusion via immune activation and/or via enhancement of the
endothelial cells barrier function.
This study explored the hypothesis that S1P may involved in the mechanisms of stress related lung infections.
Gene expression of sphingosine kinase isoenzymes (SphK1, SphK2) and S1P receptors (S1PR1and S1PR2) were detected in lung of chronic stressed male BALB/cJ mice and in controls.
Stressed an control mice were underwent to inhalations of a virulent strain of S. pneumoniae and rate of lung infections were detected.
Controls and chronic stressed mice resulted infected. However, the pneumonia was more extended in the stressed group than in controls. The bacterial size was significantly higher (p< 0.001) in the stressed animals vs controls (5x10^6 ± 2,9 CFU/lung vs 3x10^4 ± 2.3 CFU/lung). SphK1 and SphK2 expression significantly increased in control infected mice (p<0.01) while was unchanged in mice undergo to chronic exercise. No significant variations were observed in the S1PR1 and S1PR2 expression.
Thesedata confirmed that a prolonged exercise increased susceptibility to RTI; S1P could play a protective role in the bacterial diffusion via immune activation and/or via enhancement of the
endothelial cells barrier function.