RESUMO
Staphylococcus aureus(S.aureus) secretes a variety of pathogenic toxins and one of the most prominent toxins is α-hemolysin,which is considered as the main virulence factor in skin necrosis and severe infections caused by S.aureus infection. α-hemolysin is so named because of its ability to dissolve red blood cells. However,it has a wide range of effects on various cells and may cause different pathogenic re-sponses in different host cells. This review summarizes recent studies on the structure of α-hemolysin and its interaction with different cells in order to better understand the role of α-hemolysin in the process of S.aureus infection,which may provide a reference for developing new approaches to the prophylaxis and treatment of S.aureus infection.
RESUMO
BACKGROUND AND OBJECTIVES: Staphylococcus Aureus (S. Aureus) is one of the most common and predominant form of bacteria in the nasal airway that roduces toxin. Alpha toxin from S. Aureus, also known as alpha-hemolysin, causes damage to the membrane in many types of cells. The purpose of this study is to develop a rat model of rhinosinusitis induced by the intra-nasally applied alpha-toxin of S. Aureus. MATERIAL AND METHODS: Forty micro-liters of 100 microgram/ml of alpha-toxin was applied intra-nasally to 4-6 weeks-old Sprague-Dawley rats and the same amount of vehicle was applied to control rats. At days 1, 5 and 14 the rats were sacrificed and their nasal cavity prepared for histological investigation. RESULTS: Inflammatory cell clusters were observed in the alpha-toxin applied rats. The number of sinus air spaces occupied by inflammatory cell clusters increased significantly at days 1 and 5 compared with the control rats. Comparisons across the time interval demonstrated statistically significant changes, showing a peak at day 1 among alpha-toxin applied rats. CONCLUSION: Intra-nasally applied alpha-toxin induces acute rhinosinusitis in the rats. The histological evidence of rhinosinusitis revealed the appearance of inflammatory cell clusters in the sinonasal air spaces. These findings indicate that this rat model of alpha-toxin induced rhinosinusitis may be applied for better understanding of the role of bacterial toxin in the pathogenesis of rhinosinusitis.