α-toxin Of Staphylococcus Aureus Down Regulated Pulmonary AQP1 Expression In Rats

ObjectiveAquaporins(AQPs) are a family of membrane channels that are in general highly permeable to water .To date, thirteen mammalian aquaporin homologues (AQP0-AQP12) have been identified,and aquaporins are present at all levels of life.The evolutionary conservation of aquaporins suggest mediation of water homeostasis under wide-ranging environ mental conditions. aquaporin-1 (AQP1), first identified in 1992,plays fundamental roles in water and osmolyte homeostasis by facilitating water and small solute movement across plasma membranes of epithelial, endothelial and other tissues.S.A. is an important pathogen of hospital acquired pneumonia and also one of etiologies for ALI.α-Toxin is one of toxins secreted by S.A. It can form pores on cell membrance .Changes in tissue water homeostasis are a known consequence of bacterial infection, generally manifest as local or systemic edema. Mechanisms underlying disrupted water homeostasis are not fully defined.Our experiments investigated the expression of pulmonary aquaporin-1 (AQP1) in normal and effects ofα-toxin of Staphylococcus aureus on pulmonary AQP1 expression in rats.MethodsTwenty-four Wistar rats were randomly divided into control group ,α-Toxin 6h group ,α-Toxin 10h group ,α-Toxin 24h group . Lung pathology(HE) ,lung wet to dry weight ratio (W/D) ,serum level of PaO2 and AQP1 immunohistochemistry were performedResults1.Compared with control group ,the model group rats all appeared ALI symptom .α-Toxin induced pulmonary edema and bleed. Lung pathology(HE),lung wet to dry ration(W/D),serum level of PaO₂ may suguest the degree of acute lung injury . 2.Immunolabelling showed AQP1 is mainly located in the microvascular endothelia of normal lungs.3.Our data showed that AQP1 expression was down-regulated significantly byα-Toxin at 6h, 10h and 24h, in which AQP1 expression reached the lowest level at 10h. And AQP1 was resumed partly at 24h(P<0.05).Discussion1.AQP1 is the first found water channel protein. It is mainly located in microvascular endothelium in lungs.2.S.A. is an important pathogen of hospital acquired pneumonia and also one of etiologies for ALI.α-Toxin is one of toxins secreted by S.A. It can form pores on cell membrane and also called pore-forming toxins.Very low doseα-Toxin can induce permeable pulmonary edema.3.Pathologically, it can induce destruction of alveolar architecture including enlargement of interstitial cavity and injury of endothelium, which indicated that microvessels may be the target ofα-Toxin.4.The ALI animal model was made successfully by injectingα-Toxin peritoneally.We hypothesized thatα-Toxin might affect AQP1 expression of lungs.5.Our data showed that AQP1 expression was down-regulated significantly byα-Toxin at 6h, 10h and 24h, in which AQP1 expression reached the lowest level at 10h. It is suggestion that down-regulated AQP1 may involved in pulmonary water inbalance in ALI induced byα-Toxin.ConclusionExpression of pulmonary AQP1 in rats was down-regulated significantly byα-Toxin of S.A., which indicated AQP1 may play a role in abnormal fluid transportation.