Effect of transforming growth factor—β1 on monocyte Toll—like receptor 4 expression in septic rats.doc

Effect of transforming growth factor—β1 on monocyte Toll—like receptor 4 expression in septic rats BACKGROUND： Sepsis is a tough problem in critical ill patients. This study aimed to investigate the dynamic changes of monocyte Toll-like receptor （TLR） 4 expression in peripheral blood of septic rats and to determine the effects of transforming growth factor （TGF） -β1 on TLR4 expression. METHODS： Altogether 132 clean level SD rats were randomly divided into a control group （n=12）， a sepsis model group （n=60）， and a TGF-β1 intervention group （n=60）. In the sepsis model group and TGF-β1 intervention group， the rats were subdivided into five groups （2-hour group， 6-hour group， 12-hour group， 24-hour group， and 48-hour group）， with 12 rats in each group. Cecal ligation puncture （CLP） was performed in the sepsis model group and TGF-β1 intervention group to establish models of sepsis. The rats in the sepsis model group were injected with 1 mL normal saline at the caudal vein 0.5 hour after the model establishment； the rats in the TGF-β1 intervention group were injected with 20 ng/mL or 250 g TGF-β1 0.5 hour after the model establishment. Flow cytometry was used to detect the change of monocyte TLR4 in peripheral blood， and enzyme-linked immunosorbent assay （ELISA） was used to detect the change of TNF-α level in peripheral blood. RESULTS： At 6-12 hours after CLP， the monocyte TLR4 in peripheral blood started to decrease， and reached the lowest level at 12 hours. Compared to the control group， the monocyte TLR4 expression at 6 and 12 hours was lowered significantly （P0.05）. DISCUSSION 　　TLR4 can be found in many tissues， its mRNA also can be found in monocytes， neutrophils， dendritic cells， vascular endothelial cells， and intestinal epithelial tissue. Different immune cells show different TLR4 expressions after infection even in the immune cells subtypes.[5] As one of the phagocytes， monocytes play an important role in the host defense. The activation of monocytes