Résumé
Growing evidence from animal experiments and human epidemiological studies has revealed the intriguing communications between the gut,microbiota and brain,i.e.,the gut-microbiota-brain axis.The microbiota establishes its symbiotic rapport with the host early in life and participates in multiple developmental and physiological processes,including regulating brain development and influencing behavior and neurological function.Multiple perinatal factors influence neonatal colonization,and gut dysbiosis is a common finding in preterm infants.Perturbations in the delicate synergetic gut-microbiota-brain communication may have serious consequences,leading to abnormal brain development and long-term neurodevelopment disorders.
Résumé
Objective Using the technology of siRNA to inhibit gene expression of T cells'nonreceptor tyrosine protein kinase Lck in asthmatic mice,and to study the effect of siRNA inhibited Lck to the function of T cells in asthmatic mice.Methods The 21 - 23 bp RNA fragments of mouse T cell Lck were made by chemosynthesis.INTERFERinTMsiRNA Transfection Reagent was used as transfection reagent to transfect the siRNA into the spleen T cells of asthmatic mice for 48 hours.Then T cells were mixed with bone marrow dendritic cells (DC) of asthmatic mice for another 48 hours.Cell culture suspension was collected and the level of IL-4,IL-13,IL-2,INF-γ were detected with respondent ELISA kits; Western Blot was used to identify if the expression of Lck was blocked.Results The expression of Lck in T cells almost could not be detected in siRNA interference group.The levels of IL-4 and IL-13 in siRNA interference group( 10.19 ± 1.66,12.34 ±0.79) were lower than no-siRNA interference(28.06 ±2.88,27.87 ± 1.61 )and control group ( 22.07 ± 2.5 1,20.47 ± 2.37 ),and the difference was statistical significant ( P <0.01 ).Conclusions Special siRNA could block the expression of special gene,and Lck specific siRNA could block the activation and differentiation of T cells and reduce the secretion of inflammatory cytokines in asthmatic mice.