ABSTRACT
The central nervous system can produce a variety of neuroimmune factors including interleukin-6. This article reviewed the expression and signaling pathways of interleukin-6 and its receptors in the central nervous system, and advances in interleukin-6 in the regulation of central nervous system related diseases, cognitive behaviors and synaptic function, which suggested that interleukin-6 involves in various physiological or pathological functions in the central nervous system and affects central nervous system in multiple layers such as protein expression, signal transduction, neurological function, and synaptic transmission. Interleukin-6 is expected to be a biological marker in the specific state of the central nervous system. In addition, interleukin-6 can regulate the function of neurons and synapses and is an important molecule involved in synaptic transmission, synaptic plasticity, and learning and memory. Strengthening the research on the biological function and mechanism of interleukin-6 and timely regulating the interleukin-6 expression will provide a new perspective for the treatment of the central nervous system related diseases.
ABSTRACT
The central nervous system can produce a variety of neuroimmune factors including interleukin-6. This article reviewed the expression and signaling pathways of interleukin-6 and its receptors in the central nervous system, and advances in interleukin-6 in the regulation of central nervous system related diseases, cognitive behaviors and synaptic function, which suggested that interleukin-6 involves in various physiological or pathological functions in the central nervous system and affects central nervous system in multiple layers such as protein expression, signal transduction, neurological function, and synaptic transmission. Interleukin-6 is expected to be a biological marker in the specific state of the central nervous system. In addition, interleukin-6 can regulate the function of neurons and synapses and is an important molecule involved in synaptic transmission, synaptic plasticity, and learning and memory. Strengthening the research on the biological function and mechanism of interleukin-6 and timely regulating the interleukin-6 expression will provide a new perspective for the treatment of the central nervous system related diseases.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the association of gene polymorphisms of Toll-like receptor 3 (TLR3)-1377C/T and expression of TLR3 with the susceptibility to enterovirus 71 (EV71) encephalitis in children.</p><p><b>METHODS</b>A total of 187 children with EV71 infection (59 children in the encephalitis group and 128 in the non-encephalitis group) and 232 children who underwent physical examination were enrolled in the case-control study. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the TLR3-1377C/T gene polymorphisms. ELISA was used to measure the serum level of TLR3.</p><p><b>RESULTS</b>There were no significant differences in the genotype and allele frequencies of TLR3-1377C/T between the non-encephalitis group and the encephalitis group. Compared with the control group, the encephalitis group and the non-encephalitis group had significant increases in the serum level of TLR3 (P<0.05), and the non-encephalitis group had the highest level (P<0.05). The encephalitis group had a significantly higher EV71 viral load than the non-encephalitis group (P<0.01). The children aged <1 year or ≥1 year in the encephalitis group and the non-encephalitis group had significant increases in the serum level of TLR3 compared with their counterparts in the control group (P<0.05), and the children aged <1 year or ≥1 year in the non-encephalitis group had a significantly higher serum level of TLR3 than those in the encephalitis group (P<0.05). In the encephalitis group, the children aged ≥1 year had a significantly higher TLR3 concentration than those aged <1 year (P<0.05), and there were no significant differences in the TLR3 concentration between the children aged ≥1 year and <1 year in the non-encephalitis group and the control group. In the encephalitis group, the proportion of children aged <1 year was significantly higher than those aged ≥1 year (P<0.05).</p><p><b>CONCLUSIONS</b>The TLR3-1377C/T gene polymorphisms are not significantly associated with the development of EV71 encephalitis. Low expression of TLR3 might weaken the inhibitory effect on virus replication and promote the development of EV71 encephalitis. The deficiency in the expression of TLR3 in serum after EV71 infection might be an important factor for the development of encephalitis in infants.</p>
Subject(s)
Child, Preschool , Female , Humans , Infant , Male , Encephalitis, Viral , Genetics , Enterovirus A, Human , Enterovirus Infections , Genetics , Genetic Predisposition to Disease , Polymorphism, Single Nucleotide , Toll-Like Receptor 3 , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To explore the molecular mechanism of brain protection against convulsive brain damage in premature brains by observing the changes of apoptotic-regulating genes of bcl-2 and c-Jun expression in the hippocampus in Wistar rats with different ages after status convulsion (SC).</p><p><b>METHODS</b>SC was induced in infant Wistar rats (IRs) and adult Wistar rats (ARs) by intraperitoneal injection of lithium-pilocarpine. The rats were sacrificed at 3 hrs, 6 hrs, 12 hrs, 1 day, 3 days and 7 days after SC (n=8). Bcl-2 and c-Jun protein and mRNA levels were measured using immunocytochemistry, RT-PCR and in situ hybridization.</p><p><b>RESULTS</b>c-Jun protein levels increased significantly at 3 hrs and reached the peak at 6 hrs after SC in both IRs and ARs compared to those in the normal control group (P<0.01). c-Jun protein levels started to decrease 12 hrs after SC in both IRs and ARs. The expression of c-Jun protein in IRs returned to the basal level 1 day after SC, while remained higher in ARs than in the normal control group by 7 days after SC. The expression of c-Jun protein in ARs was much higher than that in IRs from 6 hrs to 7 days after SC (P<0.05). c-Jun mRNA level was in parallel with the protein level as mentioned in IRs and ARs after SC. There were no changes observed in both bcl-2 protein and bcl-2 mRNA levels after SC in IRs and ARs.</p><p><b>CONCLUSIONS</b>SC may induce an up-regulation of proapoptotic gene c-Jun in the hippocampus after SC, with a less strong extent and shorter duration in IRs compared to that in ARs. This might be one mechanism of brain protection against convulsive brain damage in IRs. The expression of bcl-2 remains unchanged after SC and is not affected by age in both IRs and ARs.</p>