OBJECTIVE: To study the relationship of tumor necrosis factor-alpha (TNF-α)-308G/A gene polymorphisms with Henoch-Sch-nlein purpura nephritis (HSPN) in children. METHODS: Using the direct DNA sequencing method, polymorphisms in the TNF-α promoter region (-308) were genotyped in 110 Han children with Henoch-Sch-nlein purpura (HSP group), including 52 children with nephritis and 58 children without nephritis. Plasma TNF-α levels were measured using ELISA. Ninety ethnically matched healthy children were used as the control group. RESULTS: There were no significant differences in the polymorphisms of TNF-α (-308G/A) between the HSP and control groups (P>0.05). The GA genotype (29% vs 10%) and A allele frequency (18% vs 7%) in HSP children with nephritis (HSPN) were more common than in those without nephritis (P<0.05). Plasma TNF-α levels in HSPN children with GA+AA genotype (7.1±2.3 pg/mL) were significantly higher than those with GG genotype (5.7±1.5 pg/mL) (P<0.05). CONCLUSIONS: TNF-α-308GA genotype and A allele may contribute to the increased risk for the development of nephritis in children with HSP.
OBJECTIVE: To investigate the change in dendritic cells (DCs) in children with chronic immune thrombocytopenia (cITP) and the effect of glucocorticoid on DCs in children with cITP. METHODS: Fifteen children with cITP and 20 healthy controls were included in the study. Flow cytometry was used to measure the DC subsets count in the 15 children with cITP before and after glucocorticoid treatment as well as the corresponding values in the 20 healthy controls. The DCs derived from peripheral blood monocytes in children with cITP were cultured in vitro and collected, and their immunophenotypes were determined by flow cytometry. RESULTS: Before glucocorticoid treatment, the children with cITP showed no notable change in the absolute count of myeloid DCs (mDCs) but showed decreased absolute count of plasmacytoid DCs (pDCs) and increased mDC/pDC ratio compared with the healthy controls (P<0.05). After glucocorticoid treatment, the children with cITP demonstrated increased absolute count of pDCs and decreased absolute count of mDCs and mDC/pDC ratio compared with before treatment (P<0.05). Before glucocorticoid treatment, the children with cITP had significantly higher positive rates of HLA-DR, CD80, CD83 and CD86 on peripheral blood DCs than the healthy controls (P<0.01). All the positive rates were significantly decreased after glucocorticoid treatment (P<0.01), so that there was no significant difference from the healthy controls (P>0.05). CONCLUSIONS: Disproportion and functional disturbance of DC subsets is associated with the pathogenesis of cITP in children. Glucocorticoid can strengthen the immunosuppression of DCs in children with cITP, which may contribute to the effectiveness of glucocorticoid as a treatment.
OBJECTIVE: To observe the expression of dynamin-1 and phosphor-dynamin-1 in the hippocampus of children and rats with mesial temporal lobe epilepsy (MTLE) and to investigate the roles of dynamin-1 and phosphor-dynamin-1 in the development of MTLE. METHODS: Male Sprague-Dawley rats (aged 25 days) were randomly divided into acute control (AC), acute seizure (AS), latent control (LC), latent seizure (LS), chronic control (CC) and chronic spontaneous seizure (CS) groups. Lithium chloride-pilocarpine was used to induce a rat model of MTLE. The hippocampus samples of 5 children with a pathologically confirmed hippocampal sclerosis who received surgical operation were collected as a human model (HM) group, and the hippocampus samples of 4 dead children (without organic lesion of the hippocampus) were collected by autopsy as a human control (HC) group. The expression of dynamin-1 and phosphor-dynamin-1 in the hippocampus of children and rats with MTLE was measured by Western blot and immunohistochemistry. RESULTS: The Western blot showed that the expression of phosphor-dynamin-1 was significantly lower in the AS and CS groups than in the corresponding control groups (AC and CC groups) (P<0.05). The expression of phosphor-dynamin-1 was significantly lower in the HM group than in the HC group (P<0.05). There were no significant differences in the expression of dynamin-1 among the AS, LS and CS groups and between the HM and HC groups (P>0.05). The immunohistochemical results showed that phosphor-dynamin-1 was highly expressed in the cytoplasm of hippocampal neurons of AC, CC and HC groups, but its expression was significantly reduced in the AS, CS and HM groups (P<0.05). CONCLUSIONS: The expression of phosphor-dynamin-1, not dynamin-1, is downregulated in the hippocampus of children and rats with MTLE during seizures, which suggests that the phosphorylation/dephosphorylation of dynamin-1 may be involved in the development of MTLE.
OBJECTIVE: Preclinical studies have demonstrated that exogenous mesenchymal stem cells (MSCs) may ameliorate kidney damage and enhance repair of renal ischemia reperfusion injury (IRI). This review will focus on the mechanism for accelerating repair of renal IRI by MSCs. Several chemokine receptors such as CXCR4 and CD44 are related to MSCs trafficking to post-ischemic kidney. MSCs differentiate into tubular epithelial cells, which is not the predominant mechanism for repair of the damaged kidney. Instead, MSCs exert their therapeutic effect mainly through paracrine action via a variety of cytokines and microvesicles, and the paracrine actions of infused MSCs work to activate intrinsic kidney cells, promote angiogenesis, inhibit oxidative stress and reduce apoptosis, inflammation and renal fibrosis.