【Abstract】Objective To study the influence of early hemofiltration on plasma concentrations of proinflammatory cytokines TNF-α and IL-1β and their transcription levels in severe acute pancreatitis (SAP) pigs. Methods The model of SAP was induced by retrograde injection of artificial bile into pancreatic duct in pigs. Animals were divided randomly into two groups: SAP hemofiltration treatment group (HF group, n=8) and SAP no hemofiltration treatment group (NHF group, n=8). TNF-α and IL-1β plasma concentrations were measured by ELISA. Their transcription levels in the tissues of pancreas, liver and lung were assayed by semi-quantitative reverse transcription polymerase chain reaction. Results After hemofiltration treatment, the plasma concentrations of TNF-α and IL-1β increased gradually but were lower than those of NHF group at the same time spot 〔at 6 h after hemofiltration treatment, (618±276) pg/ml vs (1 375±334) pg/ml and (445±141) pg/ml vs (965±265) pg/ml, P＜0.01〕. At 6 h after hemofiltration treatment, the transcription levels of TNF-α and IL-1β in tissues of pancreas, liver and lung were lower than in NHF group (57.8±8.9 vs 85.7±17.4, 48.0±8.1 vs 78.1±10.2, 46.2±9.6 vs 82.4±10.5; 55.9±9.0 vs 82.2±15.7, 40.6±9.2 vs 60.0±10.6, 35.7±9.8 vs 58.1±9.3, P＜0.01). Conclusion Early hemofiltration can reduce TNF-α and IL-1β plasma concentrations and transcription levels in SAP pigs.
ObjectiveTo explore the immunosuppressive effect of XGD1 and its mechanism. MethodsDifferent concentrations of XGD1 were added to PHA or ConA induced human peripheral blood T lymphocyte.Seventytwo hours later modified MTT assay was employed to test the effect of XGD1 on T cell proliferation. Flowcytometry was used to examine the effect of XGD1 on the expression of IL2 receptor(IL2R) on the surface of T cells individually at 48 h and 72 h.And the effects of XGD1 combined with cyclosporine A(CsA) on the proliferation of Tlymphocytes and the expression of IL2R were also investigated. ResultsIn the concentration range of 0.2～25 μg/ml,XGD1 exerted marked inhibitory effect on PHA or ConA induced T cell proliferation,which was proportional to dose. Flowcytometry showed that XGD1 inhibited the expression of IL2R,and the percentage of IL2Rα positive cells after stimulation of PHA decreased from 47.67% to 25.03% in the presence of XGD1 (1 μg/ml).XGD1 and CsA had synergism in inhibition of T cell proliferation and IL2R expression. ConclusionThe study suggests that XGD1 has immunosuppressive effect. The suppressive effect of XGD1 on T cell proliferation is most probably mediated by decreasing IL2R expression.
【Abstract】Objective The effects of tumor infiltrating lymphocytes (TIL) on cellular immunologic function of patients with breast cancer were studied. Methods Twenty five patients with breast cancer were treated by the TIL that were isolated from tissue of tumor. T cell subgroups and natural killer cell (NK cell) activity of peripheral blood, the levels of serum soluble interleukin-2 receptor (sIL-2R) were assayed before and after treatment. Results CD3, CD4, CD4/CD8 and NK cell activity were ascended obviously, and CD8, sIL-2R were descended obviously after the treatment of TIL. Conclusion TIL can enhance the cellular immunologic function of patients with breast cancer.
To study the role of endotoxin in acute hemorrhagic necrotizing pancreatitis (AHNP), the change of endotoxin were studied in rats AHNP models by injection of 5% sodium taurocholate 1 ml/kg into pancreatic duct, and the effects of recombinant interleukin-2 (IL-2) in the treatment of AHNP were observed in this experiment. The results indicated that endotoxin involved the aggravation of AHNP and was associated with the increase of serum phospholipas-2 (PLA2), and these mediators were positively correlated with severe degrees of pancreatic damage. The results also suggeste that IL-2 might inhibit the overexpression of endotoxin and PLA2 and mitigate the pancreatic injury and decrease the 72h-mortality rate of AHNP from 66.7% to 26.7% (Ｐ＜0.01). Endotoxin might play a major role in the pathogenesis of AHNP and IL-2 might have a potential role in the treatment of AHNP.
To evaluate effect of recombinant human growth hormone (rhGH) on immunologic function in patients with gastrointestinal malignant tumor (GIMT). Before and 3 weeks after surgical treatment and administration of rhGH, the amount of T lymphocyte subset (T-LS) and soluble interleukin 2 receptor (sIL-2R) level were measured in 12 patients with GIMT, which were compared with 20 cases of normal control and 18 cases of GIMT treated by surgery alone. Result: ①In all GIMT patients, the serum CD＋3, CD＋4 level and the ratio of CD＋4/CD＋8 were lower than normal control and the sIL2R level was much higher; ②After operation, the serum CD＋3, CD＋4 level and the ratio of CD＋4/CD＋8 of all patients increased, the serum sIL2R level decreased; ③In patients recieved rhGH, the serum CD＋3, CD＋4 level and the ratio of CD＋4/CD＋8 were much more increased and the serum sIL-2R level much more decreased than those of surgery alone group. Conclusion: rhGH can enhance the immunologic function of patients with GIMT.
Objective To investigate the expression of FLIP in the lung of rats and the protective effect in development of acute lung injury( ALI) with the adenovirus vector carrying FLIP gene( Ad-FLIP)inhaled. Methods Forty-eight rats were randomly divided into four groups, with 12 rats in each gruop. In treatment group, ALI rats model was eatablished by LPS intraperitoneal injection and then inhaled Ad-FLIP vector. In prevention group, the animals were infected with Ad-FLIP vector before ALI model wasestablished. Two control groups of treatment and prevention received Ad-EGFP vectors respectively.Pathological changes of lung were observed under light microscope. Wet/dry weight ( W/D) of lung lobes and lung permeability index( LPI) were also measured. The mRNA and protein expressions of FLIP in lungwere investigated by RT-PCR and immunohistochemistry, respectively. Results Lung histopathological changes were alleviated, the index of W/D and LPI were significantly lower, the expressions of FILP mRNA and protein in the lung were elevated both in the treatment group and prevention group compared to thecontrol groups ( all P lt;0. 01) . Conclusion Ad-FLIP transfection can up-regulate the expression of FLIP in lung of rats, and might protect respiratory membrane and lessen pulmonary edema to prevent the development of ALI.
【Abstract】 Objective To observe the plasma levels of adiponectin and interleukin-17 ( IL-17) in patients with chronic obstructive pulmonary disease ( COPD) at acute exacerbation or stable stage, and analyze their relationship. Methods Sixty male COPD patients with normal weight ( with BMI range of 18. 5-24. 9 kg/m2 ) were enrolled, including 30 patients with acute exacerbations of COPD ( AECOPD) and 30 patients with stable COPD. Twenty healthy nonsmoking male volunteers were included as controls. The plasma levels of adiponectin and IL-17 as well as lung function ( FEV1% pred and RV% pred) were measured in all subjects. Results The concentrations of adiponectin and IL-17 were significantly higher in the AECOPD patients than those of the patients with stable COPD and the contro1s ( P lt; 0. 001) . Theconcentrations of adiponectin and IL-17 were significantly higher in the patients with stable COPD than those of the controls ( P lt;0. 01) . Adiponectin was positively correlated with IL-17 in the AECOPD patients ( r =0. 822, P lt;0. 001) and in the patients with stable COPD ( r =0. 732, P lt;0. 001) . Adiponectin was positivelycorrelated with RV% pred in the AECOPD patients ( rs = 0. 764, P lt;0. 001) and in the patients with stable COPD ( rs =0. 967, P lt;0. 001) . There was no significant relationship between adiponectin and FEV1% pred ( P gt;0. 05) . Conclusions The plasma level of adiponectin in COPD patients is elevated which is relatedwith excessive inflation of lung. Adiponectin may be involved in the process of inflammation in COPD as a new pro-inflammatory cytokine.
Objective To identify the effects of single immunoglobin IL-1 receptor related protein （SIGIRR） on inflammation induced by high mobility group box 1 （HMGB1） in A549 derived from human alveolar epithelial cells. Methods Eukaryotic expression vectors pCDNA3.1（+） constructed with SIGIRR cDNA were transiently transfected into A549 cells，in which SIGIRR was forced to be over-expressed. Western blot and RT-PCR were applied to detect the expression level of SIGIRR after transfection. After the stimulation by HMGB1，the transcriptional activity of NF-κB in A549 cells was detected by dual-luciferase reporter assay system，and the protein levels of inflammatory cytokine TNF-α and IL-1β were measured by ELISA. Results The expression level of SIGIRR increased significantly in A549 cells transfected with SIGIRR vectors. The transcriptional activity of NF-κB was enhanced obviously after HMGB1 treatment in A549 cells by dual-luciferase reporter assay system，while the transfection of SIGIRR vectors decreased the activity. The protein levels of TNF-α and IL-1β were down-regulated in A549 cells over-expressing SIGIRR after HMGB1 stimulation compared with the non-transfected cells. Conclusions Up-regulated SIGIRR expression can inhibit HMGB1-induced proinlammatory cytokine release in A549 cells such as TNF-α and IL-1β. The transcriptional activity of NF-κB is dampened by SIGIRR transfection，implying that the anti-inflammatory effects of SIGIRR may be involved in the regulation of NF-κB.