ObjectiveTo investigate the clinical signification of plasma interleukin-17 (IL-17) 1evel in patients with acute respiratory distress syndrome (ARDS).MethodsForty-five adult ARDS patients and 22 healthy controls were enrolled in this study. The plasma cytokine levels of IL-17, IL-6 and IL-10 were measured by enzyme linked immunosorbent assay. Meanwhile, the baseline data of demographic and clinical tests including oxygenation index, procalcitonin and brain natriuretic peprtide were collected, the acute physiological and chronic health Ⅱ (APACHEⅡ) score and sequential organ failure assessment (SOFA) score were recorded. The main outcome was defined as hospital mortality within 28-day follow-up.ResultsThe plasma concentration of IL-17, IL-6 were higher in the ARDS patients (P<0.05) compared with the controls and the mean levels of IL-17, IL-6 and the APACHEⅡ score and the SOFA score in the non-survivors was higher than those in the survivors (P<0.05). In particular, there was a significant correlation between the plasma levels of IL-17 and IL-6 (P<0.05). Logistic regression and COX multivariate survival analysis suggested that age and SOFA score may be prognostic factors for ARDS.ConclusionsThe plasma concentration of IL-17 is significantly increased in ARDS patients, and its expression is linearly related to the proinflammatory factor IL-6. Both are important inflammatory markers in the acute phase of ARDS and may be important disease severity and prognostic indicators in addition to age and SOFA score.
Objective
To determine the concentration of int erleukin-12(IL-12),interleukin-2(IL-2) and tumor necrosis factor(TNF)and the irpossible role in the pathogenesis of proliferative vitreoretinopathy(PVR) ．
Methods
Patients were divided into 3 groups:18 with PVR,7 with simples retinal detachment caused by macular hole and 4 samples from normal eyes were used as control.Sample s of vitreous were obtained by aspiration through pars plana before cryotherapy ,vitrectomy and gas injection and stored in liquid nitrogen at －70℃ within 30 minites for ELISA.
Results
①The levels of IL-12,IL-2，and TNF in the vitreous of PVR were positively correlated with the degree of severity of disease.②The levels of IL-12, IL-2,and TNF in the PVR were higher than those in simple retinal detachment caused by macular hole and those in control group(Plt;0.01 ).③The levels of IL-12,IL-2，and TNF in retinal detachment caused by macular hole were also higher than those in the control group(Plt;0.01).
Conclusion
IL-12,IL-2，and TNF may play a role at lease to some extent in the pathogenesis of PVR.
(Chin J Ocul Fundus Dis,1999,15:75-77)
【Abstract】ObjectiveTo explore the effect of glutamine on immune function of rat with obstructive jaundice and its possible mechanism. MethodsFifty male Wistar rats were randomly divided into three groups: Control group (n=10)， obstructive jaundice group (n=20) and glutamine treatment group (n=20). The serum concentration of TNF-α, IL-10 was detected by using radioimmune method. Liver function was measured through automated biochemistry analyzer. The animal model of obstructive jaundice was established by ligating the rat’s common bile duct. Bacteria cultures were performed with the rat’s tissues of lung, spleen, liver and kidney respectively. ResultsCompared with control group, obstructive jaundice group showed statistically lower serum level of TNF-α, and statistically higher serum level of IL-10, TBIL, ALT and AST during the first and the second week after ligation of common bile duct. During the first and second week after administration of glutamine, the serum TNF-α of glutamine treatment group was statistically higher than that in control group and obstructive jaundice group. Meanwhile, glutamine treatment group showed statistically lower serum level of IL-10, TBIL, ALT and AST than obstructive jaundice group. There were statistically less bacteria translocations in glutamine treatment group than those in obstructive jaundice group. Conclusion Glutamine can increase the immune function by changing serum concentration of TNF-α, IL-10 and decrease the bacteria translocation.
ObjectiveTo investigate the inhibitory effects of L arginine (L arg) on systemic inflammatory response after cardiopulmonary bypass(CPB).MethodsFifty one patients with rheumatic heart disease were randomly divided into two groups: L arg group ( n =25) and control group ( n =26). For L arg group, L arg at 300mg/kg was given during operation. Plasma levels of tumor necrosis factor α(TNF α),interleukin 1β(IL 1β)and interleukin 10(IL 10) were measured by enzyme linked immunosorbent assay technique at baseline(before operation) and at 2,4,8,24 and 48 h after CPB termination.ResultsTNF α,IL 1β and IL 10 levels were increased in both groups after CPB ( P lt;0.05); levels of TNF α, IL 1β returned to normal at 48 h after CPB; In L arg group, TNF α and IL 1β levels were significantly lower than those in control group at 4,8 and 24 h after CPB ( P lt; 0 05). No significant difference were detected in IL 10 between groups( P gt;0.05).ConclusionL arg may decrease plasma levels of TNF α and IL 1β after CPB, it implies L arg may inhibit inflammation induced by CPB.
【Abstract】Objective To investigate the role of interleukin-10（IL-10） and interleukin-18 （IL-18） in the pathogenesis of acute lung injury in experimental severe acute pancreatitis.Methods Forty-eight SD rats were divided into control group and SAP group by the random data table. The model of experimental severe acute pancreatitis was established by injection of 3.5% sodium taurocholate into the bili-pancreatic duct. Lung wet weight index, ascities and level of serum amylase, IL-10 and IL-18 were quantitatively measured in different time. Intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were detected by semiquantitative RTPCR. The histopathology of pancreas and lung were observed under the light microscope.Results Lung wet weight index, ascities, level of serum amylase, IL-10 and IL-18, intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were significantly increased in SAP group (P＜0.01). The level of serum IL-18 and intrapulmonary expression of IL-18mRNA are positively correlated with lung wet weight index （r=0.68,P＜0.01; r=0.72,P＜0.01） and lung injury score （r=0.74,P＜0.01; r=0.79,P＜0.01) respectively, whereas the level of serum IL-10 and intrapulmonary expression of IL-10 mRNA are negatively correlated with lung wet weight index（r=-0.62,P＜0.01; r=-0.69,P＜0.01） and lung injury score（r=-0.66,P＜0.01; r=-0.60,P＜0.01）. Conclusion IL-18 may play a key role in the pathogenesis of acute lung injury in experimental severe acute pancreatitis, and IL-10 exerts the protection role in this process.
ObjectiveTo investigate the anti-inflammatory mechanism of sodium aescinate in preventing postoperative intestinal adhesion in rats.
MethodsThe SD rats were subjected to operation for establishing intestinal adhesion models, then randomly divided into model group, dexamethasone group(dexamethasone, i.v. 5 mg/kg), and sodium aescinate group(sodium aescinate, i.v. 2 mg/kg), 10 rats in each group. Another ten normal rats were selected as sham operation group. One times administration was administered on day 1 before establishing adhesion model, and administration for 3 d after modeling, once a day. On day 7 after operation, all of the rats were killed. The intestinal adhesion was graded and the adhesive tissues were taken for hydroxyproline determination. The levels of tumor necrosis factor(TNF)-α, interleukin(IL)-1β, and IL-6 in the serum were detected by ELISA.
ResultsCompared with the model group, sodium aescinate could obviously improve the severity of postoperative adhesion, markedly decrease hydroxyproline content in the adhesive tissues(P < 0.01), and significantly inhibit the levels of TNF-α, IL-1β, and IL-6 in the serum(P < 0.01).
ConclusionSodium aescinate could effectively prevent the formation of postoperative intestinal adhesion by inhibiting the expressions of inflammatory cytokines and decreasing the inflammatory response.
Objective To observe the alteration of anti-inflammatory cytokines (IL-10 and TGF-β) in acute pancreatitis. MethodsSD male rats were divided into 2 groups: group 1, the normal rats as a control (n＝6); group 2, the acute pancreatitis induced by intraductal injection of 5% sodium cholate sulfur with the volume of 1.0 ml/kg。 The animals were killed at 2(n＝6), 6(n＝6) and 24 hours (n＝8) after operation, the blood samples were taken for measurement of IL-10, TGF-β (by ELISA). The weight of pancreatic tissue and amylase were also observed. Results Serum IL-10 and TGF-β in control group were 32.05±14.87 pg/ml and 66.40±13.20 pg/ml, respectively. Serum IL-10 in group 2 was 36.52±9.76 pg/ml (2 hour), 37.75±6.54 pg/ml (6 hour), and 68.13±19.90 pg/ml (24 hour), respectively. Serum TGF-β in group 2 was 64.58±10.56 pg/ml (2 hour), 72.87±18.34 pg/ml (6 hour), 103.77±28.95 pg/ml (24 hour), respectively. Compared to that of normal rats, the serum level of IL-10 and TGF-β in 24 hours of acute pancreatitis increased significantly (Ｐ＜0.05). Conclusion Anti-inflammatory cytokines, both IL-10 and TGF-β were increased remarkablly in acute pancreatitis. This result indicates that there is a potential tendency of compensatory anti-inflammatory response sydrome in acute pancreatitis.
Objective
To study the expression of interleukin (IL)-37 and related factors in lung tissue of rats with acute lung injury, and explore the role and significance of IL-37 in acute lung injury so as to understand the pathogenesis of acute lung injury.
Methods
Forty-five clean-grade Wistar rats were randomly divided into a healthy control group, a bleomycin group and a dexamethasone treatment group, with 15 rats in each group. The rats in the bleomycin group and the dexamethasone group were treated with bleomycin at a dose of 4 mg/kg by intratracheal administration. The healthy control group was given the same volume of saline as control. The dexamethasone treatment group was injected with dexamethasone 3 mg/kg intraperitoneally twice a day on the basis of acute lung injury. The healthy control group and the bleomycin group were injected intraperitoneally with normal saline as control. The rats in each group were sacrificed at 7, 14 and 28 days after modeling. The histopathological changes of lung tissue were evaluated by HE staining. The levels of IL-37 in lung homogenate and tumor necrosis factor (TNF)-α in serum were measured. The expression of IL-18 mRNA in lung tissue was detected by RT-PCR.
Results
Pathological morphology showed that the lung tissue of the healthy control group was complete, no inflammatory and fibrotic changes at all time points. The lung tissues of the bleomycin group and the dexamethasone group manifested with acute alveolitis firstly and thus developed fibrosis changes lately, and the changes in the dexamethasone group were more slightly than those in the bleomycin group. The contents of IL-37 and TNF-α and the expression of IL-18 mRNA in the bleomycin group and the dexamethasone group reached to the highest point on the 7th day, and then decreased, but were significantly higher than those of the healthy control group on the 28th day (all P<0.05).
Conclusions
IL-37 plays an important role in the pathogenesis of acute lung injury in rats. This effect may be related to the regulation of IL-18 and TNF-α transduction.
Objective
To explore the mechanism of Liuhedan in promoting wound healing through applying Liuhedan to the infective wounds of New Zealand white rabbits.
Methods
A total of forty New Zealand white rabbit models of infective wounds were established after anesthesia. Five circular infective incisions were generated on the back of each rabbit, with a diameter of 2 cm. Five wounds of each rabbit were assigned respectively to the control group, model group, traditional Chinese medicine (TCM) group (Oleum Lithospermum), Western medicine group (calcium alginat), and treatment group (Liuhedan). Wound dressings were performed every day since postoperative day 1. Ten rabbits were selected randomly to be euthanized on postoperative day 3, 7, 14 and 21, respectively. Each specimen was divided into two parts. One was used for detecting interleukin-1β (IL-1β) by enzyme-linked immunosorbent assay, and the other was used for detecting tumor necrosis factor-α (TNF-α) by immunocytochemistry.
Results
On postoperative day 3 and 7, groups with the expression of IL-1β from low to high were respectively the control group, the treatment group, the Western medicine group, the TCM group, and the model group [postoperative day 3: (680.81±185.53), (1 028.67±205.57), (1 278.67±251.15), (1 449.86±230.74), (1 544.62±371.77) pg/mL; postoperative day 7: (1 024.43±239.94), (1 333.57±257.31), (1 635.14±222.40), (1 784.71±323.85), (1 953.29±324.78) pg/mL], and all the differences among the groups were significant (P<0.05); On postoperative day 14, groups with the expression of IL-1β from low to high were respectively the treatment group, the control group, the Western medicine group, the TCM group, and the model group [(908.71±108.61), (978.57±161.75), (1 120.43±265.39), (1 129.71±298.06), (1 191.14±234.92) pg/mL], and all the differences among groups were significant (P<0.05) except the difference between the Western medicine group and the TCM group (P>0.05); On postoperative day 21, the expression of IL-1β in the control group, the model group, the TCM group, and the Western medicine group was (487.19±121.80), (496.35±102.15), (500.31±139.34), (499.08±120.67) pg/mL, respectively, with no significant differences among the groups (P>0.05), which were all higher than that in the treatment group [(398.62±102.93) pg/mL] with significant difference (P<0.05). The expression of TNF-α in the model group was significantly greater than those in the other groups. The expression of TNF-α in the treatment group and Western medicine group was significantly lower compared with the model group. The expression of TNF-α in the TCM group was stronger compared with those in the treatment group and the Western medicine group.
Conclusion
Liuhedan can specifically suppress the expressions of IL-1β and TNF-α in the treatment of infective wounds, decrease the release of inflammatory factor and promote the healing.
Objective To construct gene-modified hepatic stem cells (WB-F344 cells), which have rat IL-13 gene and can secrete the recombinant rat IL-13 cytokine in the cells. Methods Firstly, the rat IL-13 sequences were synthesized. Then the sequences were amplificated in bacterium coli after recombinated with pWPXL-MOD plasmid. After PCR and sequence identification, the positive clones were packaged into lentivirus. After detecting the virus titer, the WB-F344 cells with constructed lentivirus vector with rat IL-13 gene were cultured, then the valid targets (expression level of the IL-13) were detected by real time-PCR and Western blot in cultured WB-F344 cells on 5 days. Results The valid DNA of rat IL-13 was recombinated and packaged in lentivirus vector. The recombinant gene sequence was correct by checking with gene sequence test. Then the recombinant was introducted into the WB-F344 cells cultures. The best multiplicity of infection (MOI) value for effective transfection was 5. IL-13 had been detected on day 5 after transfection by checking with real-time PCR and Western blot. Conclusion The recombinant rat IL-13 gene with lentivirus vector is constructed and gene-modified WB-F344 cells are cultured successfully, which can be used in next animal experiment.
