ObjectiveTo investigate the expressions of IL-10,tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in serum and lung tissue of COPD rats in order to elucidate the potential mechanism of airway inflammation. MethodsForty-five healthy adult male SD rats were randomly divided into a COPD model group (n=30) and a normal control group (n=15). The COPD rat model was established by intratracheal instillation of lipopolysaccharide (LPS) and exposure to cigarette smoke for 28 days. The concentrations of IL-10,TNF-α and IFN-γ in serum and lung tissue were measured by ELISA. ResultsTNF-α level of serum and lung tissue in the COPD model group increased significantly compared with the control group(P<0.05),while the levels of IFN-γ and IL-10 decreased significantly[serum:(44.68±8.67) ng/L vs. (75.96±10.59) ng/L;lung tissue:(64.55±9.03) ng/L vs. (94.06±8.71) ng/L,P<0.01]. The level of IL-10 in serum and lung tissue was negatively correlated with TNF-α (serum:r=-0.67,lung tissue:r=-0.80,P<0.01). The level of IL-10 in serum and lung tissue was positively correlated with IFN-γ (serum:r=0.64,lung tissue:r=0.72,P<0.01). The level of IL-10 in serum and lung tissue was negatively correlated with the percentage of neutrophils(serum:r=-0.70,lung tissue:r=-0.67,P<0.01). ConclusionIn COPD rats,down regulation of IL-10 plays an important role in regulation of airway inflammation.
目的 系统评价白细胞介素1β（IL-1β）与癫痫发作的相关性。 方法 2012年5月－2013年10月检索PubMed数据库（1985年1月－2013年7月）、Medline数据库（1985年1月－2013年7月）、中国知网（1998年1月－2013年7月）和万方数据库（1996年1月－2013年7月），并辅以谷歌学术搜索引擎进行手工检索。由两名研究者按照研究的纳入与排除标准进行病例对照研究的选择，对入选文献的质量参照“非随机对照临床试验质量评价标准与计分表”进行评价和计分，评估纳入研究的方法学质量并对有效的信息进行数据提取。然后采用RevMan 5.0统计软件进行Meta分析，以加权均数差（WMD）为效应指标。 结果 共纳入5个研究，包括82例癫痫发作的患者和471例正常对照。所纳入的研究未描述详细的抽样方法及其检测方法的特异性。Meta分析结果显示：癫痫发作72 h以内的患者与正常对照人群之间血浆IL-1β的浓度差异无统计学意义[WMD=0.04 pg/mL，95%CI（−0.07，0.16）pg/mL，P=0.46]。 结论 IL-1β可能没有直接参与癫痫的发作，而是通过与其他炎性因子之间的相互作用来实现。因此，需要进一步的研究来证明IL-1β在癫痫发作中的作用。
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
Objective To investigate the possible role of ulinastatin(UTI) in f lipopolysacccharide (LPS)-induced acute lung injury(ALI).Methods Thirty male SD rats were randomly divided into three groups，ie.a normal control group，a LPS group and a LPS plus UTI group.The rats were injected with 1 mL of normal saline via caudal vein in the control group，with LPS 5 mg/kg via caudal vein in the LPS group，and with UTI 100000 U/kg shortly after injection with LPS in the LPS plus UTI group.The rats were sacrificed 4 h after the injection.Lung wet/dry weight ratio was measured.IL-18 level in serum and lung tissue was determined by ELISA and the expression of NF-κB in lung tissue was determined by immunohistochemistry.Pathological changes of rats’ lung were observed by optical and electron microscope.Results Compared with the control group，IL-18 level in serum and NF-κB expression in lung tissue were significantly higher in the LPS group(Plt;0.01).The IL-8 level was somewhat elevated in the LPS+UTI group but with no significant difference from that in control group was found (Pgt;0.05).The lung inflammation in the LPS+UTI group was milder than that in the LPS rats.Conclusion UTI can alleviate LPS-induced inflammatory reaction and lung injury in rat model.
Objective To detect the expression of single immunoglobin IL-1 receptor related protein ( SIGIRR) in normal human lung tissues, and study its changes in alveolar epithelial cell acutely injured by lipopolysaccharide ( LPS) . Methods Twenty samples of human normal lung tissue were collected during the lobectomies. The expression of SIGIRR was detected by immunohistochemistry, western blot and RT-PCR. The human type II alveolar epithelial cell acute injury model was established by stimulating A549 cells with LPS of a final concentration of 10 μg/mL. The cells were collected at 0, 3, 6, 12, and 24 hours after the stimulation. The changes of SIGIRR expression at the same time points were observed by western blot. The expression vector containing full-length SIGIRR cDNA was transfected transiently into A549 cells to induce SIGIRR overexpression. MTT assay was performed to measure the injury of A549 cells caused by LPS. Results The immunohistochemistry, western blot and RT-PCR showed that there was a high expression of SIGIRR in normal human lung tissues. The expression of SIGIRR was located in alveolar epithelial cells by immunohistochemistry. The expression of SIGIRR at 3, 6, and 12 hours was down-regulated after LPSstimulation and raised again at 24 hours to the baseline. MTT assay showed that SIGIRR overexpression substantially reduced the growth inhibition ratio of A549 cells after LPS stimulation. Conclusions Expression of SIGIRR in normal human lung tissues was confirmed by different detection methods. SIGIRR alleviates the injury of alveolar epithelial cells caused by LPS, implying SIGIRR might be involved in the regulationof acute lung injury mediated by LPS.
Objective To investigate the changes of 8-isoprostane ( 8-isoPG) , leukotriene B4 ( LTB4 ) , TNF-α, IL-10 and hypersensitive C-reactive protein( Hs-CRP) in serum of patients with obstructive sleep apnea hypopnea syndrome ( OSAHS) . Methods Forty OSAHS patients ( 20 cases underwent therapeutic Auto-CPAP or UPPP treatment for over three months) and 30 normal controls were included in the study. Serum 8-isoPG, LTB4, TNF-α and IL-10 were measured by ELISA. Hs-CRP was detected by automatic biochemistry analyzer. Results ①The serum levels of 8-isoPG, LTB4, TNF-α, Hs-CRP were significantly higher and IL-10 was considerably lower after sleep in 40 OSAHS patients [ ( 36. 59 ±14. 89) ng/L, ( 14. 75 ±6. 25) μg/L, ( 1022. 13 ±97. 57 ) ng/L, ( 2. 46 ±1. 58 ) mg/L, ( 4. 68 ±3. 42) ng/L, respectively ] than those in the normal controls [ ( 19. 91 ±7. 76 ) ng/L, ( 1. 43 ±0. 72) μg/L, ( 540. 00 ±78. 70) ng/L, ( 0. 30 ±0. 16) mg/L, ( 7. 41 ±4. 49) ng/L, respectively] ( P lt;0. 01) . ② Serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels elevated gradually following the severity of OSAHS while serum IL-10 level was decreased( P lt; 0. 05) . ③Serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels in OSAHS patients after sleep were correlated positively with AHI ( r =0. 863, 0. 746, 0. 868, 0. 842,all P lt; 0. 01) and negatively with LSpO2 ( r = - 0. 623, - 0. 524, - 0. 618, - 0. 562, all P lt; 0. 01) and MSpO2 ( r = - 0. 654, - 0. 573, - 0. 537, - 0. 589, all P lt;0. 01) . SerumIL-10 level in OSAHS patients was correlated negatively with AHI ( r = - 0. 722, P lt; 0. 01) and positively with LSpO2 ( r = 0. 564, P lt; 0. 01) and MSpO2 ( r = 0. 505, P lt; 0.01) . ④ After three months of auto continuous positive air pressure( Auto-CPAP) or uvulopalatopharyngoplasty( UPPP) treatment, serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels of the OSAHS patients after sleep were obviously decreased [ ( 23. 10 ±9. 54) ng/L, ( 4. 02 ±2. 15) μg/L, ( 810. 25 ±135. 85) ng/L, ( 0. 79 ±0. 60) mg/L, respectively] , and serum IL-10 level was obviously increased[ ( 6. 93 ±3. 91) ng/L] ( P lt; 0. 01) . ⑤ serum 8-isoPG and IL-10 had no statistics difference and serum LTB4, TNF-α, Hs-CRP levels were higher in OSAHS underwent therapy compared with the normal controls. Conclusions The results suggest that inflammation and oxidative stress are activated and antiflammatory cytokines are decreased in the OSAHS patients. The serum levels of 8-isoPG, LTB4 , TNF-α, Hs-CRP and IL-10 may prove to be useful in severity monitoring and intervention efficacy judgement in OSAHS patients.
Objective To investigate the role of T helper 17 ( Th17) cells and CD4 + CD25 + Foxp3+regulatory T cells ( Treg) in the pathogenesis of asthma in a mouse model. Methods Twenty-four BALB/ c mice were randomly divided into an asthma group and a normal control group, with 12 mice in each group.Asthma model was established by ovalbumin sensitization and aerosol challenge in the asthma group. Airway reactivity was measured by plethysmography. The total and differential cell counts in bronchoalveolar lavage fluid ( BALF) were measured. The ratio of Th17 and Treg cells to mononuclear cells in the spleens of mice were detected by flow cytometry. The levels of IL-17 and IL-10 in BALF and lung homogenates were measured by ELISA. Results The bronchial provocation test showed that the average lung resistance increased remarkably in the asthma group. In spleens of the asthmatic mice, the percentage of Th17 cells was significantly higher [ ( 5.68 ±1. 99)% vs ( 2.80 ±0. 82) %, P lt; 0. 01] , and the percentage of Treg cells was significantly lower [ (2.88 ±0. 46) % vs ( 6.10 ±2.44) % , Plt; 0. 01] , with the ratio of Th17 to Treg significantly increased( 1. 93 ±0. 41 vs 0. 50 ±0. 15,P lt;0. 01) . In BALF and lung homogenates of the asthma group, the level of IL-17 was significantly higher[ ( 22. 37 ±3. 00) pg/mL vs ( 11. 42 ±2. 15) pg/mL, ( 52. 93 ±5. 39) pg/mL vs ( 19. 38 ±2. 65) pg/mL, both Plt; 0. 01] , and the level of IL-10 was significantly lower[ ( 6. 05 ±1. 25) pg/mL vs ( 14. 23 ±2. 94) pg/mL, ( 9. 33 ±1. 79) pg/mL vs ( 21. 40 ±2. 44) pg/mL, both P lt; 0. 01] compared with the control group.Conclusion The imbalance of Th17/ Treg plays an important role in the pathogenesis of asthma.
Objective To investigate the changes of interleukin-17 ( IL-17) and the effects of propofol in rats with acute lung injury ( ALI) . Methods ALI model was established by hydrochloric acid ( HCl) inhalation in a dose of 2 mL/kg. 35 adultmale SD rats were randomly divided into seven groups, ie.a control group, a HCl group, and five propofol groups ( T24b , T12b , T0 , T1a , T3a groups, respectively) . The T0 ,T24b and T12b groups were pretreated with intraperitoneal propofol injection 0, 24 and 12 hours respectively before HCl inhalation. The T1a and T3a groups were managed by intraperitoneal propofol injection 1 and 3 hours respectively after HCl inhalation. Immunohistochemistry was used to determine the expression of IL-17 in lung tissue. ELISA was adopted to detect the levels of IL-17 and IL-8 in lung tissue homogenate as well as in bronchoalveolar lavage fluid ( BALF) , meanwhile arterial partial pressure of oxygen ( PaO2 ) and myeloperoxidase ( MPO) were measured. Results Those rats in the HCl group appeared respiratory distress, cyanosis, pulmonary edema, and inflammatory cells infiltration in lung tissues after HCl inhalation.The IL-17 levels in lung tissue homogenate as well as in BALF were higher in the HCl group than those in the control group( all P lt; 0. 01) . IL-17 was mainly expressed in alveolar epithelial cells and mononuclear cells in the ALI rats and its expression level was higher than that in the control group. IL-17 concentration in lung tissue homogenate was both correlated with IL-8 concentration in lung tissue homogenate ( r=0. 98, P =0.003) and with the activity of MPO in lung tissue( r=0. 981, P =0. 003) in the HCl group. Mainwhile, a same significant correlation was found between IL-8 level in lung tissue homogenate and the MPO activity in the HCl group( r =0. 961, P =0. 009) . Propofol attenuated lung injury induced by HCl inhalation, especially in T24b group. The concentrations of IL-17 in lung tissue homogenate and in BALF were lower in T24b group when compared with the HCl group( P = 0. 011, P =0. 003, respectively) . Conclusions The expression of IL-17 increases in ALI rats. Pretreatment with propofol by 24 hours has obvious inhibiting effects on inflammatory reaction. Inhibiting IL-17 expression may be one of the mechanisms through which propofol inhibits the inflammatory reaction of ALI.