Levels of IL-17, IL-8 and VEGF in bronchoalveolar lavage fluid in asthma children

AIM: To investigate the mechanism of airway inflammation in children with asthma by determining the levels of IL-17, IL-8 and vascular endothelial growth factor(VEGF) in bronchoalveolar lavage fluid (BALF). METHODS: Eighty-eight children were enrolled in the study and divided into asthma group (n=52), pneumonia group (n=25) and control group (n=11). BALF were collected from all 88 cases. The levels of IL-17, IL-8, VEGF, IL-4 and IFN-γ in BALF were measured by ELISA. The cell types in BALF were determined. RESULTS: Compared with the control, the levels of IL-17 and IL-8 were significantly elevated in asthma group and pneumonia group (all P<0.05). The level of IL-8 (P<0.05) in the patients with asthma was lower than that in the pneumonia patients. No statistical difference of the IL-17 level between asthma group and pneumoniae group was observed (P>0.05). Compared with pneumonia group and control group, the level of VEGF was significantly increased in asthma group (all P<0.01), and the VEGF level among control group and pneumonia groups was almost similar (P>0.05). The levels of IL-4 and IFN-γ, and ratio of IL-4/IFN-γ among groups were not statistically different. The percentage of neutrophils in BALF was significantly higher in asthma group and pneumonia group than that in control group (all P<0.01). CONCLUSION: IL-17, IL-8 and VEGF play important roles in airway inflammation in children with asthma. Th17 cells may participate in the pathogenesis of asthma in children.     

Change of intestinal flora and its relationship with IL-23/IL-17 axis in patients with ulcerative colitis

AIM:To investigate the change of intestinal flora distribution and its relationship with interleukin-23 (IL-23)/IL-17 axis in ulcerative colitis (UC) patients. METHODS:The fresh fecal samples from 20 patients with active UC and 20 healthy controls were collected. The distribution of the flora was analyzed by direct smear and traditional bacterial culture. The changes of bacteria were detected by real-time PCR. The hemoglobin, albumin, erythrocyte sedimentation, and C-reactive protein levels were tested routinely. Both normal and damaged mucosal tissues of UC patients were examined and obtained by colonoscopy, and further assessed by Mayo scoring, Baron grading and HE staining. The expression of IL-17 and IL-23 was observed by immunohistochemistry and Western blot. RESULTS:(1) The degree of flora imbalance in active UC patients was higher than that in the healthy controls (P<0.05). (2) The results of aerobic culture showed that the number of Escherichia coli in the UC patients was significantly lower than that in the normal controls (P<0.01), while Enterococcus was increased obviously (P<0.01). The results of anaerobic culture revealed that the numbers of Bacteroidetes, Bifidobacterium bifidum and Lactobacilli in the UC patients were significantly decreased (P<0.01). (3) Quantitative analysis of target bacteria showed that the relative quantification of Escherichia coli, Bacteroidetes, Bifidobacterium bifidum and Lactobacilli in the UC patients was significantly lower than that in the normal subjects, and the number of Enterococcus was significantly increased (P<0.01). (4) Compared with control group, no significant change of hemoglobin in the UC patients was ovserved, albumin was significantly decreased (P<0.05), but erythrocyte sedimentation and C-reactive protein levels were elevated obviously (P<0.01). (5) The Mayo score, Baron grade, and histopathological score were all increased (P<0.01). (6) High IL-17 and IL-23 expression levels were detected in the UC patients (P<0.01). (7) Correlation analysis showed that the average absorbance values of IL-17 and IL-23 expression were positively correlated with Baron grade (r=0.717, P=0.02; r=0.849, P=0.016) and pathological score (r=0.660, P=0.03; r=0.675, P=0.032). Meanwhile, the average absorbance value of IL-23 expression was negatively correlated with the number of Escherichia coli (r=-0.699, P=0.025), and positively correlated with Enterococcus (r=0.872, P=0.010). Furthermore, the average absorbance value of IL-17 expression was positively correlated with Enterococcus (r=0.764, P=0.046), and both of them were not correlated with other bacteria. CONCLUSION:Obvious flora imbalance exists in active UC patients, changed intestinal microflora is closely related with the degree of inflammation. IL-23/IL-17 axis, as a key factor in the development of UC, may be related to the changes of intestinal microflora. The interaction between intestinal microflora and IL-23/IL-17 axis plays an important role in the pathogenesis of UC.     

Proportion of CD14+CD16+ monocytes in peripheral blood from patients with type 2 diabetic mellitus and effect of LPS and IL-15 on expression of STAT5 in monocytes

AIM: To characterize the proportion of CD14⁺CD16⁺ monocytes in peripheral blood from type 2 diabetes (T2DM) patients and to observe the response of CD14⁺CD16⁺ monocytes to lipopolysaccharide (LPS) and interleukin-15 (IL-15) for further exploring the potential mechanism of inflammatory immune response in the pathogenesis of T2DM. METHODS: Twenty-eight patients with T2DM and 20 healthy volunteers were enrolled in the study. The peripheral blood was collected for determining the percentage of CD14⁺CD16⁺ monocytes by flow cytometry. The peripheral blood mononuclear cells (PBMC) were isolated and subject to stimulation with LPS and IL-15 for 4 h. The protein expression of STAT5 was detected by Western blotting and the phosphorylated (p)-STAT5 was determined by Western blotting and immunofluorescence. Serum levels of 25-hydroxyvitamin D₃ and IL-6, and the concentrations of IL-6 and monocyte chemoattractant protein-1(MCP-1) in the culture supernatants were assessed by ELISA. Serum level of C-reactive protein (CRP) was measured by immunoturbidimetry. RESULTS: There were positive correlations between the quantity of CD14⁺CD16⁺ monocytes and serum levels of CRP and IL-6 (r=0.394, P<0.05 and r=0.741, P<0.01), while serum 25 (OH) D₃ was negatively correlated with the quantity of CD14⁺CD16⁺ monocytes (r=-0.409, P<0.01), serum CRP(r=-0.479,P<0.01) and serum IL-6 (r=-0.774,P <0.01). After stimulated with LPS and IL-15, PBMC showed significant up-regulation of p-STAT5 protein expression, and significant increases in the supernatant levels of IL-6 and MCP-1 were observed (P<0.05). The expression of p-STAT5 existed in the nucleus.CONCLUSION: These findings suggest that the functional disturbance in monocytes occurs in T2DM, which may be related to insufficiency of vitamin D₃. The aberrant activation of STAT5 signaling pathway underlies the functional abnormalities of the monocytes in T2DM.     

Elevated levels of serum IL-6, ICAM-1 and P-selectin in stable survivors with liver transplantation

AIM: To study the profile of serum IL-6， ICAM-1 and P-selectin in stable survivors with clinical liver transplantation (LTx). METHODS: Flow cytometric analysis was used to determine the phenotype of T cell subsets in peripheral blood mononuclear cells （PBMCs） from stable survivors with liver transplantation (n=22), and healthy volunteers (n=12). Serum levels of the pro-inflammatory cytokines, tumor necrosis factor (TNF-α) and interleukin (IL-6), intercellular adhesion molecules (ICAM-1) and P-selectin in stable survivors with liver transplantation and healthy volunteers were assessed by enzyme-linked immunoabsordent assay (ELISA). Recently performed 6 cases of liver transplantation were also dynamically observed in this study. RESULTS: Percentage of CD4+ T cells， CD8+ T cells and CD3+ T cells, as well as ratio of CD4 to CD8 were no difference between two groups (P>0.05). However, a significant higher percentage of CD3+CD25+ T cells was found in stable liver transplantation group as compared to healthy group (P<0.05). Significantly increased concentrations of IL-6, ICAM-1 and P-selectin were found in stable liver transplantation group as compared to healthy group (P<0.05). A high TNF-α level was detected in stable liver transplantation group while no significant difference was found as compared to healthy volunteers group (P>0.05). There was not found no regular change of serum cytokines (IL-6, TNF-α) and adhesion molecules (ICAM-1, P-selectin) in 6 liver transplanted patients during post-operation from day 1 to day 30, indicating that was associated with the different status of patients before or after transplantation. CONCLUSIONS: Our data suggesting that increased levels of ICAM-1 and P-selectin, appears to participate in the processing of immunoregulation to transplanted livers, whereas elevated concentrations of IL-6 appear to be involved in the repair of the injury induced by TNF-α in allo-transplanted livers.     

Serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in patients with multiple organ dysfunction syndrome

AIM: To determine the changes of the serum levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), IL-10, C reactive protein (CRP) and D-dimer in the patients with multiple organ dysfunction syndrome (MODS) and compare the relationship between the levels of cytokines in early stage and MODS. METHODS: The serum values of TNF-α, IL-6, IL-10, CRP and D-dimer were measured in 27 patients with MODS in 1 d, 3 d and 5 d after undergoing disease, and compared with the adult peripheral blood of 15 normal controls. The levels in the first undergoing day between the lived group (n=19) and died group (n=8) were compared. RESULTS: The serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in MODS group were higher than that in control (P<0.05). With the development of the MODS, the levels of TNF-α, IL-6, IL-10, CRP and D-dimer were higher gradually. The level of IL-10 was increased at the third day. The levels of TNF-α, IL-6, IL-10, CRP and D-dimer in the first day of MODS in died group were higher than those in lived group, especially IL-6 and D-dimer (P<0.01). CONCLUSION: Determining the serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in MODS patients is helpful to guide the diagnosis and outcome.     

Protective effects and mechanism of astragalus injection on asthmatic rats

AIM: To explore the protective effects and mechanism of astragalus injection on asthmatic rats.METHODS: OVA was injected intraperitoneally and inhaled to produce the asthmatic model.Forty rats were randomly divided into five groups: control group,asthma group and astragalus groups of high,medium and low dose.The concentrations of IL-4,IFN-γ in BALF,the expression of IL-4 mRNA,IFN-γ mRNA and phospho-p38 MAPK in lung tissues were respectively measured by ELISA,RT-PCR and Western blotting.The number of inflammatory cells in BALF and histropathology changes were observed.RESULTS: In asthmatic group,the number of inflammatory cells and the concentrations of IL-4 in BALF and the expression of IL-4 mRNA,phospho-p38 MAPK in lung tissue were higher,but IFN-γ and IFN-γ mRNA were lower than those in normal control rats (P<0.01).In astragalus group,the number of inflammatory cells,the concentrations of IL-4 in BALF and the expression of IL-4 mRNA,phospho-p38 MAPK in lung tissue were lower,but IFN-γ and IFN-γ mRNA were higher than those in normal control rats (P<0.01),and histropathology damage was alleviated significantly.The efficacies in the astragalus groups of high,medium and low dose were similar,which no significant difference was observed among them.There were positive correlations between the expression of 〖JP3〗phospho-p38 MAPK and the number of eosinophil,the concentration of IL-4,IL-4 mRNA (r=0.63,r=0.69,r=0.71,〖JP〗 P<0.01),and negative correlations between the expression of phospho-p38 MAPK and IFN-γ and IFN-γ mRNA (r=-0.65,r=-0.68,P<0.01).CONCLUSION: p38 MAPK may play a role in pathological process of asthma.Astragalus effectively treats asthma by inhibiting the expression of phospho-p38 MAPK,correcting the inbalance of IFN-γ/ IL-4 and decreasing the number of inflammatory cells.     

Plasma levels of endothelin-1, nitric oxide,malondialdehyde and superoxide dismutase in rats exposed to infrasound

AIM: To observe the changes of NO, ET-1, SOD and MDA levels in plasma of rats exposed to infrasound. METHODS: Using infrasound (frequency: 8 Hz; sound pressure level:130 dB), the rats were exposed for 1 d， 7 d， 14 d， 21 d and 28 d, 2 h daily, then the levels of NO, ET-1, SOD and MDA were measured after exposure. RESULTS: The changes of NO levels in plasma significantly declined at 7 d and 14 d （P<0.01）, then 1, 21 and 28 d normally （P>0.05）. The changes of ET-1 levels in all groups in plasma were significantly increased （P<0.01）, mostly at 7 d, least at 14 d. The changes of SOD activity in all groups in plasma were significantly declined （P<0.01）. The changes of MDA levels in all groups in plasma were significantly increased （P<0.01）. CONCLUSIONS: Infrasouns induces changes of NO, ET-1, SOD and MDA in rat plasma, and it depends on infrasound exposure time.     

Preliminary study of IL-17 signal transduction pathway in peripheral blood mononuclear cells from lupus nephritis patients

AIM: To investigate the role of IL-17 and its signal conduction component-JNK activity in the pathogenesis of LN. METHODS: Peripheral blood mononuclear cells (PBMC) were separated and cultured from 15 cases of active lupus nephritis (LN) patients. IL-6 level was detected by ELISA, IL-6 mRNA was checked with RT-PCR, and JNK activity was measured by Western blot. RESULTS: At same IL-17 end concentrations, there was a much higher level of IL-6 in LN group than in control group (all P<0.05). IL-17 induced a significant elevation of IL-6 mRNA expression and JNK activity in PBMC from LN patients in a time- and dose-dependent manner, which could be blocked markedly by IL-17 monoclonal antibody, mIgG₂₈, and dexamethasone. Much higher IL-6 mRNA expression was observed in LN group than in control group under medium culture or IL-17-conditioned culture (all P<0.01). Under medium culture or IL-17-conditioned culture, there was much higher JNK activity of PBMC in active LN group than that in control group. There was a positive linear correlation between PBMC JNK activity and their SLEDAI or IL-6 mRNA expression level in LN patients (r1=0.638, P<0.01; r2=0.644, P<0.01). CONCLUSION: These results suggest that IL-17 may take part in the initiation and progression of LN through induction of IL-6 overexpression by PBMC,and JNK hyperactivity may be necessary in the IL-17 signal transduction.     

Effects of baicalin on serum levels of IL-6 and IL-4 in mouse periodontitis

AIM: To investigate the effect of baicalin on experimental periodontitis in mouse model by comparing the histological changes in periodontal tissues and serum levels of inter leukin(IL)-6/IL-4 in mice, and to analyze the role of baicalin in immune regulation and anti-inflammatory mechanisms. METHODS: Twenty-seven male Kunming mice (SPF grade, 12-week-old) were randomly divided into 3 groups. The naive mice were used in normal control group. In experimental periodontitis group, the periodontitis model was produced by ligature of braided silk around the first maxillary molar and inoculation with putative periodontopathic bacteria. Five weeks after the ligature, the mice were fed with 10% glucose, and gavaged with distilled water. In baicalin treatment+periodontitis group, the periodontitis model was induced as above, then gavaged with baicalin at the beginning of the fifth week after the ligature. The mice were sacrificed at week 4, 6 and 8. The histological changes of the periodontal tissues were observed under microscope with hematoxylin and eosin (HE) staining. The serum level of IL-6 and IL-4 in the mice were determined by ELISA. RESULTS: The periodontal tissues showed moderate inflammatory damages in experimental periodontitis group. The periodontal destruction was significantly reduced in baicalin treatment+periodontitis group. The serum level of IL-6 in experimental periodontitis group was significantly higher than that in control group and baicalin treatment+periodontitis group (P<0.01), and the serum level of IL-6 in baicalin treatment+periodontitis group was significantly lower than that in periodontitis group at week 6 and 8 (P<0.01). The serum level of IL-4 in periodontitis group was significantly lower than that in control and baicalin treatment+periodontitis group (P<0.01). The serum level of IL-4 in baicalin treatment+periodontitis group was significantly higher than that in periodontitis group at weeks 6 and 8 (P<0.01).CONCLUSION: The pathogenesis of periodontitis is closely related to the imbalance of Th1/Th2 cytokines, characterized by increased serum level of IL-6 and the decreased serum level of IL-4. Baicalin plays a significant role in treating mouse periodontitis by decreasing the serum level of IL-6 and increasing the serum level of IL-4.     

Polymorphisms in IL-4 and IL-4R genes in children with allergic asthma

AIM: To determine whether interleukin 4 and interleukin 4 receptor α chain are associated with allergic asthma in children and to study the impact of such polymorphism upon plasma IgE.METHODS: Two polymorphism sites of IL-4 and IL-4R were studied by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).RESULTS: (1)The results showed that the IL-4 promoter -589 was not associated with children allergic asthma, however, the IL-4R α chain 576RR genotype and R allele were significantly increased in the subjects with asthma in children compared with age-matched control subjects (χ2=11.84, P＜0.01; χ2=13.03, P＜0.01). The IL-4R α chain 576RR genotype was associated with higher plasma IgE. CONCLUSION: These date suggest that the IL-4R α chain R576 is a risk factor of allergic asthma in children in Chinese, and is also related with higher plasma IgE level.     

Expression of PCNA,IL-6,IL-11 and galectin-3 in human umbilical cord mesenchymal stem cells during long-term culture

AIM: To investigate the changes of the mRNA and protein levels of proliferating cell nuclear antigen(PCNA),interleukin-6(IL-6),IL-11 and galectin-3 in human umbilical cord mesenchymal stem cells (hUC-MSCs) during long-term culture in vitro. METHODS: Human umbilical cords from neonates via caesarean section were collected, and the hUC-MSCs were isolated and sub-cultured. The cells and culture supernatants at passages 3, 8, 18, 28 and 33 were collected. The mRNA expression and protein secretion of PCNA,IL-6,IL-11 and galectin-3 in different passages of hUC-MSCs were detected by qRT-PCR, ELISA, and Western blotting. RESULTS: The mRNA expression of PCNA,IL-6 and IL-11 and protein secretion of IL-6 and IL-11 reduced gradually along with the passage.Comparing the 33rd passage with the 3rd passage of MSCs, the mRNA expression of PCNA,IL-6 and IL-11 decreased by 33%, 56% and 37%, and the protein secretion decreased by 50.3% and 58.9%, respectively. The differences were statistically significant (P<0.01). No statistically significant difference of galectin-3 mRNA expression and the protein band brightness (P>0.05) in the MSCs among different passages was observed. CONCLUSION: The multiplication and haematogenesis support capabilities of the might decrease or even lose during long-term culture in vitro. Long-term culture might have no effect on hUC-MSCs immunoregulatory capability of hUC-MSCs, which requires further study.     

Effect of recombinant plasmids encoding IL-1RII and IL-1RAcP on rat experimental autoimmune myocarditis and possible mechanism

AIM To evaluate the effects of recombinant plasmids encoding interleukin-1 type II receptor （IL-1RII） and interleukin-1 receptor accessory protein （IL-1RAcP） on rat experimental autoimmune myocarditis （EAM） and the possible mechanism. METHODS The recombinant plasmids pCAGGS-IL-1RII and pCAGGS-IL-1RAcP were constructed， and pCAGGS-SP （signal peptide） served as the control plasmid. Male Lewis rats （n=29） were divided into 4 groups： control group （rats without immunization or injection， n=5）， EAM+SP group （immunized rats injected with pCAGGS-SP， n=9）， EAM+IL-1RII group （immunized rats injected with pCAGGS-IL-1RII， n=8） and EAM+IL-1RII+IL-1RAcP group （immunized rats injected with pCAGGS-IL-1RII and pCAGGS-IL-1RAcP， n=7）. The rats were immunized to induce EAM on day 0， and injected with recombinant plasmids by hydrodynamics-based delivery on day 6. Echocardiography was performed， and the rats were killed on day 17. The ratio of heart weight to body weight （HW/BW） was evaluated， and the histopathological changes of the myocardial tissues were observed by HE staining. The mRNA expression of atrial natriuretic peptide （ANP）， brain natriuretic peptide （BNP） and inflammatory factors in the myocardial tissues was detected by RT-qPCR. Recombinant plasmids pUC19-IL-1RII-actin and pUC19-IL-1RAcP-tub were transfected into Cos7 cells， and the culture supernatants were collected and added to lipopolysaccharide （LPS）-induced H9c2 cells. The expression of inflammatory genes were detected by RT-qPCR. Recombinant plasmids pEGFP-IL-1RII-actin and pEGFP-IL-1RAcP-tub were transfected into the Cos7 cells to identify the formation of IL-1RII/IL-1RAcP heterodimer by co-immunoprecipitation （Co-IP）. RESULTS Compared with EAM+SP group， injection with plasmids effectively attenuated EAM in EAM+IL-1RII group and EAM+IL-1RII+IL-1RAcP group， as indicated by the decreases in HW/BW， left ventricular end-systolic diameter， and myocardial expression of ANP， BNP， TNF-α， IL-2， IFN-γ and TGF-β， and the increase in expression of IL-4 in the hearts. In LPS-induced H9c2 cells， compared with LPS group， the levels of TGF-β and IL-6 in the culture supernatants were significantly decreased （P<0.01）， and the level of IL-10 was significantly increased （P<0.05） in LPS+IL-1RII group and LPS+IL-1RII+IL-1RAcP group. Compared with LPS+IL-1RII group， the expression of TNF-α and IL-2 was significantly decreased （P<0.05）， and the expression of IL-13 was significantly increased in LPS+IL-1RII+IL-1RAcP group （P<0.01）. The formation of IL-1RII/IL-1RAcP heterodimer was detected by Co-IP. CONCLUSION Plasmids encoding IL-1RII and IL-1RAcP effectively attenuate EAM， and the possible mechanism may be related to the inhibition of inflammatory factor expression and the formation of IL-1RII/IL-1RAcP heterodimer.     

Alteration of serum IL-6, IL-8, TNF-α and sICAM-1 in patients with pre-menstruation recurrent aphthous ulceration

AIM:To investigate the serum levels of interleeukin-6(IL-6), interleukin-8(IL-8), tumor necrosis factor-alpha(TNF-α) and soluble intercellular adhesion molecule-1 (sICAM-1)in female patients with pre-menstruation recurrent aphthous ulceration(RAU).METHODS:Serum levels of IL-6, IL-8, TNF-α and sICAM-1 in 21 pre-menstruation RAU patients were examined using ELISA technique, and compared to 10 healthy individuals and 22 the female RAU patients unrelated to menstrual cycle.RESULTS:The serum levels of IL-6, IL-8, TNF-α in patients with pre-menstruation RAU were not only significantly higher than that in the normal control group(P＜0.01), but also higher than that in the RAU patients without pre-menstruous recurrence (P＜0.01).The level of serum TNF-α in the RAU patients without pre-menstruous recurrence was slightly higher than that in the normal control group(P＜0.05).The level of sICAM-1 had not changed.CONCLUSION:The serum levels of IL-6, IL-8 and TNF-α increase in pre-menstruation RAU patients, which might play a role in local lesion of RAU.     

Effect of recombinant rat CC16 protein on LPS-induced expression of TNF-α, IL-6 and IL-8 in rat tracheal epithelial cells

AIM: To explore the effect of recombinamt rat CC16 protein (rCC16) on LPS-induced expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-8 in the rat tracheal epithelial (RTE) cells.METHODS: The RTE cells were incubated with rCC16 at concentrations of 0.5, 1.0 and 2.0 mg/L in serum-free media for 2 h prior to LPS (0.1 mg/L) treatment for further 24 h. The cells were harvested for assessing the mRNA levels of TNF-α, IL-6 and IL-8 by RT-qPCR. The cell culture supernatants were collected for analyzing the protein levels of TNF-α, IL-6 and IL-8 by ELISA. In addition, the nuclear translocation of nuclear factor-κB (NF-κB) p65 was tested by Western blot.RESULTS: rCC16 inhibited LPS-induced IL-6 and IL-8 expression at both mRNA and protein levels in the RTE cells in a concentration-dependent (0~2 mg/L) manner, as demonstrated by RT-qPCR and ELISA. However, no concentration-dependent manner between the dose of rCC16 and TNF-α expression was observed, and rCC16 inhibited LPS-induced TNF-α expression at lower concentration (0.5 mg/L). rCC16 concentration-dependently inhibited the effects of LPS on the level of nuclear translocation of NF-κB p65.CONCLUSION: rCC16 suppresses LPS-mediated TNF-α, IL-6 and IL-8 production through inactivation of NF-κB activity in RTE cells.[KEY WORDS] CC16 protein; Airway inflammation; LPS; Inflammatory mediators; Nuclear factor-κB     

Changes of IL-4, IL-10, IL-12 levels in rat serum and lung during acute respiratory distress syndrome induced by oleic acid

AIM:To observe the dynamic changes of interleukin-4(IL-4), IL-10, IL-12 in rat serum and lung tissues during acute respiratory distress syndrome (ARDS).METHODS:The ARDS model of rats was induced by intravenous injection of oleic acid. The levels of IL-4, IL-10, IL-12 in serum and the supernatant of lung tissues were measured by enzyme linked immunosorbent assay (ELISA).RESULTS:The Levels of serum and lung IL-10, IL-12 in ARDS rats were increased in 4 h, 8 h, 16 h group compared with control group. The levels in IL-10 in serum in 16 h group and IL-10 in lung tissues of 8 h group were lower than that in 4 h group. The Levels of IL-4 in serum in 4 h, 8 h group were higher than that in control group, while IL-4 in 16 h group was lower than that in 8 h group. IL-4 of lung tissues in 4 h, 8 h, 16 h group were increased significantly, but in 16 h group were lower than that in 8 h group. The biggest changes of pulmonary coefficient and histopathology were observed at 4 h after injection of oleic acid.CONCLUSIONS:IL-4, IL-10 and IL-12 might play important roles in inflammatory reaction induced by oleic acid. The pro-and anti-inflammatory cytokines produced successively during ARDS.The relationship between unbalanced cytokines and lung injury in ARDS needs to be further studied.     

Advance in biological properties of IL-38 and its role in pulmonary diseases

Interleukin-38 （IL-38） is the most recently discovered cytokine of the IL-1 family and is an IL-36 receptor inhibitor. IL-38 is mainly expressed in human immune organs and associated with a variety of diseases. In the process of apoptosis and necrosis caused by injury or inflammation， researchers have studied quiet a lot about the kinase， cleavage sites， activity regulatory mechanism， signal transduction ligand， transduction mode and potential receptors of IL-38， but many mechanisms are still unknown. This article reviews the role of IL-38 in the pathogenesis and progression of lung tumors， asthma and interstitial lung disease. We also discussed the role of IL-38 in the treatment of these diseases， the possible relationship between IL-38 and tuberculosis， and the direction of future studies on the mechanism of IL-38 action.