A new independent subtype CD4+ T cell which massively secreted interleukin-17 (IL-17) was found at the beginning of the 21st century, and thus it was named as T helper cell 17 (Th17 cell). With the progress of the research in recent years, Th17 cells were found to be widely involved in a variety of the human diseases such as autoimmune diseases, infections and tumors through secretion of IL-17. The relationship between Th17 cells, IL-17 and the occurrence, development and prognosis of lung cancer was reviewed.
Objective To explore the role of macrophage-stimulating protein ( MSP) and receptor tyrosine kinase RON in the airway inflammation of chronic obstructive pulmonary disease( COPD) , and investigate its possible mechanism. Methods The rat COPDmodel was established by exposing the rats to cigarette smoke daily for three months. Rat alveolar macrophages ( AMs) were isolated in vivo and cultured,and then challenged with different concentrations of MSP for 24 hours. The concentrations of MSP in broncho-alveolar lavage fluid ( BALF) and serum, and the levels of IL-1β, TNF-α, IL-8, and IL-10 in the supernatants were measured by ELISA. The expression of RONmRNA in lung tissue was assessed by reverse transcription-polymerase chain reaction. The levels of RON protein in the lung tissue and AMs cultured in vitro were observed by immunohistochemistry. The activity of superoxide dismutase ( SOD) and malondialdehyde ( MDA) content in the culture solution were measured with chromatometry method. Results Compared with the control group, the concentrations of MSP in serum and BALF of the COPD rats were significantly higher ( P lt;0. 01) . The levels of RONmRNA and RON protein in the COPD rats were also upregulated significantly ( P lt; 0. 01) . MSP evoked the AMs isolated from the normal and COPD rats to generate more content of MDA and caused a reduction in activity of SOD. In addition, MSP stimulated TNF-α, IL-8, IL-1βand IL-10 release fromAMs of the normal and COPD rats dose-dependently. The levels of TNF-α, IL-8, and IL-1βwere higher, while the level of IL-10 and the SOD activity were lower in AMs of the COPD group than those of the control group in the same dose of MSP ( P lt;0. 01) . The more significant increase in the levels of TNF-α, IL-8, IL-1β, and the more notable decrease in the activity of SOD was found in the COPD group compared with the control group. But the degree of increasing MDA and IL-10 in the AMs of the COPD group was lower than that in the control group. Linear correlation analysis showed that the MSP concentration and the RON protein level in the COPD rats were positively associated with the total cellcounts and AM counts in BALF, and were related to the indexes for pulmonary emphysema. Conclusions There is a close correlation between the MSP and receptor tyrosine kinase RON with the airway inflammation of COPD. The mechanism might be that MSP promote the macrophages release inflammatory factors and increase the production of oxygen free radicals.
Objective This study aims to investigate the changes of inflammatory markers of oropharynx and its correlation with prognosis in the stable phase of chronic obstructive pulmonary disease (COPD). Methods Sixty-two patients with COPD in stable stage were divided into smoking and non-smoking groups, and 31 healthy persons were selected as controls. The pharyngeal swabs were collected to determine tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), collagen type Ⅳ (COL-4), and fibronectin (FN) by an enzyme-linked immunosorbent assay. Meanwhile, eosinophil count and C-reactive protein (CRP) in peripheral blood were measured. The correlations between the above metrics and COPD and the prognosis of the patients were analyzed. Results TNF-α, IL-8, COL-4, FN and CRP levels in patients with COPD were significantly higher compared with control groups (P<0.05), and there were significant differences between smoking and non-smoking groups in inflammatory markers such as TNF-α, IL-8, FN, CRP (P<0.05). The forced expiratory volume in one second (FEV1) and FEV1%pred of patients with COPD were significantly lower than the control group (P<0.05). The smoking index of patients with COPD in smoking group was significantly higher than that in smoking control group (P<0.05). TNF- α and IL-8 were positively associated with blood CRP in patients with COPD. Conclusion The inflammatory markers of oropharynx in patients with COPD are different from those in healthy persons and smoking may promote the increase of inflammatory markers of oropharynx in patients with COPD; the non-invasive detection of paired pharyngeal inflammatory markers may be helpful in determining acute onset and prognosis.
Objective To investigate the difference of anticoagulant efficacy of heparin and citric acid during continuous renal replacement therapy (CRRT) in patients with severe acute pancreatitis, and analyze their effects of on filter life span, length of hospital stay and mortality. Methods Patients with severe acute pancreatitis in Intensive Care Unit of the First Affiliated Hospital of Hebei North University between January 2018 and July 2022 were retrospectively enrolled, and they were divided into heparin group (control group) and citric acid group (research group) according to anticoagulation methods. The differences of anticoagulant catheter blockage during CRRT, filter life span, length of hospital stay, and 90-day mortality between the two groups were analyzed. Results A total of 108 patients were enrolled, including 56 in the research group and 52 in the control group. In pre-CRRT treatment, the balance value of fluid intake and outflow in the research group was significantly lower than that in the control group (P<0.05). The 108 patients received 217 times of CRRT treatment totally, with a median length of treatment of 63 h (range 44-87 h). The severity of catheter blockage in the research group was lower than that in the control group (P=0.003). The filter life span was longer in the research group than that in the control group [42.5 vs. 29.0 h; hazard ratio=1.83, 95% confidence interval (1.23, 2.73), P<0.001]; in the comparison of 90-day mortality, there was no significant difference between the two groups (P>0.05). The mean use of filters in the research group was less than that in the control group (1.93±0.09 vs. 2.17±0.14, P<0.001). The downtime of CRRT due to filter life in the research group was obviously shorter than that in the control group [120 (0, 720) vs. 300 (0, 890) min, P=0.029], while the duration of CRRT in the research group was remarkably better than that in the control group [10.6 (4.9, 27.7) vs. 8.1 (3.6, 25.0) d, P=0.024], and the risk of filter replacement due to special conditons in the research group was lower than that in the control group (46.4% vs. 65.4%, P=0.048). There was no statistically significant difference in the length of intensive care unit hospitalization or total hospitalization between the two groups (P>0.05). Conclusion Both heparin and citric acid could assist the treatment of CRRT, while citric acid might be apt to improve local coagulation and systemic inflammatory response.
Objective To investigate the protective effect of annexin A1 (ANXA1) derived from human umbilical cord mesenchymal stem cells (HucMSCs) on lipopolysaccharide (LPS) -induced acute lung injury (ALI). Methods Six-week-old male C57BL/6 mice were randomly divided into a sham group, a LPS group, a LPS+HucMSC-cm (LPS+cm) group, a LPS+nc-cm group, and a LPS+si-cm group, with 6 mice in each group. LPS (5 mg/kg) was intratracheally injected to induce ALI model. Then, normal saline, HucMSC-cm (HucMSC conditioned medium), HucMSC-nc-cm (normal ANXA1 expression) and HucMSC-si-cm (knockout of ANXA1) were injected intratracheally with 50 μL each after LPS treatment for 4 hours. After 72 hours of LPS administration, the mice were killed, and the blood and lung tissues were retained. After corresponding treatment, the blood and lung tissues were preserved. The expression of IL-6 in peripheral blood of mice was detected by enzyme-linked immunosorbnent assay, the pathological changes of lung tissues were observed by hematoxylin-eosin staining, and the expressions of interleukin-6 (IL-6) and vascular cell adhesion molecule-1 (VCAM-1) in lung tissues of each group were detected by Western blot and immunohistochemistry. Results Compared with the sham group, the lung histopathology of mice in the LPS group showed significantly increased inflammatory factor infiltration, alveolar collapse, and lung tissue structure destruction as well as lung tissue injury score and wet/dry weight ratio (W/D) increased (all P<0.05). Accordingly, IL-6 and VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were increased (all P<0.05). Compared with the LPS group, the pathological injury of lung tissue in the LPS+cm group was improved, the lung tissue injury score and the W/D ratio decreased while IL-6, VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were decreased (all P<0.05). But there were no significant differences between the LPS+cm group and the LPS+ nc-cm group (all P>0.05). Compared with the LPS+nc-cm group, lung tissue pathological injury was aggravated again, lung tissue injury score and W/D were also increased in the LPS+si-cm group (all P<0.05). IL-6 and VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were increased again (all P<0.05). Conclusion ANXA1 derived from HucMSCs has certain protective effect in LPS-induced ALI model.
Objective To study the effect of interleukin-6,10 (IL-6,10), C-reactive protein (CRP), and fibrinogen (FIB) on inflammatory response of lower limbs deep vein thrombosis (DVT). Methods Thirty patients with acute lower limb DVT (DVT group) and 30 volunteers (normal control group) were included in this study, and then the concentrations of serum IL-6, IL-10, CRP, and FIB were detected. Results The concentrations of serum IL-6, IL-10, CRP, and FIB of patients in DVT group before treatment were higher than those in normal control group (Plt;0.001). Compared with before treatment, the concentrations of serum IL-6, CRP, and FIB of patients after treatment were lower in DVT group (Plt;0.001), however, the concentration of serum IL-10 was higher (Plt;0.001). There was no difference of the concentrations of serum FIB between DVT group after treatment and normal control group (Pgt;0.05), but the concentrations of serum IL-6, IL-10, and CRP of patients in DVT group after treatment were higher than those in normal control group (Plt;0.05). Conclusion Inflammatory factors may involve in DVT. Therein IL-6, CRP, and FIB play important roles in acute stage of DVT, and IL-10 may have an anti-inflammatory effect.
ObjectiveTo explore the effect of preoperative glucocorticoid on systemic inflammatory indexes and pulmonary inflammation after radical esophagectomy.MethodsA total of 44 patients with esophageal cancer treated in the First Affiliated Hospital of Xiamen University from July 2019 to September 2020 were selected and randomly divided into an intervention group and an observation group by random number table. There were 22 patients in the intervention group, including 20 males and 2 females with an average age of 62.86±5.22 years and 22 patients in the observation group, including 19 males and 3 females with an average age of 63.00±6.19 years. Two groups were given thoracoscope-assisted incision via right chest, upper abdomen and left neck. The intervention group was given an intravenous infusion of methylprednisolone 500 mg before induction of anesthesia, and the observation group was given the same dose of normal saline. The second generation cephalosporins were routinely used to prevent infection in the two groups. The levels of interleukin-6 (IL-6) and C-reactive protein (CRP), lymphocyte and neutrophil count before operation and 1 day, 3 days and 5 days after operation were recorded and compared between the two groups. Utrecht Pneumonia Scoring System (UPSS) score 1 day after operation, the healing of the surgical incision and the anastomotic leakage within 2 weeks after the operation were evaluated.ResultsThe level of IL-6 in the intervention group was significantly lower than that in the observation group at 1 hour and 1 day after operation (both P<0.05). CRP showed significant difference between the two groups 2 days after operation (P=0.044). The white blood cell count in the intervention group was significantly less than that in the observation group 1 day and 3 days after operation (both P<0.05). There was no significant difference in lymphocyte or neutrophil count between the two groups 1 day after operation. There was no significant difference in the rate of non-grade A wound healing or the incidence of anastomotic leakage between the two groups within 2 weeks after operation. The pneumonia score of UPSS in the intervention group was lower than that in the observation group 1 day after operation (P=0.027).ConclusionThe use of glucocorticoid before radical esophagectomy can reduce the systemic inflammatory reaction and improve the short-term postoperative pulmonary inflammation. At the same time, no adverse effect on the healing of surgical incision and anastomotic stoma is found, which has certain safety.
ObjectiveTo investigate the changes of interleukin-8 (IL-8), tumor necrosis factor-α(TNF-α) and phospholipase A2 (PLA2) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue of COPD rats and the effects of tiotropium.To identify the anti-inflammatory function of tiotropium. MethodsRat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide(LPS).Thirty male SD rats were randomly divided into a control group, a COPD group and a tiotropium bromide treatment group (n=10 in each group).The pathologic changes of the lung tissue and airway were observed by HE staining.The total and differential cell counts in BALF were observed.The levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue were measured by enzyme-linked immunosorbent assay. ResultsHE staining revealed that the rat COPD model was successfully established.The COPD group appeared obvious emphysema, while the treatment group appeared mild emphysema.The total inflammatory cells, the proportion of neutrophils and lymphocyte, and the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue in the COPD group were obviously higher than those in the control group (P < 0.01).The total inflammatory cells, the proportion of neutrophils and lymphocyte, and the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue in the treatment group were significantly lower than those in the COPD group but higher than those in the control group (P < 0.01). ConclusionsTiotropium bromide can reduce the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue of COPD rats by reducing the leakage of inflammatory cells, and alleviate the airway inflammation and the degree of emphysema.
Objective To investigate the effects of glutathione S-transferase M5 (GSTM5) on the inflammation in human bronchial epithelial 16HBE cells and its possible molecular mechanisms. Methods Acute lung injury cell model was constructed with 16HBE cells induced by tumour necrosis factorα (TNF-α, 10 ng/mL). The cells were devided into a control group, a TNF-α group (TNF-α), a GSTM5 group (GSTM5+TNF-α), a negative control group (negative control plasmid+TNF-α). GSTM5-GFP plasmid and negative control plasmid were respectively transfected to the cells of the GSTM5 group and the negative control group using Lipofectamine2000. The contents of interleukin-6(IL-6), IL-8, IL-10 in the cell supernatant were measured by ELISA.The expression of nuclear factor-κB (NF-κB) mRNA was detected by RT-PCR, and the expression of NF-κB, phospho-NF-κB, p38, phospho-p38 protein were detected by Western blot. Results The GSTM5-GFP eukaryotic expression vector was successfully constructed and transfected successfully confirmed by fluorescence microscope. The contents of IL-6, IL-8, IL-10 in the TNF-α-induced cell supernatant were significantly higher than those in the control group(P < 0.05), and the contents of IL-6, IL-8, IL-10 in the GSTM5 group were lower than those in the TNF-α group (P < 0.05)with statistically significant difference. At the same time, the total NF-κB mRNA, phospho -NF-κB and phospho-p38 protein were increased in TNF-α stimulated cells compared with the control group (P < 0.05), while the GSTM5 group was lower than that in the TNF-α group and the negative control group (P < 0.05). Conclusion Overexpression of GSTM5 inhibits the phosphorylation of p38MAPK and NF-κB and down-regulates the inflammation of TNF-α-induced human bronchial epithelial 16HBE cells.