Therapeutic Effect and Mechanism of Chaige Qinlian Tang on Young Mouse MRSA Pneumonia Model / 中国实验方剂学杂志

Objective::To explore the therapeutic effect and mechanism of Chaige Qinlian Tang on pneumonia in young mice. Method::The pneumonia model was duplicated by slowly dripping Staphylococcus aureus into the nasal cavity of mice.After successful modeling, the mice were randomly divided into model group, clindamycin group, and high and low-dose Chaige Qinlian Tang groups, with sham operation group as negative control group.The rats were given 200 mg·kg-1 high-dose Chaige Qinlian Tang, 100 mg·kg-1 low-dose Chaige Qinlian Tang and 120 mg·kg-1 clindamycin.The mice were observed every day.Colonies were counted in the lungs of each group five days later.The expression levels of interleukin(IL)-16, tumor necrosis factor (TNF)-α in lung lavage fluid of each group were determined by enzyme linked immunosorbent assay (ELISA). Real-time fluorescent quantitative polymerase chain reaction (Real-time PCR) and Western blot were used to measure the expression levels of IL-16, TNF-α in lung lavage fluid of each group.The expressions of tumor necrosis factor receptor (TNFR) 1, Caspase-3 and Caspase-7 in lung and the pathological changes of lung were observed. Result::Compared with the sham operation group, the respiratory state and the activity state of the model mice were worse, and the survival rate was higher in the high-dose Chaige Qinlian Tang group.Compared with the sham operation group, the pulmonary colony counts in the model group and treatment groups were increased, compared with the model group, the lung colony counts in clindamycin group and high-dose Chaige Qinlian Tang group were improved significantly (P<0.05, P<0.01). Compared with the control group, the expression levels of IL-16, TNF-α, TNFR1, Caspase-3, Caspase-7 mRNA and protein in the lung of model group and treatment groups were significantly increased (P<0.01). Compared with model group, the expression levels of IL-16, TNF-α and TNFR1, Caspase-3, Caspase-7 in the lung of clindamycin group and high and low-dose Chaige Qinlian Tang groups were significantly increased (P<0.01). The expression levels of protein and mRNA were significantly decreased (P<0.05, P<0.01), and the pathological changes of lung were improved, especially in clindamycin group and high-dose Chaige Qinlian Tang group. Conclusion::Chaige Qinlian Tang has a certain therapeutic effect on Staphylococcus aureus pneumonia in young mice.This effect may be related to regulating TNFR1, Caspase-3 and Caspase-7 pathways, reducing the secretion of IL-16 and TNF-alpha, and enhancing the clearance of staphylococcus aureus.

Study on effects and mechanism of interleukin 16 on pathogenesis of atherosclerosis / 国际检验医学杂志

Objective To analyze the expression of interleukin 16 (IL-16) in atherosclerosis (AS) patients, and to study the roles of IL-16in the pathogenesis of AS.Methods Thirty AS patients in Affiliated Hospital of Jining Medical College from August 2015to August 2016were randomly selected as the case group and twenty-nine healthy subjects were selected as the healthy control group.Peripheral blood of the subjects were collected.IL-16levels were determined with enzyme-linked immunosorbent assay (ELISA).Reverse transcriptase-polymerase chain reaction was applied to analyze IL-16mRNA level.IL-16expression in the atherosclerotic plaque samples was detected with immunohistochemical analysis.IL-16expression in aortic atherosclerotic plaque of AS patients and atherosclerotic ApoE-/-mice were analyzed by immunohistochemical staining.The aortic plaque changes of AS mice injected intraperitoneally with recombinant IL-16were detected.Results Both IL-16protein levels and IL-16mRNA levels were higher in case group than those of healthy control group, the difference was statistically significant (P＜0.05).The IL-16mRNA was highly expressed in the atherosclerotic plaque.The aortic plaque area of the mice underwent IL-16intraperitoneal injection were decreased while the plaque stability increased.Conclusion IL-16levels elevated in both AS patients and AS mice, which suggested that IL-16might play aprotective role against AS.

Expressions of IL-16, IFN-γ and CXCR3 in plasma of patients with chronic obstructive pulmonary disease and their clinical significance / 实用医学杂志

Objective Toexplore the expressions of interleukin-16 (IL-16), interferon-γ (IFN-γ), CXC chemokine receptor 3 (CXCR3), and CRP and their clinical significance in acute exacerbation chronic obstructive pulmonary disease by observing the changes in these factors in patients with AECOPD. Methods 103 patients with AECOPD and 20 healthy controls were collected. According to the 2013 GOLD guideline, all the patients with AECOPD were divided into4 groups(group A of 21 patients, B of 30, C of 27, andD of 25). Results As compared withthe control group, plasma concentrations of IL-16, IFN-γ, CXCR3. and CRP were significantly increased in the patients with AECOPD (P < 0.01), and as the severity of the disease was elevating, these expression levels were significantly increased.While the expression levels of IL-16, IFN-γ, CXCR3, and CRP levels were significantly reduced after treatment, but they were still higherthan those in the control group (P < 0.05). The expression levels of serum IL-16, IFN-γ, CXCR3, and CRP were significantly correlated in patients with AECOPD. Conclusions Expressions of IL-16, IFN-γ and CXCR3 are significantly increased in AECOPD, which is correlated with disease severity and decreased after treatment, suggesting that these three factors may be associated with the occurrence and development of COPD.

The changes and significance of interleukin-16 and CXC chemokine receptor 3 expression in pulmonary artery of smokers with chronic obstructive pulmonary disease / 中华内科杂志

Objective To study the pathological characteristics of interleukin-16 (IL-16) and CXC chemokine receptor 3 (CXCR3) in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD). Methods We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: group NS(nonsmokers with normal lung function, n=10); group S (smokers with normal lung function, n=13); group COPD (smokers with stable COPD, n=10). The clinical datas including blood gas analysis, pulmonary function,BMI, smoking index, BODE index, six-minute-walk distance (6MWD), Medical Research Council dyspened scale (MRC), St. George Respiratory Questionnaire (SGRQ) were recorded in all subjects before the operation. We applied technique of hematoxylin-eosin staining to observe pathomorphological changes of the pulmonary arteries. The concentration of IL-16 in lung tissues were measured by ELISA. Muscularized arteries were examined with immunohistochemical methods to identify T-lymphocytes (CD_3), CD_4 T-lymphocytes, CD_8 T-lymphocytes, IL-16, CXCR3. The correlation of IL-16 and CXCR3 in muscnlarized arteries in smokers with stable COPD were analysed. Results (1) The group COPD showed the highest concentration of IL-16 in lung tissue (P <0. 01) . The concentration of IL-16 in group S was higher than group NS (P<0.05). (2) Both in group S and group COPD, the percentage of the muscularized arteries that contained CXCR3 and IL-16 were increased as compared with group NS (P < 0. 01). Moreover there were statistical significance have been observed between group COPD and group S(P < 0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes, CD_8~+ T-lymphocytes, CXCR3 (r=0.639,0. 803,0. 696; P < 0. 05 or P < 0. 01), smoking index, BODE index (r= 0.737,0. 704; P < 0. 05). There was inverse relationship between the content of IL-16 in the muscularized arteries in group COPD and forced expiratory volume in one second% predicted (FEV_1 % Pred) and 6MWD (r=-0.803,-0.787; P<0.01). We also found the intensity of CXCR3 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes,CD_8~+ T-lymphocytes(r=0.650,0.767; P<0.05), smoking index, BODE index (r=0.650,0.767; P< 0.05). There was inverse relationship between the content of CXCR3 in the muscularized arteries in group COPD and FEV_1 % Pred and 6MWD (r=-0.778,-0.774;P<0.01). Conclusions (1) Both in group S and group COPD, IL-16 and CXCR3 were mainly expressed in lymphocytes which were correlated with CD_8~+ T-lymphocytes infiltrating the muscularized arteries. There were some suggestion that IL-16 prohaly recruited CD_8~+ T-lymphocytes into muscularized arteries by enhancing the expression of CXCR3. (2) The intensity of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function that suggested pulmonary arterial inflammation might be one of the key factors associated with the progression of COPD, and inhibiting the pulmonary artery inflammation played an important role in prevention and cure of COPD.

IL-17 induces the production of IL-16 in rheumatoid arthritis

The purpose of this study was to investigate the expression of IL-16 in the rheumatoid synovium and the role of inflammatory cytokines and Toll-like receptor (TLR) ligands in IL-16 production by fibroblast- like synoviocytes (FLS) of rheumatoid arthritis (RA) patients. Immunohistochemical staining was performed with a monoclonal antibody to IL-16 in synovial tissues from patients with RA and likewise in patients with osteoarthritis (OA). FLS were isolated from RA synovial tissues and stimulated with IL-15, IL-1beta, IFN-gamma, and IL-17. The IL-16 mRNA level was assessed by semiquantitative RT-PCR and real time (RT) PCR and a comparison was made between IL-16 mRNA levels produced by RA-FLS and OA-FLS. Production of IL-16 was identified by a western blot assay, and IL-16 production after stimulation by specific ligands of TLR2 and TLR4 was assessed by RT-PCR. While immunohistochemical staining demonstrated strong expression of IL-16 mRNA in synovial tissues from patients with RA, similar findings were not present in the OA group. Moreover, mRNA expression of IL-16 by RA-FLS increased after treatment with IL-17 but not with IL-15, IL-1beta, and IFN-gamma. Specifically, IL-17 increased IL-16 mRNA level by RA-FLS and peripheral blood mononuclear cells in a dose-dependent manner. However, IL-17 did not stimulate IL-16 production in OA-FLS. Peptidoglycan, a selective TLR2 ligand, also increased production of IL-16 by RA-FLS dose- dependently, whereas LPS, a selective TLR4 ligand, had no such stimulatory effect. The results from our data demonstrate that IL-17 and TLR2 ligands stimulate the production of IL-16 by RA-FLS.

Measurement of Serum Interleukin-16,-10 and Immunoglobulin E in Asthmatic Children and Its Significance / 实用儿科临床杂志

Objective To discuss the level and its relativity analysis of IL-16 and IgE in asthmatic children .Methods Compare and analyze the level of IL-16,IL-10 and IgE between 18 asthmatic children and 14 healthy children.Results The serum level of IL-16 and IgE in asthmatic children was much higher than the contrast, P

Tumor Vaccine Effect by IL-16 Gene Transfer into Murine Neuroblastoma Model

PURPOSE: Interleukin(IL)-16 is a potent chemoattractant factor for CD4+ T cells, monocytes, and eosinophils. It up-regulates IL-2R on CD4+ T lymphocytes and regulates the function of antigen presenting cells. We used retrovirus-mediated gene transfer of the human IL-16 gene into the neuro-2a cells, which is the murine neuroblastoma cell lines, to investigate whether locally secreted IL-16 might generate anti-tumor immune responses. METHODS: We estimated whether the local secretion of IL-16 from the genetically-modified tumor cells would affect their tumorigenicity in vivo, and then, IL-16 transfected neuroblastoma cells would protect mice from tumor development after wild-type tumor cell challenges. And we investigated the mechanism of IL-16 by nude mice trial of an anti-tumor immune response. RESULTS: The IL-16 gene-transduced neuro-2a clones secreted 4.2-6.0ng of IL-16 per mL per 10(5) cells during 24 hr. None of the mice(N=6) injected with 2x10(6) of irradiated, IL-16 gene-transfected neuro-2a cells developed tumors within 6 weeks while all of the mice(N=6) injected with wild-type neuro-2a cells developed tumors. Immunization of mice(N=6) with 2x106 IL-16 gene- transfected, irradiated neuro-2a cells protected these animals against a subsequent challenge with 2x10(6) wild-type tumor cells. Nude mice also showed an anti-tumorigenicity effect. However, the mice did not reveal the prophylactic effect against murine neuroblastoma. CONCLUSION: The local secretion of IL-16 gene-transduced tumor cells abrogated their tumorigenicity and induced protective immunity.

Levels of IL-18, IL-16, IL-8, eotaxin and the chymase activity in the sputum of asthmatics / 中国病理生理杂志

AIM: To investigate the levels of IL-18, IL-16, IL-8, eotaxin and the chymase activity in the sputum of asthmatics. METHODS: IL-18, IL-16, IL-8 and eotaxin levels were detected with sandwich ELISA procedures and chymase activity was determined spectrophotometrically (410 nm) by the rate of hydrolysis of N-succinyl-L-Ala-L-Ala-L-Pro-L-Phe-p-nitroanilide (SAAPP). RESULTS: The specific chymase activities in the severe and moderate asthmatics were higher than that in controls. Native protease inhibitors ?_1-antitrypsin (?_1-AT) and soybean trypsin inhibitor (SBTI) inhibited 71.9% and 72.1% enzymatic chymase activity, respectively. The levels of IL-18, IL-16, IL-8 and eotaxin were significantly elevated in the sputum of patients with acute asthma. There were correlations between the levels of IL-8 and IL-16 (r=0.55, P