Shao-xi Cai

Nanfang Hospital, Shengcheng, Guangdong, China

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Publications (65)16.2 Total impact

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    ABSTRACT: To investigate the effect of thymic stromal lymphopoietin (TSLP) on the permeablily of monolayer bronchial epithelial cells in vitro.
    06/2014; 34(6):802-6.
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    ABSTRACT: To investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro. Human airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10(-8) mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA. 16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58). Both 1,25VD3 and HDM can induce TSLP expression and release in 16HBE cells, but pretreatment with 1,25VD3 can decrease HDM-augmented TSLP expression in the cells.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 04/2014; 34(4):492-6.
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    ABSTRACT: Rationale: Accumulating evidence has demonstrated that up-regulation of the angiotensin-converting enzyme (ACE)/angiotensin (Ang) II/AngII type 1 receptor (AT1R) axis aggravates pulmonary fibrosis. The recently discovered ACE2/Ang-(1-7)/Mas axis, which counteracts the activity of the ACE/AngII/AT1R axis, has been shown to protect against pulmonary fibrosis. However, the mechanisms by which ACE2 and Ang-(1-7) attenuate pulmonary fibrosis remain unclear. Objectives: We hypothesized that up-regulation of the ACE2/Ang-(1-7)/Mas axis protects against bleomycin-induced pulmonary fibrosis by inhibiting the MAPK/NF-κB pathway. Methods: In vivo, Ang-(1-7) was continuously infused into Wistar rats that had received bleomycin or AngII. In vitro, HFL-1 cells were pretreated with compounds that block the activities of AT1R, Mas (A-779), and MAPKs before exposure to AngII or Ang-(1-7). The HFL-1 cells were infected with lentivirus- mediated ACE2 before exposure to AngII. Measurements and main results: In vivo, Ang-(1-7) prevented bleomycin-induced lung fibrosis and AngII-induced lung inflammation by inhibiting the MAPK phosion anation and NF-κB signaling cascades. However, exogenous Ang-(1-7) alone clearly promoted lung inflammation. In vitro, Ang-(1-7) and lentivirus-mediated ACE2 inhibited the AngII-induced MAPK/NF-κB pathway, thereby attenuating inflammation and α-collagen I production, which could be reversed by the Mas inhibitor A779. Ang-(1-7) inhibited AngII-induced lung fibroblast apoptotic resistance via inhibition of the MAPK/NF-κB pathway and activation of the bax/caspase-dependent mitochondrial apoptotic pathway. Ang-(1-7) alone markedly stimulated ERK1/2 phosphorylation and the NF-κB cascade. Conclusion: Up-regulation of the ACE2/Ang-(1-7)/Mas axis protected against pulmonary fibrosis by inhibiting the MAPK/NF-κB pathway. However, close attention should be paid to the proinflammatory effects of Ang-(1-7).
    American Journal of Respiratory Cell and Molecular Biology 10/2013; · 4.15 Impact Factor
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    ABSTRACT: To establish a chronic obstructive pulmonary disease (COPD) model by passive cigarette smoking and (or) intratracheal instillation of lipopolysaccharide (LPS) in spontaneously hypertensive (SH) rats. Fifteen male SH rats were randomly divided into control group, cigarette smoking exposure (CS) group and CS+LPS (cigarette smoking exposure plus intratracheal instillation of LPS) group. After 8 weeks' treatment, the COPD model was validated by inspecting the general condition and examining lung function and pulmonary pathological changes. The expressions of surfactant-associated protein A (SP-A), NF-κB, histone, p-Iκ-Kα/β, Iκ-Kα/β, and IκB-α were determined with Western blotting, and the expression of TNF-α and IL-6 mRNA were measured using qRT-PCR. The rats in both CS and CS+LPS groups were marantic with intermittent cough and tachypnea. Lung function test showed increased RI and lowered peak expiratory flow in CS group, which were more prominent in CS+LPS group (P<0.05). HE staining demonstrated typical chronic bronchitic inflammation and emphysema in the lungs of the two model groups with significantly decreased mean alveolar number and significantly increased mean lining intermiment and destrction index. The emphysema level was more serious in CS+LPS group than in CS group. Western blotting showed markedly decreased expressions of SP-A and IκB-α in CS group and CS+LPS , especially the latter group. The protein levels of NF-κB, Iκ-K phosphorylation and mRNA expressions of TNF-α and IL-6 increased obviously in the two model groups. COPD model can be established by passive smoking and (or) intratracheal instillation of LPS in SH rats, and the model induced by combined exposures is optimal.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 09/2013; 33(9):1341-6.
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    ABSTRACT: To explore the expression and effect of Toll-like receptor 4 (TLR-4) in the lung tissue of rats established by passive smoking or intratracheal instillation of lipopolysaccharide (LPS). Eight-week-old male Sprague-Dawley rats (n = 15) were randomly divided into 3 groups, including: (1) group A: conventional breeding; (2) group B: the rats were placed into a 120-L organic glass box with twice-daily exposure to cigarette smoking plus an intratracheal instillation of water at Day 1 and 14; (3) Group C: exposure to cigarette smoking the same as group B plus intratracheal instillation of lipopolysaccharide (1 mg/kg) at Day 1 and 14. Four weeks later, general status, arterial blood gas, pulmonary function and histopathology were analyzed. The expressions of TLR-4 and nuclear factor kappa-B (NF-κB) were determined by immunohistochemistry. Western blot was used to measure the protein contents of TLR-4, NF-κB, p-Iκ-Kα/β, Iκ-Kα/β, IκB-α. And real-time polymerase chain reaction (PCR) was employed to detect the mRNA levels of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6). Rats in Groups B and C were marantic with intermittent cough and dyspnea. Peak expiratory flow (PEF) and 50% expiratory flow-volume (EP50) were much lower in Group C ((10.6 ± 1.4), (0.77 ± 0.14) ml/s) than that in Groups A ((13.5 ± 2.0), (1.01 ± 0.08) and B (12.3 ± 0.9), (0.91 ± 0.10) ml/s) (all P < 0.05). Accumulated volume (AV) and carbon dioxide pressure (PCO2) were much higher in Groups B ((4358 ± 1501) ml, (52.77 ± 1.97) mm Hg) (1 mm Hg = 0.133 kPa) and C ((10 077 ± 1866) ml, (51.03 ± 4.96) mm Hg) than that in Group A ((1735 ± 798) ml, (39.57 ± 1.43) mm Hg) (all P < 0.05). Hematoxylin and eosin stain showed chronic bronchitis and emphysema in Groups B and C. Besides, quantitative analysis demonstrated that in unit area, mean lining interval (MLI) and destruction index (DI) in Group B ((84 ± 13) µm, 0.228 ± 0.047) and Group C ((86 ± 10) µm, 0.294 ± 0.060) significantly increased versus Group A ((65 ± 6) µm, 0.036 ± 0.012) (all P < 0.05). Immunohistochemical staining indicated that the expression of TLR-4 in cytoplasm and cytomembrane and NF-κB in nucleus markedly increased in Groups B and C versus Group A. Relative expressions of TLR-4 and NF-κB assayed by Western blot increased in Group B (0.68 ± 0.03, 0.21 ± 0.08) and Group C (1.12 ± 0.11, 0.59 ± 0.06) than that in Group A (1.36 ± 0.07, 1.04 ± 0.08). Compared with Group A, the expression levels of TLR-4, NF-κB and IκB-α and the phosphorylation levels of Iκ-Kα/β in Group B and C significantly increased (all P < 0.05). The mRNA levels of TNF-α and IL-6 increased in Group B (3.95 ± 0.29, 5.04 ± 0.28) and C (5.33 ± 0.26, 7.23 ± 0.39) versus that in Group C (1.00 ± 0.37, 1.00 ± 0.25) (all P < 0.05). Both passive smoking and intratracheal instillation of LPS may cause lung injury analogous to chronic obstructive pulmonary disease via NF-κB signaling pathway. And TLR4 plays an important role in this process.
    Zhonghua yi xue za zhi 07/2013; 93(28):2230-4.
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    ABSTRACT: Abstract Previous studies have shown that matrix metalloproteinase-9 (MMP-9) and its cognate inhibitor TIMP-1, inflammatory cytokine TNF-a, and the OPG/RANK/RANKL system may each play individual roles in the pathogenesis of osteoporosis in patients with COPD. In the present study, we investigated the interrelationships of these factors in male COPD patients with and without osteoporosis. The serum levels of MMP-9, MMP-9/TIMP-1 ratio, TNF-a, RANKL, OPG, and the RANKL/OPG ratio were higher in COPD patients with osteoporosis than in individuals with normal or low bone mineral density (BMD) (N 5 30, all P < 0.05 or < 0.01). The lung function FEV1%Pre and the BMD of the lumbar spine and femoral neck were found to be negatively correlated with MMP-9 serum level (r 5 20.36, P < 0.05, r 5 20.58, P < 0.001, and r 5 20.62, P < 0.01, respectively), RANKL serum level (r 5 20.21, P < 0.05, and r 5 20.25, P < 0.05, and r 5 20.26, P < 0.05, respectively), and RANKL/OPG ratio (r 5 20.23, P < 0.05, r 5 20.33, P < 0.05, and r 5 20.38, P < 0.05, respectively). However, they had no correlation with TIMP-1, TNF-a, OPG, or RANK. The MMP-9 serum level was found to be positively correlated with TNF-a level (r 5 0.35, P < 0.05) and RANKL/OPG ratio (r 5 0.27, P < 0.05) but not associated with RANKL. These results suggest that MMP-9, TNF-a, and the OPG/RANK/RANKL system may be closely interrelated and may play interactive roles in pathogenesis of osteoporosis in COPD.
    COPD Journal of Chronic Obstructive Pulmonary Disease 07/2013; · 2.73 Impact Factor
  • Ying Meng, Chang-Hui Yu, Shao-Xi Cai, Xu Li
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    ABSTRACT: To explore the anti-fibrotic effects of angiotensin (Ang) 1-7 on bleomycin (BLM) -induced pulmonary fibrosis in rats. Eighteen Wister male rats were randomly divided into 3 groups, including control group (intratracheal instillation with physiological saline and subcutaneous micro-pump with bi-distilled water at the rate of 0.29 µl/h), BLM group (intratracheal instillation with bleomycin and subcutaneous micro-pump with bi-distilled water at the same rate) and BLM+Ang1-7 group (intratracheal instillation with bleomycin and subcutaneous micro-pump with Ang1-7 at a dose of 25 µg·kg(-1) · h(-1) at the same rate). At Day 28, lung tissues were collected. Histological changes of lungs were evaluated by hematoxylin and eosin and Masson's trichrome stains. Collagen content of lung tissues was assessed by hydroxyprolin concentration. Then the products of protein and RNA were collected. And Western blot and realtime polymerase chain reaction (RT-PCR) were used to detect the protein or mRNA of TGF-β1 and α-collagenI. Human embryonic lung fibroblast (HFL-1) was divided into 5 groups: (1) control group: no stimulation; (2) AngII group: stimulation of AngII (10(-7)mol/L) ; (3) Ang1-7 group: stimulation of Ang1-7 (10(-7)mol/L); (4) Ang1-7 plus AngII group: stimulation by AngII (10(-7)mol/L) with Ang1-7 (10(-7)mol/L) pre-treatment; (5) Ang1-7+AngII+A-779 group: stimulation by AngII and Ang1-7 (10(-7) mol/L) with Mas receptor inhibitor A-779 (10(-6)mol/L) pre-treatment. Then the products of protein and RNA were collected. And QuantiGene and RT-PCR were used to detect the activation of TGF-β1, and α-collagenI mRNA. Compared with control group, fibrosis score and hydroxyproline concentrations increased significantly in BLM group, but declined in BLM+Ang1-7 group. The difference was statistically significant (P < 0.05). TGF-β1 mRNA, α-collagenI mRNA and α-collagenI protein level were up-regulated by BLM (4.45 ± 0.45 vs 1.00 ± 0.20, 5.14 ± 0.55 vs 1.00 ± 0.08, 1.48 ± 0.34 vs 0.23 ± 0.11) (all P < 0.05); while compared with BLM group, those of BLM+Ang1-7 group were down-regulated (2.80 ± 0.35, 3.10 ± 0.52, 0.49 ± 0.11) (all P < 0.05). In vitro: TGF-β1 mRNA and α-collagen I mRNA level were up-regulated by AngII (1.67 ± 0.26 vs 1.00 ± 0.10, 4.86 ± 1.36 vs 1.46 ± 0.54) (all P < 0.05); while those of AngII+Ang1-7 group were down-regulated (0.91 ± 0.30, 1.57 ± 0.27) compared with AngII group (all P < 0.05); no significant difference existed between the AngII+Ang1-7+A-779 group (1.25 ± 0.14, 1.29 ± 0.49) and AngII+Ang1-7 group (P > 0.05). Ang1-7 has anti-fibrous effect upon bleomycin-induced pulmonary fibrosis in rats andsuch an effect of Ang1-7 may be associated with AngII-induced expression of TGF-β1.
    Zhonghua yi xue za zhi 05/2013; 93(20):1585-9.
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    ABSTRACT: To explore the risk factors for hospitalization case fatality of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). A retrospective review of medical records was performed for 182 hospitalized AECOPD patients at Nanfang Hospital from January 2010 to August 2012. Their general information, condition in stable stage, the results of spirometry, blood routine test, blood gas analysis and C-reactive protein (CRP) were collected and analyzed. The risk factors for mortality were analyzed by multivariable Logistic regression. Among them, 42 died during hospitalization. Univariate analysis revealed that 8 factors had significant differences between two groups (all P < 0.05): high exacerbation risk (death vs improvement group, 90.4% vs 70.0%) , low peripheral absolute lymphocyte count (73.8% vs 47.1%), high CRP (50.0% vs 17.1%), concurrent anemia (50.0% vs 27.1%), hypoproteinemia (71.4% vs 46.4%), hypercapnia (64.3% vs 30.7%), chronic pulmonary heart disease (76.1% vs 40.7%) and ischemic heart disease (19.0% vs 7.0%). By multiple Logistic regression analysis, high CRP (OR = 3.226, P = 0.009), hypercapnia (OR = 2.928, P = 0.013), chronic pulmonary heart disease (OR = 2.510, P = 0.045), low peripheral absolute lymphocyte count (OR = 2.488, P = 0.045) were the independent risk factors for hospitalization case fatality of AECOPD patients. Low peripheral absolute lymphocyte count, high CRP, hypercapnia and chronic pulmonary heart disease were the independent risk factors for mortality in hospitalized AECOPD patients.
    Zhonghua yi xue za zhi 05/2013; 93(18):1374-7.
  • Ying Meng, Shao-Xi Cai, Xu Li
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    ABSTRACT: To summarize the features of disease history, clinical manifestations, adjuvant examination results, diagnosis, treatments and outcome of patients with histoplasmosis. The clinical data of 14 patients with biopsy-confirmed histoplasmosis between 2000 and 2012 in Nanfang Hospital were analyzed retrospectively. The clinical manifestations of histoplasmosis included fever, productive cough, chest pain, and abdominal pain, accompanied occasionally by neurological symptoms, lymph node enlargement or surface mass. Seven out of the 14 o patients had underlying immunosuppressive conditions, 9 had chest imaging changes, and 2 showed reduced white blood cells, red blood cells and platelets. The cases were initially diagnosis as tuberculosis, malignant tumor, or malignant lymphoma before the definite diagnosis was established pathologically. Ten patients received treatments with itraconazole, amphotericin B, fluconazole or voriconazole, and 9 of them responded favorably to the treatments. Histoplasmosis, with a low incidence and diverse clinical manifestations, presents with no specific imaging features to easily cause misdiagnosis and missed diagnosis, and its definite diagnosis relies on pathological examination.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 02/2013; 33(2):296-8.
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    ABSTRACT: To test the effect of high-mobility group box protein 1 (HMGB1) alone or in synergy with interleukin-1β (IL-1β) on the expression of IL-8 in human airway epithelial cells in vitro. Human airway epithelial 16HBE and A549 cell lines were incubated with HMGB1 (100 ng/ml) in the absence or presence of IL-1β (10 ng/ml) for 24 h, and the changes of IL-8 mRNA and protein expressions were assessed using quantitative PCR and enzyme-linked immunosorbent assay (ELISA). In the two human airway epithelial cell lines, HMGB1 alone did not produce obvious effect on the expression of IL-8, but in the presence of IL-1β, HMGB1 caused a significant increase of IL-8 expressions at both the mRNA and protein levels. HMGB1 in synergy with IL-1β increases the expression of IL-8 in human airway epithelial cells, which provides new evidence that HMGB1 contributes to neutrophilic airway inflammation by regulating IL-8 expression.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 12/2012; 32(12):1764-7.
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    ABSTRACT: To investigate the effect of hydrogen dioxide (H(2)O(2)) on the release and translocation of high mobility group box 1 release (HMGB1) from normal human bronchiolar epithelial cells (HBE). MTT assay was used to assess the viability of HBE135-E6E7 cells exposed to different concentrations of H(2)O(2). The expression and location of HMGB1 in the cytoplasm, nuclei and culture medium of the exposed cells were determined using Western blotting and immunofluorescence assay. Exposure to 125 µmmol/L H(2)O(2) did not obviously affect the cell viability. At the concentration of 250 µmmol/L, H(2)O(2) significantly decreased the cell viability (P<0.05), but significant cell death occurred only after exposure to 400 µmmol/L H(2)O(2) (P=0.000). Compared with the control cells, the cells exposed to 12.5, 125 and 250 µmmol/L H(2)O(2) for 24 h showed significantly increased levels of HMGB1 in the culture medium (P<0.05), and exposure to 125 µmmol/L H(2)O(2) for 12 and 24 h also caused significantly increased HMGB1 level (P<0.05). Exposure to 125 µmmol/L H(2)O(2) for 24 h significantly increased HMGB1 expression in the cytoplasm but decreased its expression in the nucleus. HMGB1 translocation from the nuclei to the cytoplasm and to the plasmalemma occurred after 125 µmmol/L H(2)O(2) exposure for 12 h and 24 h, respectively. H(2)O(2) can induce HMGB1 translocation and release in human bronchial epithelial cells, suggesting the involvement of HMGB1 in airway oxidative stress in chronic inflammatory diseases such as asthma and COPD.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 08/2012; 32(8):1131-4.
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    ABSTRACT: To establish an improved method for culturing primary mouse pulmonary microvascular endothelial cells (PMVECs). An improved tissue block adherent culture method was used to isolate and culture the PMVECs from C57 mice. The cultured cells were identified by factor VIII-related antigen and CD31 antigen, and the growth of cells cultured using the improved method and the conventional method was compared. The cultured primary pulmonary microvascular endothelial cells showed a short fusiform or round morphology, and the cell monolayer displayed a cobble stone-like appearance. The cultured cells were positive for VIII-related antigen and CD31 antigen. The cell growth was accelerated in the cell cultures with the improved method compared with that in conventional cell cultures. The improved culture method allows more efficient acquisition of primary mouse PMVECs of a greater purity.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 08/2012; 32(8):1151-3.
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    ABSTRACT: To explore the post-therapeutic change of cathelicidin LL-37 in asthmatics of different inflammatory phenotypes. Thirty-four patients with initially diagnosed asthma (asthma group) and 14 normal subjects (control group) were recruited at Nanfang Hospital from August 2009 to August 2010 for this prospective study. Sputum and venous blood samples were collected and analyzed for cell differential. Eosinophilic asthma was defined as the count of sputum eosinophils ≥ 3%. The LL-37 concentrations in plasma and sputum supernatant were measured by enzyme-linked immunosorbent assay (ELISA) kit. The subjects were treated with budesonide/formoterol (160/4.5 µg) one inhalation twice daily and re-examined after 1 month. Prior to treatment, there were no differences between the asthma and control groups in the levels of LL-37 in plasma and sputum supernatant (P = 0.427,0.427). The plasma concentrations of LL-37 in asthma group were negatively correlated with baseline forced expiratory volume in one second (FEV(1), r = -0.470, P = 0.005), percent predicted of FEV(1) (FEV(1)%pred, r = -0.421, P = 0.013) and forced vital capacity (FVC, r = -0.367, P = 0.033). After treatment, the plasma and sputum supernatant concentrations of LL-37 (M (Q(R))) in the asthma group (5.6 (16.2), 65.6 (184.0) µg/L) were significantly higher than those baseline concentrations (5.03 (9.21), 28.40(109.76) µg/L, P = 0.005, 0.015). In the eosinophilic asthma subgroup, the plasma and sputum supernatant concentrations of LL-37 (M (Q(R))) after treatment (5.3 (19.3), 65.6 (185.2) µg/L) were significantly higher than those baseline concentrations (6.7 (8.9) L, 35.3 (102.0) µg/L, P = 0.021,0.014). And in the non-eosinophilic asthma subgroup, the changes of plasma and sputum supernatant concentrations of LL-37 showed no significant differences (P = 0.139, 0.386). In the asthma group, the correlations between plasma concentrations of LL-37 and FEV(1), FEV(1)%pred, FVC were not statistically significant (P = 0.283, 0.706,0.272) after treatment. LL-37 may participate in the aggravation of asthma. The elevated concentrations of LL-37 in eosinophilic asthma is probably due to the resolved suppression of LL-37 expression by eosinophilic inflammation. But its mechanism needs further researches.
    Zhonghua yi xue za zhi 03/2012; 92(12):818-21.
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    ABSTRACT: High microvascular permeability plays an essential role in pathological process of multiple diseases such as septic shock, acute lung injury and acute respiratory distress syndrome, and burns. Inhibiting hyperpermeability is significant for controlling these conditions. Cdc42, as a main member of the small Rho GTPase family, plays a critical role in controlling and regulating the endothelial junctional permeability. We aimed to generate and identify endothelial specific cdc42-deficient mice by the Cre/loxp recombination approach, for examination in an animal model of the contribution of the cdc42 gene in the microvascular barrier function. We crossed cdc42(Flox/Flox) mice with mice expressing endothelial cell-specific Cre recombinase, and the offspring with the genotype cdc42(Flox/+)Tie2Cre(+/-) were back-crossed with the cdc42(Flox/Flox) mice. The cdc42(Flox/Flox)Tie2Cre(+/-) mice in the F2 generation were the target mice. If the cdc42 deficient mice did not survive, we would observe the cdc42 deficient mice embryos, and compare them with wild-type mice embryos. Cdc42(flox/+)Cre(+/-) mice were mated with the cdc42(Flox/Flox) mice and among the living offspring there were no cdc42(Flox/Flox)Cre(+/-) target mice. We found the endothelial special cdc42 deficient embryos at the E7.5-E16.5 stage. We observed that cdc42 deficient embryos were much smaller, had fewer vessels and were a little more swollen compared with the wild-type embryos. Endothelial specific knockout of cdc42 caused embryonic lethality and the mice did not survive to birth. The target embryos were much smaller, had fewer vessels and were a little more swollen compared with the wild-type embryos. These results demonstrated that the cdc42 plays an important role in development of embryos and in development of microvessels as well as microvascular permeability.
    Chinese medical journal 12/2011; 124(24):4155-9. · 0.90 Impact Factor
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    ABSTRACT: To investigate the role of AdeABC efflux pump in carbapenems resistance of Acinetobacter baumannii in light of the phenotype and genetype of the efflux pump. The phenotype of the efflux pump was detected in 138 clinical isolates of A.baumannii using the efflux pump inhibitor carbonyl cyanide 3-chlorophenylhydrazone (CCCP). The mRNA expression of pump-encoding gene adeB in the strains was detected using quantitative real-time RT-PCR. Of the 138 strains, 28 showed positivities for AdeABC efflux pump identified by Mueller-Hinton Broth with CCCP. Of the 39 strains resistant to meropenem, 15 (38.4%) showed positive results in CCCP assay, a rate significantly higher than that among the 99 sensitive strains (13.1%, 13/99) (X(2)=12.477(b), P=0.01). The mRNA expression of efflux pump-encoding gene adeB was detected by real-time RT-PCR at a level of 0.899∓∓1.172 in meropenem-sensitive strains, significantly lower than the level of 21.101∓∓21.443 in meropenem-resistant strains (t=4.403, P=0.000). Efflux plays a role in carbapenems resistance in the clinical isolates of A. baumannii. The AdeABC efflux pump may be an important factor in reducing carbapenems sensitivity in A. baumannii.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 08/2011; 31(8):1378-81.
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    ABSTRACT: Damage-associated molecular pattern molecules such as high-mobility group box 1 protein (HMGB1) and heat shock protein 70 (HSP70) have been implicated in the pathogenesis of asthma. The aim of our study was to examine the induced sputum and plasma concentrations of HSP70 in asthmatic patients to determine their relationship with airway obstruction. Thirty-four healthy controls and 56 patients with persistent bronchial asthma matched for gender and age were enrolled in this study. Spirometry measurements were performed before sputum induction. HSP70 levels in induced sputum and plasma were measured using the ELISA Kit. Sputum and plasma concentrations of HSP70 in asthmatics patients were significantly higher than that in control subjects (sputum, (0.88 ng/ml (0.27–1.88 ng/ml) versus 0.42 ng/ml (0.18–0.85 ng/ml), p < 0.001); plasma, (0.46 ng/ml (0.20–0.98 ng/ml) versus 0.14 ng/ml (0.11–0.37 ng/ml), p < 0.001) and were significantly negatively correlated with forced expiratory volume in 1 s (FEV1), FEV1 (percent predicted), and FEV1/FVC in all 90 participants and 56 patients with asthma. There were no significant differences in HSP70 levels between patients with eosinophilic and non-eosinophilic asthma. HSP70 levels in plasma were positively correlated with neutrophil count, and HSP70 levels in induced sputum were positively correlated with lymphocyte count. In multivariate analysis, independent predictors of sputum HSP70 were diseases and disease severity but not smoking, age, or gender, and independent predictors of plasma HSP70 were also diseases and disease severity. In conclusion, this study indicates that induced sputum and plasma HSP70 could serve as a useful marker for assessing the degree of airway obstruction in patients with asthma. However, further investigation is needed to establish the role of circulating and sputum HSP70 in the pathogenesis of asthma.
    Cell Stress and Chaperones 07/2011; · 2.48 Impact Factor
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    ABSTRACT: To observe the effect of 25-hydroxyvitamin D3 on the permeability and ZO-1 expression in normal human airway epithelial cells. MTT assay was used to assess the viability of human airway epithelial cell line 16HBE following a 24-hour exposure to different concentrations of 25-hydroxy vitamin D3, and the transepithelial electrical resistance (TER) of the cell monolayer was measured using a Millicell-ERS voltohmmeter. Real-time quantitative RT-PCR was employed to determine the changes of ZO-1 mRNA expression in the cells following the exposures. Exposure to 25-hydroxyvitamin D3 resulted in significantly increased permeability of 16HBE cells, but the exspression of ZO-1 showed no obvious changes. 25-hydroxyvitamin D3 at 4×10(-9) mol/L showed the strongest effect in increasing the permeability of cell monolayer. 25-hydroxyvitamin D3 increases the permeability of normal bronchial airway epithelial cell monolayer in vitro, but this effect is not mediated by upregulation of ZO-1 expression.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 07/2011; 31(7):1187-9.
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    ABSTRACT: To compare the change of lung tissue and vasopermeability between the vascular endothelial cells special cdc42-deficient heterozygous mice and the non-knockout mice in acute lung injury. The mice with vascular endothelial cell-specific expression of cre recombinase were crossed with cdc42(flox/flox) mice. The cdc42(flox/+)Cre(+/-) F1 offspring mice were crossed back with cdc42(flox/flox) mice, resulting in the F2 generation mice with three genotypes, namely cdc42(flox/+)Cre(+/-), cdc42(flox/flox)Cre(-/-) and cdc42(flox/+)Cre(+/-). The heterozygous mice with cdc42(flox/+)Cre(+/-) genotype were selected as the model mice, with the other two genotype groups as the control. After intratracheal instillation of 2 mg/kg LPS to induce acute lung injury, the mice were sacrificed to examine the lung pathologies, lung wet/dry ratio and lung microvascular permeability. The heterozygous mice with cdc42 gene knockout (cdc42(flox/+)Cre(+/-)) showed no significant differences from the two control groups in the lung pathological score, lung wet/dry ratio or the lung microvascular permeability coefficient. There were no significant difference on lung tissue and vasopermeability between the vascular endothelial cells special cdc42-deficient heterozygous mice and the non-knockout mice.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 06/2011; 31(6):995-8.
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    ABSTRACT: Eosinophils play a pivotal role in asthmatic airway inflammation. We previously found a significantly high expression of Slingshot-1L (SSH-1L) in peripheral eosinophils in acute exacerbations of asthma. Objective To investigate the expression and localization patterns of SSH-1L in peripheral blood eosinophils of asthmatic patients and their changes after treatment with inhaled corticosteroids. We recruited 4 outpatients with acute exacerbations of asthma who received no previous corticosteroid treatment and 1 healthy volunteer. From all the subjects 30 ml peripheral venous blood samples were collected before and after a 3-month treatment with inhaled fluticasone. The eosinophils were isolated, purified and counted, and the expressions of SSH-1L in the eosinophils were examined by RT-PCR and Western blotting. The localization of SSH-1L phosphatases in the peripheral eosinophils was detected by immunofluorescence assay in one patient. SSH-1L phosphatases distributed diffusely in the cytoplasm, especially dense near the membrane of the peripheral eosinophils. Glucocorticoids treatment resulted in a significant reduction in both the SSH-1L mRNA expression (0.7403∓0.1124 vs 0.4101∓0.0363, P=0.001) and SSH-1L protein expression (0.3410∓0.1337 vs 0.1543∓0.0551, P=0.039). A high expression of SSH-1L in peripheral eosinophils in acute exacerbations of asthma may play a role in the activation and migration of eosinophils. The efficacy of inhaled corticosteroids in asthma control might be partly attributed to a down-regulated expression of SSH-1L.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 06/2011; 31(6):928-32.
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    ABSTRACT: Damage-associated molecular pattern molecules such as high-mobility group box 1 protein (HMGB1) and heat shock protein 70 (HSP70) have been implicated in the pathogenesis of asthma. The aim of our study was to examine the induced sputum and plasma concentrations of HSP70 in asthmatic patients to determine their relationship with airway obstruction. Thirty-four healthy controls and 56 patients with persistent bronchial asthma matched for gender and age were enrolled in this study. Spirometry measurements were performed before sputum induction. HSP70 levels in induced sputum and plasma were measured using the ELISA Kit. Sputum and plasma concentrations of HSP70 in asthmatics patients were significantly higher than that in control subjects (sputum, (0.88 ng/ml (0.27-1.88 ng/ml) versus 0.42 ng/ml (0.18-0.85 ng/ml), p < 0.001); plasma, (0.46 ng/ml (0.20-0.98 ng/ml) versus 0.14 ng/ml (0.11-0.37 ng/ml), p < 0.001) and were significantly negatively correlated with forced expiratory volume in 1 s (FEV1), FEV1 (percent predicted), and FEV1/FVC in all 90 participants and 56 patients with asthma. There were no significant differences in HSP70 levels between patients with eosinophilic and non-eosinophilic asthma. HSP70 levels in plasma were positively correlated with neutrophil count, and HSP70 levels in induced sputum were positively correlated with lymphocyte count. In multivariate analysis, independent predictors of sputum HSP70 were diseases and disease severity but not smoking, age, or gender, and independent predictors of plasma HSP70 were also diseases and disease severity. In conclusion, this study indicates that induced sputum and plasma HSP70 could serve as a useful marker for assessing the degree of airway obstruction in patients with asthma. However, further investigation is needed to establish the role of circulating and sputum HSP70 in the pathogenesis of asthma.
    Cell Stress and Chaperones 06/2011; 16(6):663-71. · 2.48 Impact Factor