scholarly journals Moderate hyperoxia plays a protective role in lung bronchial epithelial cells

2019 ◽  
Vol 42 (4) ◽  
pp. E28-E36
Author(s):  
Shimiao Tang ◽  
Siyu Sun ◽  
Dongyang Zhang ◽  
Dongyan Liu
Keyword(s):  
Epithelial Cells ◽  
Survival Rates ◽  
Protective Role ◽  
Secretory Component ◽  
Bronchial Epithelial Cells ◽  
Control Group ◽  
Mrna Levels ◽  
Bronchial Epithelial ◽  
Inflammatory Reactions ◽  
Tnf Α

Purpose: Oxygen therapy is commonly used in clinical settings, but several problems may result from improper use. Oxygen poisoning involves the initiation of a series of inflammatory reactions. In this study, we compared the effects of moderate hyperoxia (40% O2) and extreme hyperoxia (85% O2) on pulmonary bronchial epithelial cells. Methods: Normal human tracheobronchial epithelium (NHBE) cells were exposed to hyperoxia (40% and 85%) for 24 hours, and their survival rates were determined by the colorimetic assay, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide). The protein and mRNA levels of RelA, RelB, ASK1, TNF-α and secretory component (SC) were detected by immunohistochemical staining, western blot, and real-time polymerase chain reaction. Results: The NHBE cell survival increased in the presence of moderate hyperoxia. RelA, RelB, ASK1, TNF-α and SC expressions were significantly higher in the 85% O2 group in comparison with the control group and the 40% O2 group. In the 40% O2 group, RelA, RelB, ASK1 and TNF-α were upregulated, but SC expression was not significantly different than that of the control group. However, compared with the 85% O2 group, SC expression was significantly lower in the 40% O2 group. Conclusion: These results suggest that moderate hyperoxia promotes proliferation in NHBE cells and activates TNF-α and downstream ASK1. Then TNF-α activates NF-κB and SC to play a protective role.

Induction of MMP-9 in normal human bronchial epithelial cells by TNF-α via NF-κB-mediated pathway

2001 ◽  
Vol 281 (6) ◽  
pp. L1444-L1452 ◽  
Author(s):  
Atsuko Hozumi ◽  
Yoshihiro Nishimura ◽  
Teruaki Nishiuma ◽  
Yoshikazu Kotani ◽  
Mitsuhiro Yokoyama
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Interleukin 1Β ◽  
Pyrrolidine Dithiocarbamate ◽  
Mrna Levels ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Tnf Α ◽  
Normal Human

In this study, we determined whether the proinflammatory cytokines tumor necrosis factor (TNF)-α and interleukin-1β contribute to the regulation of matrix metalloproteinase (MMP)-9 in human bronchial epithelial cells and whether the induction of MMP-9 is regulated by the transcription factor nuclear factor (NF)-κB. We demonstrated that TNF-α induced MMP-9 at both the protein and mRNA levels in human bronchial epithelial cells and that interleukin-1β did not. In contrast, induction of the tissue inhibitor of metalloproteinase-1 by TNF-α was less than that of interleukin-1β. Increased expression of MMP-9 and NF-κB activation induced by TNF-α were inhibited by pyrrolidine dithiocarbamate and N-acetyl-l-cysteine but were not inhibited by curcumin. These results suggest that TNF-α induces the expression of MMP-9 in human bronchial epithelial cells and that this induction is mediated via the NF-κB-mediated pathway.

Reactive oxygen intermediates stimulate interleukin-6 production in human bronchial epithelial cells

1999 ◽  
Vol 276 (6) ◽  
pp. L900-L908 ◽  
Author(s):  
Yoshimasa Yoshida ◽  
Muneharu Maruyama ◽  
Tadashi Fujita ◽  
Nobuki Arai ◽  
Ryuji Hayashi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Lung Fibroblasts ◽  
Mrna Levels ◽  
Airway Epithelial ◽  
Human Bronchial Epithelial Cells ◽  
Oxygen Intermediates ◽  
Bronchial Epithelial ◽  
Tnf Α

Reactive oxygen intermediates (ROIs) play an important role in the initiation and progression of lung diseases. In this study, we investigated whether ROIs were involved in the induction of interleukin (IL)-6 in human bronchial epithelial cells. We exposed normal human bronchial epithelial cells as well as a human bronchial epithelial cell line, HS-24, to ROIs. We measured the amount of IL-6 in the culture supernatants using ELISA and the IL-6 mRNA levels using RT-PCR. Superoxide anions ([Formula: see text]), but not hydrogen peroxide (H2O2), increased IL-6 production. To examine whether it is a cell type-specific mechanism of airway epithelial cells, the experiments were also performed in human lung fibroblasts, WI-38-40. In WI-38-40 cells, neither [Formula: see text] nor H2O2increased IL-6 production. In contrast, tumor necrosis factor (TNF)-α (200 U/ml) induced IL-6 at the protein and mRNA levels in both airway epithelial cells and lung fibroblasts. This cytokine-induced IL-6 production was significantly suppressed by several antioxidants, including dimethyl sulfoxide (DMSO), in airway epithelial cells. In WI-38-40 cells, DMSO was not able to suppress IL-6 production induced by TNF-α. Pretreatment with DMSO recovered the TNF-α-induced depletion of intracellular reduced glutathione in HS-24 cells. These findings indicate that oxidant stress specifically induces IL-6 production in human bronchial epithelial cells and that in these cells ROIs may be involved in IL-6 production after stimulation with cytokines such as TNF-α. Presumably, ROIs participate in the local immune response in lung diseases via IL-6 release from bronchial epithelial cells.

scholarly journals Expression of lipocortins in human bronchial epithelial cells: effects of IL-1β , TNF-α, LPS and dexamethasone

1996 ◽  
Vol 5 (3) ◽  
pp. 210-217
Author(s):  
M. M. Verheggen ◽  
H. I. M. de Bont ◽  
P. W. C. Adriaansen-Soeting ◽  
B. J. A. Goense ◽  
C. J. A. M. Tak ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelium ◽  
Northern Blotting ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Annexin I ◽  
Tnf Α

In this study, we investigated the expression of lipocortin I and II (annexin I and I in the human bronchial epithelium, bothin vivoandin vitro. A clear expression of lipocortin I and II protein was found in the epithelium in sections of bronchial tissue. In cultured human bronchial epithelial cells we demonstrated the expression of lipocortin I and II mRNA and protein using Northern blotting, FACScan analysis and ELISA. No induction of lipocortin I or II mRNA or protein was observed after incubation with dexamethasone. Stimulation of bronchial epithelial cells with IL-1β, TNF-α or LPS for 24 h did not affect the lipocortin I or II mRNA or protein expression, although PGE2and 6-keto-PGF1αproduction was significantly increased. This IL-1β- and LPS-mediated increase in eicosanoids could be reduced by dexamethasone, but was not accompanied by an increase in lipocortin I or II expression. In human bronchial epithelial cells this particular glucocorticoid action is not mediated through lipocortin I or II induction.

IL-4 induces ICAM-1 expression in human bronchial epithelial cells and potentiates TNF-α

1999 ◽  
Vol 277 (1) ◽  
pp. L58-L64 ◽  
Author(s):  
Ilja Striz ◽  
Tadashi Mio ◽  
Yuichi Adachi ◽  
Peggy Heires ◽  
Richard A. Robbins ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Macrophage Cells ◽  
Tnf Α

Interleukin (IL)-4 is thought to contribute to the Th2 type of immune response and hence the development of allergic reactions such as asthma. In asthmatic patients, the airway epithelium expresses increased amounts of the cell surface adhesion molecule intercellular adhesion molecule (ICAM)-1 (CD54). One cytokine capable of inducing ICAM-1 in airway epithelial cells, tumor necrosis factor-α (TNF-α), is present in asthma. This study evaluated if IL-4 either alone or together with TNF-α costimulation might modulate CD54 expression by human bronchial epithelial cells (HBECs). CD54 positivity increased in response to IL-4 (16 ± 2% positive vs. 3 ± 1%, P < 0.01); greater induction of CD54 resulted from TNF-α (45 ± 2%, P < 0.001). Costimulation with TNF-α plus IL-4 further augmented expression (56 ± 1%, P < 0.05). Immunoperoxidase results were confirmed by flow cytometry. RT-PCR revealed no increase in ICAM-1 mRNA expression under control conditions or after stimulation with IL-4 alone. TNF-α increased IL-4 mRNA, and IL-4 potentiated this. Functionally, IL-4 augmented the adhesion of THP-1 monocyte/macrophage cells to monolayers of HBECs both alone and in the presence of TNF-α. We conclude that 1) IL-4 augments epithelial cell ICAM-1 expression, 2) IL-4 potentiates the adhesion of THP-1 monocyte/macrophage cells to epithelial cells, and 3) modulation of epithelial cell ICAM-1 expression by IL-4 may play a role in the immunopathology of bronchial asthma.

scholarly journals cAMP-dependent protein kinase activation decreases cytokine release in bronchial epithelial cells

2014 ◽  
Vol 307 (8) ◽  
pp. L643-L651 ◽  
Author(s):  
Todd A. Wyatt ◽  
Jill A. Poole ◽  
Tara M. Nordgren ◽  
Jane M. DeVasure ◽  
Art J. Heires ◽  
...  
Keyword(s):  
Cell Migration ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Wound Repair ◽  
Bronchial Epithelial Cells ◽  
Dependent Protein Kinase ◽  
Bronchial Epithelial ◽  
Cyclic Monophosphate ◽  
Tnf Α ◽  
Dependent Protein

Lung injury caused by inhalation of dust from swine-concentrated animal-feeding operations (CAFO) involves the release of inflammatory cytokine interleukin 8 (IL-8), which is mediated by protein kinase C-ε (PKC-ε) in airway epithelial cells. Once activated by CAFO dust, PKC-ε is responsible for slowing cilia beating and reducing cell migration for wound repair. Conversely, the cAMP-dependent protein kinase (PKA) stimulates contrasting effects, such as increased cilia beating and an acceleration of cell migration for wound repair. We hypothesized that a bidirectional mechanism involving PKA and PKC regulates epithelial airway inflammatory responses. To test this hypothesis, primary human bronchial epithelial cells and BEAS-2B cells were treated with hog dust extract (HDE) in the presence or absence of cAMP. PKC-ε activity was significantly reduced in cells that were pretreated for 1 h with 8-bromoadenosine 3′,5′-cyclic monophosphate (8-Br-cAMP) before exposure to HDE ( P < 0.05). HDE-induced IL-6, and IL-8 release was significantly lower in cells that were pretreated with 8-Br-cAMP ( P < 0.05). To exclude exchange protein activated by cAMP (EPAC) involvement, cells were pretreated with either 8-Br-cAMP or 8-(4-chlorophenylthio)-2'- O-methyladenosine-3',5'-cyclic monophosphate (8-CPT-2Me-cAMP) (EPAC agonist). 8-CPT-2Me-cAMP did not activate PKA and did not reduce HDE-stimulated IL-6 release. In contrast, 8-Br-cAMP decreased HDE-stimulated tumor necrosis factor (TNF)-α-converting enzyme (TACE; ADAM-17) activity and subsequent TNF-α release ( P < 0.001). 8-Br-cAMP also blocked HDE-stimulated IL-6 and keratinocyte-derived chemokine release in precision-cut mouse lung slices ( P < 0.05). These data show bidirectional regulation of PKC-ε via a PKA-mediated inhibition of TACE activity resulting in reduced PKC-ε-mediated release of IL-6 and IL-8.

Retinoic acid reduces p11 protein levels in bronchial epithelial cells by a posttranslational mechanism

2000 ◽  
Vol 279 (6) ◽  
pp. L1103-L1109 ◽  
Author(s):  
M. T. Gladwin ◽  
X. L. Yao ◽  
M. Cowan ◽  
X. L. Huang ◽  
R. Schneider ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Calcium Ionophore ◽  
Bronchial Epithelial Cells ◽  
26S Proteasome ◽  
Mrna Levels ◽  
Bronchial Epithelial ◽  
Protein Levels ◽  
Cytosolic Phospholipase ◽  
Protein Reduction

p11 is a member of the S100 family of proteins, is the cellular ligand of annexin II, and interacts with the carboxyl region of 85-kDa cytosolic phospholipase A2 (cPLA2), inhibiting cPLA2activity and arachidonic acid (AA) release. We studied the effect of retinoic acid (RA) on PLA2 activity in human bronchial epithelial cells and whether p11 contributes to these effects. The addition of 10−6 M RA resulted in reduced p11 protein levels at 4 days, with the greatest effect observed on days 6 and 7. This effect was dose related (10−6 to 10−9 M). RA treatment (10−6 M) had no effect on cPLA2 protein levels. p11 mRNA levels were unchanged at 6 and 8 days of treatment (correlating with maximum p11 protein reduction). Treatment with RA reduced p11 levels in control cells and in cells transfected with a p11 expression vector, suggesting a posttranslational mechanism. Lactacystin (10−6 M), an inhibitor of the human 26S proteasome, blocked the decrease in p11 observed with RA treatment. Compared with control cells ( n = 3), RA-treated cells ( n = 3) had significantly increased AA release after treatment with the calcium ionophore A-23187 ( P = 0.006). Therefore, RA reduces p11 protein expression and increases PLA2 activity and AA release.

scholarly journals Increased expression of placenta growth factor in COPD

Thorax ◽  
2008 ◽  
Vol 63 (6) ◽  
pp. 500-506 ◽  
Author(s):  
S-L Cheng ◽  
H-C Wang ◽  
C-J Yu ◽  
P-C Yang
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Serum Levels ◽  
Bronchial Epithelial Cells ◽  
Angiogenic Factor ◽  
Concomitant Treatment ◽  
Placenta Growth Factor ◽  
Bronchial Epithelial ◽  
Tnf Α ◽  
Fluid Levels

Background:Vascular endothelial growth factor (VEGF) and its receptor may have an important role in the pathogenesis of emphysema. The effect of another angiogenic factor, placenta growth factor (PlGF), in chronic obstructive pulmonary disease (COPD) is unknown.Methods:The serum levels of VEGF and PlGF in patients with COPD (n = 184), smokers (n = 212) and non-smokers (n = 159) and the bronchoalveolar lavage (BAL) fluid levels of VEGF and PlGF in another group (20 patients with COPD, 18 controls) were measured. In vitro cell culture experiments were performed to investigate the effect of PlGF on VEGF.Results:The mean (SE) serum levels of PlGF were significantly higher in patients with COPD than in controls (27.1 (7.4) pg/ml vs 12.3 (5.1) pg/ml in smokers and 10.8 (6.3) pg/ml in non-smokers, p = 0.005). The levels of PlGF in BAL fluid were also significantly higher in patients with COPD than in controls (45.7 (12.3) pg/ml vs 23.9 (7.6) pg/ml, p = 0.005), associated with an increase in the cytokines tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). In patients with COPD the levels of PlGF correlated inversely with forced expiratory volume in 1 s (FEV1) in serum (r = −0.59, p = 0.002) and in BAL fluid (r = −0.51, p = 0.001). While the serum levels of VEGF were the same in patients with COPD and controls, the BAL fluid levels were significantly lower in patients with COPD than in controls (127.5 (30.1) pg/ml vs 237.8 (36.1) pg/ml, p = 0.002). In cultured bronchial epithelial cells, proinflammatory cytokines induced an increase in the protein expression of both PlGF and VEGF. Continuous concomitant treatment with PlGF, TNF-α and IL-8 stimulation reduced VEGF expression and induced cell death. This phenomenon was suppressed by VEGF receptor inhibitor (CBO-P11).Conclusions:The serum and BAL fluid levels of PlGF are increased in patients with COPD and are inversely correlated with FEV1. Concomitant treatment with PlGF, TNF-α and IL-8 causes detrimental effects on airway epithelial cells. These data suggest that bronchial epithelial cells can express PlGF, which may contribute to the pathogenesis of COPD.

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