scholarly journals Glucocorticoid receptor mRNA levels in bronchial epithelial cells of patients with COPD: influence of glucocorticoids

1998 ◽  
Vol 92 (9) ◽  
pp. 1102-1109 ◽  
Author(s):  
S.H. Korn ◽  
F.B.J.M. Thunnissen ◽  
G.J. Wesseling ◽  
J.-W. Arends ◽  
E.F.M. Wouters
Keyword(s):  
Epithelial Cells ◽  
Glucocorticoid Receptor ◽  
Bronchial Epithelial Cells ◽  
Mrna Levels ◽  
Bronchial Epithelial ◽  
Receptor Mrna ◽  
Glucocorticoid Receptor Mrna

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 Epithelial SERPINB10, a novel marker of airway eosinophilia in asthma, contributes to allergic airway inflammation

2019 ◽  
Vol 316 (1) ◽  
pp. L245-L254 ◽  
Author(s):  
Yuqing Mo ◽  
Kan Zhang ◽  
Yuchen Feng ◽  
Lingling Yi ◽  
Yuxia Liang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Murine Model ◽  
Allergic Airway Inflammation ◽  
Bronchial Epithelial Cells ◽  
Mrna Levels ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Airway Eosinophilia

Serine peptidase inhibitor, clade B, member 10 (SERPINB10) expression is increased in IL-13-stimulated human bronchial epithelial cells and in a murine model of allergic airway inflammation. However, the role of SERPINB10 in asthma remains unknown. We examined the association between epithelial SERPINB10 expression and airway eosinophilia in subjects with asthma and the role of Serpinb10 in allergic airway inflammation in an animal model. Epithelial SERPINB10 mRNA and protein expression were markedly increased in subjects with asthma ( n = 60) compared with healthy controls ( n = 25). Epithelial SERPINB10 mRNA levels were significantly correlated with airway hyperresponsiveness (AHR) and three parameters reflecting airway eosinophilia including the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa, and fraction of exhaled nitric oxide in subjects with asthma. Moreover, epithelial SERPINB10 expression was strongly correlated with the epithelial gene signature ( CLCA1, POSTN, and SERPINB2) for type 2 status. In normal human bronchial epithelial cells cultured at air-liquid interface, knockdown of SERPINB10 suppressed IL-13-stimulated periostin (encoded by POSTN) and CCL26 (eotaxin-3) expression by inhibiting the activation of p38 MAPK. Epithelial CCL26 mRNA levels were correlated with SERPINB10 expression in subjects with asthma. Airway knockdown of Serpinb10 alleviated AHR, airway eosinophilia and the expression of periostin and Ccl26 in a murine model of allergic airway disease. Taken together, epithelial SERPINB10 is a novel marker for airway eosinophilia in asthma. Epithelial SERPINB10 contributes to allergic airway eosinophilic inflammation, at least in part, by regulating the expression of periostin and CCL26.

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.

Regulation of SLPI and elafin release from bronchial epithelial cells by neutrophil defensins

2000 ◽  
Vol 278 (1) ◽  
pp. L51-L58 ◽  
Author(s):  
Sandra van Wetering ◽  
Abraham C. van der Linden ◽  
Marianne A. J. A. van Sterkenburg ◽  
Willem I. de Boer ◽  
Astrid L. A. Kuijpers ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Proteinase Inhibitor ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Protein Release ◽  
Mrna Levels ◽  
Main Function ◽  
Airway Epithelial ◽  
Dynamic Regulation ◽  
Bronchial Epithelial

Secretory leukocyte proteinase inhibitor (SLPI) is a serine proteinase inhibitor that is produced locally in the lung by cells of the submucosal bronchial glands and by nonciliated epithelial cells. Its main function appears to be the inhibition of neutrophil elastase (NE). Recently, NE was found to enhance SLPI mRNA levels while decreasing SLPI protein release in airway epithelial cells. Furthermore, glucocorticoids were shown to increase both constitutive and NE-induced SLPI mRNA levels. In addition to NE, stimulated neutrophils also release α-defensins. Defensins are small, antimicrobial polypeptides that are found in high concentrations in purulent secretions of patients with chronic airway inflammation. Like NE, defensins induce interleukin-8 production in airway epithelial cells. This induction is sensitive to inhibition by the glucocorticoid dexamethasone and is prevented in the presence of α1-proteinase inhibitor. The aim of the present study was to investigate the effect of defensins on the production of SLPI and the related NE inhibitor elafin/SKALP in primary bronchial epithelial cells (PBECs). Defensins significantly increase SLPI protein release by PBECs in a time- and dose-dependent fashion without affecting SLPI mRNA synthesis. In the presence of α1-proteinase inhibitor, the defensin-induced SLPI protein release is further enhanced, but no effect was observed on SLPI mRNA levels. Dexamethasone did not affect SLPI protein release from control or defensin-treated PBECs. In addition, we observed a constitutive release of elafin/SKALP by PBECs, but this was not affected by defensins. The present results suggest a role for defensins in the dynamic regulation of the antiproteinase screen in the lung at sites of inflammation.

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.

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