scholarly journals Effect of mineral particles containing iron on primary cultures of rabbit tracheal epithelial cells: possible implication of oxidative stress.

1993 ◽  
Vol 101 (5) ◽  
pp. 436-442 ◽  
Author(s):  
C Guilianelli ◽  
A Baeza-Squiban ◽  
E Boisvieux-Ulrich ◽  
O Houcine ◽  
R Zalma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Primary Cultures ◽  
Tracheal Epithelial Cells ◽  
Mineral Particles ◽  
Tracheal Epithelial

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

Application of glutathione to antagonize H2O2-induced oxidative stress in rat tracheal epithelial cells

2016 ◽  
Vol 11 (1) ◽  
pp. 59-63
Author(s):  
Jian Zou ◽  
Jinbo Yu ◽  
Yuqing Zhu ◽  
Jiali Zhu ◽  
Jing Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

scholarly journals Protective Effects of Licochalcone A Improve Airway Hyper-Responsiveness and Oxidative Stress in a Mouse Model of Asthma

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 617 ◽  
Author(s):  
Wen-Chung Huang ◽  
Chien-Yu Liu ◽  
Szu-Chuan Shen ◽  
Li-Chen Chen ◽  
Kuo-Wei Yeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Therapeutic Potential ◽  
Intercellular Adhesion Molecule ◽  
Eosinophil Infiltration ◽  
Licochalcone A ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
Oxidative Responses

Licochalcone A was isolated from Glycyrrhiza uralensis and previously reported to have antitumor and anti-inflammatory effects. Licochalcone A has also been found to inhibit the levels of Th2-associated cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. However, the molecular mechanism underlying airway inflammation and how licochalcone A regulates oxidative stress in asthmatic mice are elusive. In this study, we investigated whether licochalcone A could attenuate inflammatory and oxidative responses in tracheal epithelial cells, and whether it could ameliorate oxidative stress and airway inflammation in asthmatic mice. Inflammatory human tracheal epithelial (BEAS-2B) cells were treated with licochalcone A to evaluate oxidative responses and inflammatory cytokine levels. In addition, BALB/c mice were sensitized with ovalbumin (OVA) and injected intraperitoneally with licochalcone A (5 or 10 mg/kg). Licochalcone A significantly inhibited reactive oxygen species, eotaxin, and proinflammatory cytokines in BEAS-2B cells. Licochalcone A also decreased intercellular adhesion molecule 1 levels in inflammatory BEAS-2B cells, blocking monocyte cell adherence. We also found that licochalcone A significantly decreased oxidative responses, reduced malondialdehyde levels, and increased glutathione levels in the lungs of OVA-sensitized mice. Furthermore, licochalcone A decreased airway hyper-responsiveness, eosinophil infiltration, and Th2 cytokine production in the BALF. These findings suggest that licochalcone A alleviates oxidative stress, inflammation, and pathological changes by inhibiting Th2-associated cytokines in asthmatic mice and human tracheal epithelial cells. Thus, licochalcone A demonstrated therapeutic potential for improving asthma.

Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells

2000 ◽  
Vol 278 (3) ◽  
pp. L560-L571 ◽  
Author(s):  
Tomoko Suzuki ◽  
Mutsuo Yamaya ◽  
Kiyohisa Sekizawa ◽  
Norihiro Yamada ◽  
Katsutoshi Nakayama ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Cultures ◽  
Viral Rna ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tracheal Epithelial Cells ◽  
Rhinovirus Infection ◽  
Infected Cells ◽  
Tracheal Epithelial ◽  
Viral Titers

To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection.

Molecular responses of rat tracheal epithelial cells to transmembrane pressure

2000 ◽  
Vol 278 (6) ◽  
pp. L1264-L1272 ◽  
Author(s):  
Barbara Ressler ◽  
Richard T. Lee ◽  
Scott H. Randell ◽  
Jeffrey M. Drazen ◽  
Roger D. Kamm
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Muscle Activation ◽  
Primary Cultures ◽  
Transmembrane Pressure ◽  
Apical Surface ◽  
Dependent Manner ◽  
Tracheal Epithelial Cells ◽  
Compressive Stresses ◽  
Tracheal Epithelial

Smooth muscle constriction in asthma causes the airway to buckle into a rosette pattern, folding the epithelium into deep crevasses. The epithelial cells in these folds are pushed up against each other and thereby experience compressive stresses. To study the epithelial cell response to compressive stress, we subjected primary cultures of rat tracheal epithelial cells to constant elevated pressures on their apical surface (i.e., a transmembrane pressure) and examined changes in the expression of genes that are important for extracellular matrix production and maintenance of smooth muscle activation. Northern blot analysis of RNA extracted from cells subjected to transmembrane pressure showed induction of early growth response-1 (Egr-1), endothelin-1, and transforming growth factor-β1 in a pressure-dependent and time-dependent manner. Increases in Egr-1 protein were detected by immunohistochemistry. Our results demonstrate that airway epithelial cells respond rapidly to compressive stresses. Potential transduction mechanisms of transmembrane pressure were also investigated.

scholarly journals Levofloxacin Inhibits Rhinovirus Infection in Primary Cultures of Human Tracheal Epithelial Cells

2012 ◽  
Vol 56 (8) ◽  
pp. 4052-4061 ◽  
Author(s):  
Mutsuo Yamaya ◽  
Hidekazu Nishimura ◽  
Yukimasa Hatachi ◽  
Hiroyasu Yasuda ◽  
Xue Deng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Bacterial Infections ◽  
Mrna Level ◽  
Primary Cultures ◽  
Intercellular Adhesion Molecule ◽  
Soluble Form ◽  
Chronic Obstructive ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACTRespiratory virus infections, including infections with rhinoviruses (RVs), are related to exacerbations of chronic obstructive pulmonary disease (COPD). A new quinolone antibiotic, levofloxacin (LVFX), has been used to treat bacterial infections that cause COPD exacerbations as well as bacterial infections that are secondary to viral infection in COPD patients. However, the inhibitory effects of LVFX on RV infection and RV infection-induced airway inflammation have not been studied. We examined the effects of LVFX on type 14 rhinovirus (RV14) (a major human RV) infection of human tracheal epithelial cells pretreated with LVFX. LVFX pretreatment reduced the RV14 titer, the level of cytokines in the supernatant, the amount of RV14 RNA in the cells after RV14 infection, and the cells' susceptibility to RV14 infection. LVFX pretreatment decreased the mRNA level of intercellular adhesion molecule 1 (ICAM-1), a receptor for RV14, in the cells and the concentration of the soluble form of ICAM-1 in the supernatant before RV14 infection. LVFX pretreatment also decreased the number and the fluorescence intensity of the acidic endosomes from which RV14 RNA enters the cytoplasm. LVFX pretreatment inhibited the activation of nuclear factor κB proteins, including p50 and p65, in nuclear extracts. LVFX pretreatment did not reduce the titers of RV2 (a minor human RV) but reduced the titers of RV15 (a major human RV). These results suggest that LVFX inhibits major-group rhinovirus infections in part by reducing ICAM-1 expression levels and the number of acidic endosomes. LVFX may also modulate airway inflammation in rhinoviral infections.

Prostaglandin secretion by guinea pig tracheal epithelial cells caused by eosinophil major basic protein

1993 ◽  
Vol 265 (3) ◽  
pp. L234-L242 ◽  
Author(s):  
S. R. White ◽  
K. S. Sigrist ◽  
S. M. Spaethe
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Basic Protein ◽  
Primary Cultures ◽  
Thromboxane B2 ◽  
Major Basic Protein ◽  
Tracheal Epithelial Cells ◽  
Subsequent Response ◽  
Tracheal Epithelial ◽  
Eosinophil Major Basic Protein

We examined the effect of eosinophil major basic protein (MBP) on prostaglandin (PG) secretion from guinea pig tracheal epithelial (GPTE) cells. Primary cultures of GPTE cells were incubated with 10(-6) M MBP for up to 6 h and then stimulated with 10(-6) M bradykinin (BK). PGE2, 6-ketoprostaglandin F1 alpha (PGF1 alpha), PGF2 alpha, and thromboxane B2 (TxB2) concentrations in media were determined by enzyme-linked immunoabsorbent assay (EIA). Incubation with MBP for 6 h caused secretion of both PGE2 (17,614 +/- 4,416 vs. 1,426 +/- 555 pg/10(6) cells at baseline, P < 0.001, n = 7) and PGF2 alpha (20,303 +/- 5,724 vs. 3,790 +/- 1.075 pg/10(6) cells at baseline, P < 0.002, n = 7). Secretion of PGE2 and PGF2 alpha stimulated by MBP required at least 2 h. Incubation with MBP for 6 h also augmented the subsequent response to BK: PGE2 secretion was 29,215 +/- 6,853 vs. 3,445 +/- 1,041 pg/10(6) cells for BK alone (P < 0.0001), and PGF2 alpha secretion was 25,407 +/- 6,237 vs. 5,213 +/- 1,535 pg/10(6) cells for BK alone (P < 0.0001). MBP did not change 6-keto-PGF1 alpha and TxB2 secretion. Incubation of GPTE cells from seven animals with polylysine, a protein with mass and ion charge similar to MBP, for 2 h, both caused secretion of PGE2 (8,579 +/- 3,244 vs. 788 +/- 419 pg/10(6) cells at baseline, P < 0.01) and augmented the response to BK (12,732 +/- 4,788 vs. 1,653 +/- 680 pg/10(6) cells after BK alone, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Formoterol and budesonide inhibit rhinovirus infection and cytokine production in primary cultures of human tracheal epithelial cells

2014 ◽  
Vol 52 (4) ◽  
pp. 251-260 ◽  
Author(s):  
Mutsuo Yamaya ◽  
Hidekazu Nishimura ◽  
Lusamba Nadine ◽  
Hiroshi Kubo ◽  
Ryoichi Nagatomi
Keyword(s):  
Epithelial Cells ◽  
Cytokine Production ◽  
Primary Cultures ◽  
Tracheal Epithelial Cells ◽  
Rhinovirus Infection ◽  
Tracheal Epithelial
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