A Comparative Study on the Model of PM2.5 Direct or Indirect Interaction with Bronchial Epithelial Cells.

Abstract The impact of PM2.5 on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM2.5 direct interaction with epithelia, macrophages that engulf PM2.5 may also influence the function of epithelial cells. However, among the toxic researches of PM2.5, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM2.5. In this present research, PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model, while the contrast is to indirect stimulation model, which takes advantage of transwell co-culture system to carry out that PM2.5 is promptly contacted with macrophages rather than BEAS-2B. By comparing these two modes of interaction, we determined the viability of BEAS-2B and mRNA and/or protein expression profile of transcription factors Nrf2,NF-kB and according inflammatory indicators, with a view to evaluating the effects of different interaction modes of PM2.5 on epithelial cell damage in vitro. We have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while strengthen the inflammation response.

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Corticosteroids differentially regulate secretion of IL-6, IL-8, and G-CSF by a human bronchial epithelial cell line

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1993.265.4.l360 ◽

1993 ◽

Vol 265 (4) ◽

pp. L360-L368 ◽

Cited By ~ 8

Author(s):

S. J. Levine ◽

P. Larivee ◽

C. Logun ◽

C. W. Angus ◽

J. H. Shelhamer

Keyword(s):

Epithelial Cell ◽

Epithelial Cells ◽

Cell Line ◽

Bronchial Epithelial Cell ◽

Bronchial Epithelial Cells ◽

Human Bronchial Epithelial Cell ◽

Tnf Alpha ◽

Epithelial Cell Line ◽

Human Bronchial Epithelial Cells ◽

Bronchial Epithelial

Human airway epithelial cells play an active role in modulating airway inflammation by elaborating a variety of proinflammatory molecules, including cytokines. The purpose of this study was to define the role of corticosteroids in the regulation of cytokine gene transcription and secretion by human bronchial epithelial cells. In particular, we assessed whether dexamethasone was capable of inhibiting the tumor necrosis factor-alpha (TNF-alpha)-mediated secretion of interleukin-6 (IL-6), interleukin-8 (IL-8), and granulocyte colony-stimulating factor (G-CSF) by a human bronchial epithelial cell line (BEAS-2B). Stimulation with 20 ng/ml of TNF-alpha resulted in significant increases in secretion of immunoreactive IL-6, IL-8, and G-CSF that were maximal at 24 h. TNF-alpha-mediated IL-6, IL-8, and G-CSF secretion was concentration dependent and specific. In addition, stimulation with TNF-alpha resulted in significant increases in the quantity of IL-6, IL-8, and G-CSF mRNA as detected by reverse-transcription polymerase chain reaction. Dexamethasone preconditioning significantly inhibited both the secretion of immunoreactive IL-6 and the accumulation of IL-6 mRNA. Although dexamethasone appeared to reduce both the secretion of immunoreactive IL-8 and accumulation of IL-8 mRNA, the inhibitory effects did not reach statistical significance. Finally, dexamethasone did not inhibit either the secretion of immunoreactive G-CSF or the accumulation of G-CSF mRNA. In summary, our results suggest that corticosteroids have a differential effect on the regulation of cytokine secretion by human bronchial epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Interleukin-9 and Interleukin-13 augment UTP-induced Cl ion transport via hCLCA1 expression in a human bronchial epithelial cell line

Clinical & Experimental Allergy ◽

10.1111/j.1365-2222.2007.02646.x ◽

2007 ◽

Vol 37 (2) ◽

pp. 219-224 ◽

Cited By ~ 5

Author(s):

Y. Endo ◽

K. Isono ◽

M. Kondo ◽

J. Tamaoki ◽

A. Nagai

Keyword(s):

Epithelial Cell ◽

Ion Transport ◽

Cell Line ◽

Bronchial Epithelial Cell ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Bronchial Epithelial ◽

Interleukin 13 ◽

Interleukin 9

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In vitro genotoxicity assay of sidestream smoke using a human bronchial epithelial cell line

Food and Chemical Toxicology ◽

10.1016/s0278-6915(02)00034-0 ◽

2002 ◽

Vol 40 (6) ◽

pp. 845-850 ◽

Cited By ~ 37

Author(s):

L. Wolz ◽

G. Krause ◽

G. Scherer ◽

M. Aufderheide ◽

U. Mohr

Keyword(s):

Epithelial Cell ◽

Cell Line ◽

Bronchial Epithelial Cell ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Bronchial Epithelial ◽

Sidestream Smoke ◽

In Vitro Genotoxicity

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Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00289.2003 ◽

2004 ◽

Vol 286 (4) ◽

pp. L777-L785 ◽

Cited By ~ 14

Author(s):

Kei Takamura ◽

Yasuyuki Nasuhara ◽

Motoko Kobayashi ◽

Tomoko Betsuyaku ◽

Yoko Tanino ◽

...

Keyword(s):

Retinoic Acid ◽

Epithelial Cell ◽

Cell Line ◽

Nuclear Translocation ◽

Bronchial Epithelial Cell ◽

Inhibitory Effect ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Transcriptional Level ◽

Bronchial Epithelial

Retinoic acid (RA) is known to accelerate wound healing and induce cell differentiation. All- trans RA (ATRA) exerts its effect by binding retinoic acid receptors, which are members of the nuclear receptor family. We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-κB. We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. ATRA and its stereodimer 9- cis retinoic acid (9- cis RA) inhibited IL-4-induced release of eotaxin at 10-6M by 78.0 and 52.0%, respectively ( P < 0.05). ATRA and 9- cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10-6M by 52.3 and 53.5%, respectively ( P < 0.05). In contrast, neither ATRA nor 9- cis RA had any effects on TNF-α-induced eotaxin production. In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Interestingly, ATRA had no effects on IL-4-induced tyrosine phosphorylation, nuclear translocation, or DNA binding activity of STAT6. Activating protein-1 was not involved in ATRA-mediated transrepression of eotaxin with IL-4 stimulation. The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. These findings raise the possibility that RA may reduce eosinophilic airway inflammation, one of the prominent pathological features of allergic diseases such as bronchial asthma.

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