scholarly journals Adherence of Streptococcus pneumoniae to Human Bronchial Epithelial Cells (BEAS-2B)

1998 ◽  
Vol 66 (2) ◽  
pp. 820-822 ◽  
Author(s):  
John E. Adamou ◽  
Theresa M. Wizemann ◽  
Philip Barren ◽  
Solomon Langermann
Keyword(s):  
Streptococcus Pneumoniae ◽  
Epithelial Cells ◽  
Cell Line ◽  
Pneumococcal Infection ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Bronchial Epithelial

ABSTRACT Pneumococcal adherence to alveolar epithelial cells and nasopharyngeal epithelial cells has been well characterized. However, the interaction of Streptococcus pneumoniae with bronchial epithelial cells has not been studied. We have now shown that pneumococci bind specifically to a human bronchial epithelial cell line (BEAS-2B cells). Pneumococci adhered to BEAS-2B cells in a time- and dose-dependent manner. These results suggest that the bronchial epithelium may serve as an additional site of attachment for pneumococci and demonstrate the utility of the BEAS-2B cell line for studying mechanisms of pneumococcal infection.

Stimulation of both human bronchial epithelium and neutrophils is needed for maximal interactive adhesion

1996 ◽  
Vol 270 (1) ◽  
pp. L80-L87 ◽  
Author(s):  
P. G. Bloemen ◽  
M. C. Van den Tweel ◽  
P. A. Henricks ◽  
F. Engels ◽  
M. J. Van de Velde ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cultured Cells ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Tnf Alpha ◽  
Epithelial Cell Line ◽  
Ifn Gamma ◽  
Bronchial Epithelial ◽  
Stimulation Of

It has become clear that the bronchial epithelium is not just a passive barrier but plays an active role in inflammation. It can produce several inflammatory mediators and does express cell adhesion molecules of which intercellular adhesion molecule (ICAM)-1 can be upregulated by cytokines like interferon (IFN)-gamma. In the present study, we analyzed in detail the interaction of neutrophils with human bronchial epithelial cells, both primary cultured cells and the bronchial epithelial cell line BEAS-2B. Confluent monolayers of epithelial cells were incubated with freshly isolated 51Cr-labeled neutrophils for 30 min at 37 degrees C; then the nonadherent cells were removed by washing gently. Stimulation of the epithelial cells with IFN-gamma or the combination of IFN-gamma and tumor necrosis factor-alpha (TNF-alpha) (which doubles the ICAM-1 expression) increased neutrophil adhesion. Activation of the neutrophils themselves with N-formylmethionyl-leucyl-phenylalanine (fMLP), platelet-activating factor, or TNF-alpha also caused a profound enhancement of the adhesion. A significant additional increase was found when the epithelial cells had been exposed to IFN-gamma and the neutrophils were stimulated with fMLP simultaneously. This effect was even more pronounced with epithelium preincubated with IFN-gamma and TNF-alpha. With the use of monoclonal antibodies against CD18 and ICAM-1, it was demonstrated that the increased adhesion was mainly mediated by the ICAM-1/beta 2-integrin interaction. This study highlights that both the activation state of the bronchial epithelial cells and the activation state of the neutrophils are critical for their interactive adhesion.

Feedlot dust stimulation of interleukin-6 and -8 requires protein kinase Cε in human bronchial epithelial cells

2007 ◽  
Vol 293 (5) ◽  
pp. L1163-L1170 ◽  
Author(s):  
Todd A. Wyatt ◽  
Rebecca E. Slager ◽  
Jane DeVasure ◽  
Brent W. Auvermann ◽  
Michael L. Mulhern ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Cell Line ◽  
Bronchial Epithelial Cells ◽  
Dominant Negative ◽  
Dependent Manner ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Dust Extract

Individuals exposed to dusts from concentrated animal feeding operations report increased numbers of respiratory tract symptoms, and bronchoalveolar lavage samples from such individuals demonstrate elevated lung inflammatory mediators, including interleukin (IL)-8 and IL-6. We previously found that exposure of bronchial epithelial cells to hog barn dusts resulted in a protein kinase C (PKC)-dependent increase in IL-6 and IL-8 release. We hypothesized that cattle feedlot dusts would also generate bronchial epithelial interleukin release in vitro. To test this, we used interleukin ELISAs and direct PKC isoform assays. We found that a dust extract from cattle feedlots [feedlot dust extract (FLDE)] augments PKC activity of human bronchial epithelial cells in vitro. A 5–10% dilution of FLDE stimulated a significant release of IL-6 and IL-8 at 6–24 h in a PKC-dependent manner vs. control medium-treated cells. An increase in PKCα activity was observed with 1 h of FLDE treatment, and PKCε activity was elevated at 6 h of FLDE exposure. The PKCα inhibitor, Gö-6976, did not inhibit FLDE-stimulated IL-8 and IL-6 release. However, the PKCε inhibitor, Ro 31-8220, effectively inhibited FLDE-stimulated IL-8 and IL-6 release. Inhibition of FLDE-stimulated IL-6 and IL-8 was confirmed in a dominant-negative PKCε-expressing BEAS-2B cell line but not observed in a PKCα dominant negative BEAS-2B cell line. These data support the hypothesis that FLDE exposure stimulates bronchial epithelial IL-8 and IL-6 release via a PKCε-dependent pathway.

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

1993 ◽  
Vol 265 (4) ◽  
pp. L360-L368 ◽  
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)

scholarly journals STING Mediates Cytosolic Dna-Induced Muc5ac Mrna Expression in Human Bronchial Epithelial Cells

2020 ◽  
Author(s):  
Masaya Ohta ◽  
Yutaka Nishida ◽  
Hisako Yagi ◽  
Aikira Aizawa ◽  
Takahito Oyanagi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
Cell Types ◽  
Bronchial Epithelial Cells ◽  
Epithelial Cell Line ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Dna Sensing ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Abstract Background: Non-autologous and autologous cytosolic DNA are recognized as danger signals by cytoplasmic sensor molecules that activate signal-transduction pathways. An important molecule in cytosolic DNA sensing is stimulator of interferon genes (STING), an endoplasmic reticulum protein activated by cyclic GMP–AMP (cGAMP) produced in response to cytosolic DNA. STING is important for innate immune responses to cytosolic DNA in immune cells; however, knowledge about its role in bronchial epithelial cells is limited. Methods: We stimulated NCI-H292 cells with poly(dA:dT) and silenced STING and other regulatory proteins, and then determined MUC5AC mRNA expression levels. Results: Cytosolic DNA increased the expression of a major respiratory mucin protein, MUC5AC, in the human respiratory epithelial cell line NCI-H292 in a STING-dependent manner. Introducing poly(dA:dT) into the cytoplasm induced MUC5AC and interferon-β (IFNβ) expression. Silencing STING by RNA interference decreased poly(dA:dT)-induced MUC5AC mRNA expression but increased IFN-β mRNA levels. Furthermore, cGAMP treatment increased MUC5AC expression but not IFN-β expression. In contrast, silencing retinoic acid-inducible gene-I (RIG-I), which is a component of a different nucleic acid-sensing system, suppressed poly(dA:dT)-induced IFN-β expression and increased MUC5AC expression. Conclusions: Unlike its role in other cell types, in human bronchial epithelial cells, STING is central to cytosolic DNA-induced MUC5AC expression, whereas IFN-β expression is dependent on RIG-I. Our data indicate a functional interaction between the STING and RIG-I pathways, suggesting the existence of intricate and cell-specific cytosolic DNA-sensing systems.

scholarly journals Vitamin D Modulates the Response of Bronchial Epithelial Cells Exposed to Cigarette Smoke Extract

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2138 ◽  
Author(s):  
Carolien Mathyssen ◽  
Jef Serré ◽  
Annelore Sacreas ◽  
Stephanie Everaerts ◽  
Karen Maes ◽  
...  
Keyword(s):  
Vitamin D ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Bronchial Epithelium ◽  
Cigarette Smoke Extract ◽  
Bronchial Epithelial Cells ◽  
Epithelial Cell Line ◽  
Impaired Wound Healing ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition

In chronic obstructive pulmonary disease (COPD), the bronchial epithelium is the first immune barrier that is triggered by cigarette smoke. Although vitamin D (vitD) has proven anti-inflammatory and antimicrobial effects in alveolar macrophages, little is known about the direct role of vitD on cigarette smoke-exposed bronchial epithelial cells. We examined the effects of vitD on a human bronchial epithelial cell line (16HBE) and on air–liquid culture of primary bronchial epithelial cells (PBEC) of COPD patients and controls exposed for 24 h to cigarette smoke extract (CSE). VitD decreased CSE-induced IL-8 secretion by 16HBE cells, but not by PBEC. VitD significantly increased the expression of the antimicrobial peptide cathelicidin in 16HBE and PBEC of both COPD subjects and controls. VitD did not affect epithelial to mesenchymal transition or epithelial MMP-9 expression and was not able to restore impaired wound healing by CSE in 16HBE cells. VitD increased the expression of its own catabolic enzyme CYP24A1 thereby maintaining its negative feedback. In conclusion, vitD supplementation may potentially reduce infectious exacerbations in COPD by the upregulation of cathelicidin in the bronchial epithelium.

Biosynthesized matrix provides a key role for survival signaling in bronchial epithelial cells

2004 ◽  
Vol 286 (3) ◽  
pp. L596-L603 ◽  
Author(s):  
Sam J. Wadsworth ◽  
Anette M. Freyer ◽  
Randolph L. Corteling ◽  
Ian P. Hall
Keyword(s):  
Growth Factors ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Survival ◽  
Cell Line ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial Cells ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Survival Signals

The extracellular matrix (ECM) influences a variety of cellular functions, including survival, adhesion molecule expression, differentiation, and migration. The ECM composition of the epithelial basement membrane is altered in asthmatics. In this study, we elucidate the major survival signals received by bronchial epithelial cells in vitro by studying the effects of a variety of ECM factors and soluble growth factors on bronchial epithelial cell survival. Our findings indicate that the insulin family of soluble growth factors provides important survival signals but also that adhesion to ECM is a crucial determinant of bronchial epithelial cell survival. In the BEAS-2B bronchial epithelial cell line, collagens I and IV, laminin, fibronectin, and vitronectin provide significant levels of protection from apoptosis. Tenascin-C has no effect, whereas elastin and collagen V increase apoptosis to above control levels. BEAS-2B cells secrete their own biosynthesized matrix (BSM), which also provides rescue from apoptosis. Protection by collagen I, fibronectin, and vitronectin was found to be via an RGD domain. Laminin-, collagen IV-, and BSM-mediated survival is not RGD dependent. Primary bronchial epithelial cells exhibit a similar pattern of apoptosis rescue to the BEAS-2B cell line, although we did not observe any vitronectin-mediated protection in the primary cells. These data indicate that bronchial epithelial cell survival is dependent both on soluble growth factors and on a variety of ECM-derived signals.

scholarly journals Haemophilus influenzae causes cellular trans-differentiation in human bronchial epithelia

2021 ◽  
Vol 27 (3) ◽  
pp. 251-259
Author(s):  
Michael Glöckner ◽  
Sebastian Marwitz ◽  
Kristina Rohmann ◽  
Henrik Watz ◽  
Dörte Nitschkowski ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Haemophilus Influenzae ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Respiratory Pathogen ◽  
Chronic Obstructive ◽  
Bronchial Epithelial ◽  
Extracellular Matrix Components ◽  
The Impact ◽  
Primary Bronchial Epithelial Cells

Non-typeable Haemophilus influenzae (NTHi) is the most common respiratory pathogen in patients with chronic obstructive disease. Limited data is available investigating the impact of NTHi infections on cellular re-differentiation processes in the bronchial mucosa. The aim of this study was to assess the effects of stimulation with NTHi on the bronchial epithelium regarding cellular re-differentiation processes using primary bronchial epithelial cells harvested from infection-free patients undergoing bronchoscopy. The cells were then cultivated using an air-liquid interface and stimulated with NTHi and TGF-β. Markers of epithelial and mesenchymal cells were analyzed using immunofluorescence, Western blot and qRT-PCR. Stimulation with both NTHi and TGF-ß led to a marked increase in the expression of the mesenchymal marker vimentin, while E-cadherin as an epithelial marker maintained a stable expression throughout the experiments. Furthermore, expression of collagen 4 and the matrix-metallopeptidases 2 and 9 were increased after stimulation, while the expression of tissue inhibitors of metallopeptidases was not affected by pathogen stimulation. In this study we show a direct pathogen-induced trans-differentiation of primary bronchial epithelial cells resulting in a co-localization of epithelial and mesenchymal markers and an up-regulation of extracellular matrix components.

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.

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