Expression and Modulation of Adhesion Molecules on Human Bronchial Epithelial Cells

Bloemen, P. G. M.; Tweel, M.C. van den; Henricks, Paul A.J.; Engels, Ferdi; Wagenaar, Sjoerd Sc.; Rutten, A.A.J.J.L.; Nijkamp, Frans P.

doi:10.1165/ajrcmb/9.6.586

Cited by 133 publications

(90 citation statements)

References 33 publications

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“…The in vivo model system used for our studies does not differentiate the role of direct interaction between bacteria and epithelial cells from the better understood cytokine-dependent mechanisms for inflammatory gene regulation. IFN-␥ and TNF-␣ appear to be the predominant cytokine stimulants of airway epithelial cell ICAM-1 expression (4,5,67), and epithelial cell induction of ICAM-1 by LPS in vivo may be TNF-␣ dependent (72). However, rapid induction of ICAM-1 and other mediators by direct bacterial interaction with epithelial cells, independent of inflammatory mediator release by other cell types, may allow for early targeting of neutrophils to sites of H. influenzae infection resulting in efficient innate defense in the airway.…”

Section: Discussionmentioning

confidence: 99%

Haemophilus influenzaeStimulates ICAM-1 Expression on Respiratory Epithelial Cells

Frick¹,

Joseph²,

Pang³

et al. 2000

The Journal of Immunology

119

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Epithelial cells interact directly with bacteria in the environment and play a critical role in airway defense against microbial pathogens. In this study, we examined the response of respiratory epithelial cells to infection with nontypable Haemophilus influenzae. Using an in vitro cell culture model, we found that epithelial cell monolayers released significant quantities of IL-8 and expressed increased levels of ICAM-1 mRNA and surface protein in response to H. influenzae. In contrast, levels of IL-1β, TNF-α, and MHC class I were not significantly affected, suggesting preferential activation of a specific subset of epithelial genes directed toward defense against bacteria. Induction of ICAM-1 required direct bacterial interaction with the epithelial cell surface and was not reproduced by purified H. influenzae lipooligosaccharide. Consistent with a functional role for this response, induction of ICAM-1 by H. influenzae mediated increased neutrophil adherence to the epithelial cell surface. Furthermore, in an in vivo murine model of airway infection with H. influenzae, increased epithelial cell ICAM-1 expression coincided with increased chemokine levels and neutrophil recruitment in the airway. These results indicate that ICAM-1 expression on human respiratory epithelial cells is induced by epithelial cell interaction with H. influenzae and suggest that an ICAM-1-dependent mechanism can mediate neutrophil adherence to these cells independent of inflammatory mediator release by other cell types. Direct induction of specific epithelial cell genes (such as ICAM-1 and IL-8) by bacterial infection may allow for rapid and efficient innate defense in the airway.

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Section: Discussionmentioning

confidence: 99%

Haemophilus influenzaeStimulates ICAM-1 Expression on Respiratory Epithelial Cells

Frick¹,

Joseph²,

Pang³

et al. 2000

The Journal of Immunology

119

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“…BEAS-2B cell line is derived from epithelial cells, which were isolated from normal human bronchial epithelium and infected with and adenovirus 12-SV40 virus hybrid in order to increase culture longevity [18]. We used BEAS-2B cells as noncancerous control because this cell line is nontumorigenic and retains features of human bronchial epithelial cells [18,19]. As shown in Fig.…”

Section: Activation Of P2x7 Receptor Is Involved In Tgf-β1-induced MImentioning

confidence: 99%

Autocrine signaling via release of ATP and activation of P2X7 receptor influences motile activity of human lung cancer cells

Takai

Tsukimoto

Hishida

et al. 2014

Purinergic Signalling

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Extracellular nucleotides, such as ATP, are released from cells and play roles in various physiological and pathological processes through activation of P2 receptors. Here, we show that autocrine signaling through release of ATP and activation of P2X7 receptor influences migration of human lung cancer cells. Release of ATP was induced by stimulation with TGF-β1, which is a potent inducer of cell migration, in human lung cancer H292 cells, but not in noncancerous BEAS-2B cells. Treatment of H292 cells with a specific antagonist of P2X7 receptor resulted in suppression of TGF-β1-induced migration. PC-9 human lung cancer cells released a large amount of ATP under standard cell culture conditions, and P2X7 receptor-dependent dye uptake was observed even in the absence of exogenous ligand, suggesting constitutive activation of P2X7 receptor in this cell line. PC-9 cells showed high motile activity, which was inhibited by treatment with ecto-nucleotidase and P2X7 receptor antagonists, whereas a P2X7 receptor agonist enhanced migration. PC-9 cells also harbor a constitutively active mutation in epidermal growth factor receptor (EGFR). Treatment with EGFR tyrosine kinase inhibitor AG1478 suppressed both cell migration and P2X7 receptor expression in PC-9 cells. Compared to control PC-9 cells, cells treated with P2X7 antagonist exhibited broadened lamellipodia around the cell periphery, while AG1478-treated cells lacked lamellipodia. These results indicate that P2X7-mediated signaling and EGFR signaling may regulate migration of PC-9 cells through distinct mechanisms. We propose that autocrine ATP-P2X7 signaling is involved in migration of human lung cancer cells through regulation of actin cytoskeleton rearrangement.

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“…Such immunoliposomes can bind to cells expressing the target antigen by multivalent interactions [20,211. Immunoliposomes specifically directed against the adhesion molecule ICAM-1 were prepared, using the anti-ICAM-I mAb F 10.2 [22], characterised and evaluated for their in vitro binding capacity to cells expressing ICAM-1. As target cells we used human umbilical vein endothelial cells (HUVEC) and the bronchial epithelial cell line BEAS-2B, which are well characterized for their ICAM-1 expression [23,24]. We show that the F10.2-mediated targeting of liposomes to ICAM-1 expressing cells is rapid, specific and positively correlated with the degree of ICAM-1 expression.…”

Section: Introductionmentioning

confidence: 99%

Adhesion molecules: a new target for immunoliposome‐mediated drug delivery

et al. 1995

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The anti-ICAM-1 monoclonal antibody FI0.2 was conjugated to liposomes to target to cells expressing the cell adhesion molecule ICAM-1. We demonstrate that F10.2 immunoliposomes bind to human bronchial epithelial cells (BEAS-2B) and human umbilical vein endothelial cells (HUVEC) in a specific, dose-and time-dependent manner. It appears that the degree of ICAM-I expression is the limiting factor in the degree of immunoliposome binding to the cells. These results are a first step in the strategy for specific drug delivery to target sites characterised by increased expression of adhesion molecules.

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Expression and Modulation of Adhesion Molecules on Human Bronchial Epithelial Cells

Cited by 133 publications

References 33 publications

Haemophilus influenzaeStimulates ICAM-1 Expression on Respiratory Epithelial Cells

Haemophilus influenzaeStimulates ICAM-1 Expression on Respiratory Epithelial Cells

Autocrine signaling via release of ATP and activation of P2X7 receptor influences motile activity of human lung cancer cells

Adhesion molecules: a new target for immunoliposome‐mediated drug delivery

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