Circulating Adhesion Molecules in Cystic Fibrosis

Rose, Virginia De; Oliva, Anthony M.; Messore, Barbara; Grosso, B.; Mollar, C.; Pozzi, Elisa

doi:10.1164/ajrccm.157.4.9704134

Cited by 50 publications

(40 citation statements)

References 33 publications

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“…Further studies are needed to characterize the expression of the counterligands of PMN from airways in its adhesion to airway epithelial cells. Our data showing that ICAM-1 is more expressed in cftr-deficient IB3-1 cells compared with C38 and BEAS-2B cells corroborates with other studies showing high ICAM-1 expression in the CFTE29o Ϫ cell line (⌬F508 homozygote tracheal epithelial cells) (22) and elevated soluble ICAM-1 levels in blood samples from CF patients (14).…”

Section: Discussionsupporting

confidence: 92%

Adherence of airway neutrophils and inflammatory response are increased in CF airway epithelial cell-neutrophil interactions

Tabary¹,

Corvol²,

Boncoeur³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Persistent presence of PMN in airways is the hallmark of CF. Our aim was to assess PMN adherence, percentage of apoptotic airway PMN (aPMN), and IL-6 and IL-8 production when aPMN are in contact with airway epithelial cells. Before coculture, freshly isolated CF aPMN have greater spontaneous and TNF-α-induced apoptosis compared with blood PMN from the same CF patients and from aPMN of non-CF patients. We then examined cocultures of PMN isolated from CF and non-CF airways with bronchial epithelial cells bearing mutated cftr compared with cftr-corrected bronchial epithelial cells. After 18-h coculture, the number of CF aPMN adhered on cftr-deficient bronchial epithelial cells was 2.3-fold higher compared with the coculture of non-CF aPMN adhered on cftr-corrected bronchial epithelial cells. The percentage of CF apoptotic aPMN (9.5 ± 0.2%) adhered on cftr-deficient bronchial epithelial cells was similar to the percentage of non-CF apoptotic aPMN adhered on cftr-corrected bronchial epithelial cells (10.3 ± 0.7%). IL-6 and IL-8 levels were enhanced 6.5- and 2.9-fold, respectively, in coculture of CF aPMN adhered on cftr-deficient bronchial epithelial cells compared with coculture of non-CF aPMN adhered on cftr-corrected bronchial epithelial cells. Moreover, blocking surface adhesion molecules ICAM-1, VCAM-1, and E-selectin on cftr-deficient bronchial epithelial cells with specific MAbs inhibited the adherence of CF aPMN by 64, 51, and 50%, respectively. Our data suggest that in CF patients a high number of nonapoptotic PMN adhered on airway epithelium associated with elevated IL-6 and IL-8 levels may contribute to sustained and exaggerated inflammatory response in CF airways.

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Section: Discussionsupporting

confidence: 92%

Adherence of airway neutrophils and inflammatory response are increased in CF airway epithelial cell-neutrophil interactions

Tabary¹,

Corvol²,

Boncoeur³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Thus, IL-8, in concert with ENA-78 and the GRO family, plays a vital role in the pathophysiology of inflammatory lung disease. These potent chemokines attract neutrophils to inflammatory sites, where their transepithelial passage is facilitated by ICAM-1 and their survival is prolonged by the hemopoietic cytokine GM-CSF (49,50). In this study both A46R and A52R were found to inhibit IL-1-and NE-induced GM-CSF up-regulation in bronchial epithelial cells.…”

Section: Discussionmentioning

confidence: 53%

Viral Inhibition of IL-1- and Neutrophil Elastase-Induced Inflammatory Responses in Bronchial Epithelial Cells

Carroll

Greene

Taggart

et al. 2005

The Journal of Immunology

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Previously, we elucidated the intracellular mechanisms by which neutrophil elastase (NE) up-regulates inflammatory gene expression in bronchial epithelial cells. In this study, we examine the effects of both IL-1 and NE on inflammatory gene expression in 16HBE14o− bronchial epithelial cells and investigate approaches to abrogate these inflammatory responses. IL-1 induced IL-8 protein production in time- and dose-dependent fashions, an important observation given that IL-8 is a potent neutrophil chemoattractant and a key inflammatory mediator. IL-1 and NE were shown to activate the p38 MAPK pathway in 16HBE14o− cells. Western blot analysis demonstrated IL-1R-associated kinase 1 (IRAK-1) degradation in response to stimulation with both IL-1 and NE. In addition, the expression of dominant negative IRAK-1 (IRAK-1Δ), IRAK-2Δ, or IRAK-4Δ inhibited IL-1- and NE-induced NF-κB-linked reporter gene expression. Dominant negative versions of the intracellular adaptor proteins MyD88 (MyD88Δ) and MyD88 adaptor-like (Mal P/H) abrogated NE-induced NF-κB reporter gene expression. In contrast, only MyD88Δ was found to inhibit IL-1-induced NF-κB reporter activity. We also investigated the vaccinia virus proteins, A46R and A52R, which have been shown to antagonize IL-1 signaling. Transfection with A46R or A52R cDNA inhibited IL-1- and NE-induced NF-κB and IL-8R gene expression and IL-8 protein production in primary and transformed bronchial epithelial cells. Furthermore, cytokine array studies demonstrated that IL-1 and NE can up-regulate the expression of IL-6, oncostatin M, epithelial cell-derived neutrophil activating peptide-78, growth-related oncogene family members, vascular endothelial growth factor, and GM-CSF, with induction of these proteins inhibited by the viral proteins. These findings identify vaccinia virus proteins as possible therapeutic agents for the manifestations of several inflammatory lung diseases.

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“…Among the adhesion molecules up-regulated in the P. aeruginosa-infected airway is ICAM-1 (21,22). To our knowledge, our studies were the first to examine the effect of P. aeruginosa phenazines on ICAM-1 expression (20).…”

mentioning

confidence: 86%

Pyocyanin and Its Precursor Phenazine-1-Carboxylic Acid Increase IL-8 and Intercellular Adhesion Molecule-1 Expression in Human Airway Epithelial Cells by Oxidant-Dependent Mechanisms

Look¹,

Stoll²,

Romig³

et al. 2005

The Journal of Immunology

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Pseudomonas aeruginosa secretes numerous factors that alter host cell function and may contribute to disease pathogenesis. Among recognized virulence factors is the redox-active phenazine pyocyanin. We have recently demonstrated that the precursor for pyocyanin, phenazine-1-carboxylic acid (PCA), increases oxidant formation and alters gene expression in human airway epithelial cells. We report in this work that PCA and pyocyanin increase expression of ICAM-1 both in vivo and in vitro. Moreover, phenazines enhanced cytokine-dependent increases in IL-8 and ICAM-1. Antioxidant intervention studies indicated both similarities and differences between PCA and pyocyanin. The thiol antioxidant N-acetyl cysteine, extracellular catalase, and inducible NO synthase inhibitors inhibited ICAM-1 and IL-8 increases in response to both phenazines. However, pyocyanin was significantly more sensitive to N-acetylcysteine inhibition. Interestingly, hydroxyl radical scavengers inhibited the response to pyocyanin, but not to PCA. These studies suggest that P. aeruginosa phenazines coordinately up-regulate chemokines (IL-8) and adhesion molecules (ICAM-1) by mechanisms that are, at least in part, oxidant dependent. However, results indicate that the mechanisms by which PCA and pyocyanin exert their effects are not identical, and not all antioxidant interventions are equally effective in inhibiting phenazine-mediated proinflammatory effects.

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Circulating Adhesion Molecules in Cystic Fibrosis

Cited by 50 publications

References 33 publications

Adherence of airway neutrophils and inflammatory response are increased in CF airway epithelial cell-neutrophil interactions

Adherence of airway neutrophils and inflammatory response are increased in CF airway epithelial cell-neutrophil interactions

Viral Inhibition of IL-1- and Neutrophil Elastase-Induced Inflammatory Responses in Bronchial Epithelial Cells

Pyocyanin and Its Precursor Phenazine-1-Carboxylic Acid Increase IL-8 and Intercellular Adhesion Molecule-1 Expression in Human Airway Epithelial Cells by Oxidant-Dependent Mechanisms

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