Mutual activation of pulmonary fibroblasts and eosinophils, and modulation by drugs in relation to asthma

Spoelstra, FM; Postma, Dirkje S.; Kauffman, Hf

doi:10.1046/j.1365-2222.2001.01111.x

Cited by 17 publications

(18 citation statements)

References 69 publications

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“…Our data on ICAM-1 and VCAM-1 expression on lung fibroblasts are in accordance with the results of the adhesion of eosinophils to lung fibroblasts. In addition to the adhesion of eosinophils to lung fibroblasts, they produce granulocyte-macrophage colony-stimulating factor (GM-CSF), which leads to the activation, chemotaxis, and survival of eosinophils in the pulmonary tissues [28]. Procaterol significantly inhibited the release of GM-CSF from lung fibroblasts, and the additive interaction was found with the combination of procaterol and budesonide (unpubl.…”

Section: Discussionmentioning

confidence: 99%

Procaterol Potentiates the Anti-Inflammatory Activity of Budesonide on Eosinophil Adhesion to Lung Fibroblasts

Yoshida

Muraguchi²,

Kamata³

et al. 2009

Int Arch Allergy Immunol

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Background: The interaction between leukocytes and various parenchymal cells is the first step of inflammation. Therefore, the adhesion of eosinophils to lung fibroblasts is thought to be a crucial step in the inflammatory process of asthma. Procaterol, a β₂-selective full agonist, is currently prescribed for patients with asthma. In addition to its potent bronchodilatory action, the agonist has been reported to have anti-inflammatory actions. In this study, to examine whether procaterol can potentiate the anti-inflammatory action of glucocorticoids, the effect of procaterol on eosinophil adhesion to normal human lung fibroblasts (NHLF) was assessed in the presence and absence of budesonide, one of the most potent glucocorticoids. Methods: Following pretreatment of NHLF with tumor necrosis factor-α (TNF-α) in the presence of various concentrations of procaterol and/or budesonide, the eotaxin-stimulated eosinophil adhesion was determined using the peroxidase activity of eosinophils. To investigate the mechanism of the inhibitory action of procaterol, TNF-α-induced expression of adhesion molecules, ICAM-1 and VCAM-1, in NHLF was also evaluated. Results: Pretreatment with procaterol inhibited the adhesion of eosinophils to NHLF in a concentration-dependent manner, and shifted the concentration-response curve of budesonide to the left. Both procaterol and budesonide resulted in concentration-dependent inhibition of expression of ICAM-1 and VCAM-1 in NHLF, and an additive inhibitory effect was found when the agents were combined. Conclusions: Given the results of this study which indicated that procaterol exerted an additive action on the anti-inflammatory effect of budesonide, procaterol and glucocorticoids may provide better control for asthma when used together than when used separately.

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Section: Discussionmentioning

confidence: 99%

Procaterol Potentiates the Anti-Inflammatory Activity of Budesonide on Eosinophil Adhesion to Lung Fibroblasts

Yoshida

Muraguchi²,

Kamata³

et al. 2009

Int Arch Allergy Immunol

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“…In addition, eosinophil-derived secondary granule proteins and expression of IL-1, IL-13, and TGF-b contribute to fibroblast migration and the release of additional growth factors, proteases, and cytokines. 46 Collectively, these eosinophil-fibroblast interactions appear to be not only important contributors to local immune responses but also critical components of tissue remodeling and repair events associated with many organ/tissue-specific inflammatory events.…”

Section: Fibroblastsmentioning

confidence: 99%

Eosinophils: Singularly destructive effector cells or purveyors of immunoregulation?

Jacobsen¹,

Taranova²,

Lee³

et al. 2007

Journal of Allergy and Clinical Immunology

184

138

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“…The inflammatory process underlying asthma results from a highly complex interaction of various cell types (3)(4)(5). In addition, ECM interacts with inflammatory cells (6), forms a reservoir for cytokines and growth factors (7,8), influences trafficking of cells (9), and activates granulocytes to increase mediator release and enhance their survival (10,11).…”

mentioning

confidence: 99%

Regulation of Activin A Expression in Mast Cells and Asthma: Its Effect on the Proliferation of Human Airway Smooth Muscle Cells

Cho¹,

Yao²,

Wang³

et al. 2003

The Journal of Immunology

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Activin A, a homodimeric protein (βAβA) and a member of the TGF-β superfamily, is involved in the inflammatory repair process. Using cDNA microarray analysis, we discovered strong induction of the activin βA gene in human mast cells (MC) on stimulation with PMA and calcium ionophore (A23187). Activin βA mRNA was also highly induced in primary cultured murine bone marrow MC (BMMC) after stimulation by IgE receptor cross-linking. Secretion of activin A was evident in human mast cell-1 line cells 3 h after stimulation and progressively increased over time. Activin A was present in the cytoplasm of activated but not unstimulated murine bone marrow MC as demonstrated by immunofluorescence studies, suggesting that secretion of activin A by MC was due to de novo synthesis rather than secretion of preformed protein. Activin A also colocalized with human lung MC from patients with asthma by double-immunofluorescence staining. Furthermore, secretion of activin A was significantly increased in the airway of wild-type mice after OVA sensitization followed by intranasal challenge. Secretion of activin A, however, was greatly reduced in MC-deficient WBB6F1-W/Wv mice as compared with wild-type mice, indicating that MC are an important contributor of activin A in the airways of a murine asthma model. Additionally, activin A promoted the proliferation of human airway smooth muscle cells. Taken together, these data suggest that MC-derived activin A may play an important role in the process of airway remodeling by promoting the proliferation of airway smooth muscle.

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Mutual activation of pulmonary fibroblasts and eosinophils, and modulation by drugs in relation to asthma

Cited by 17 publications

References 69 publications

Procaterol Potentiates the Anti-Inflammatory Activity of Budesonide on Eosinophil Adhesion to Lung Fibroblasts

Procaterol Potentiates the Anti-Inflammatory Activity of Budesonide on Eosinophil Adhesion to Lung Fibroblasts

Eosinophils: Singularly destructive effector cells or purveyors of immunoregulation?

Regulation of Activin A Expression in Mast Cells and Asthma: Its Effect on the Proliferation of Human Airway Smooth Muscle Cells

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