Fibroblast-eosinophil interaction - Modulation of adhesion molecules expression and chemokine release by human fetal lung fibroblasts in response to IL-4 and TNF-α

Federica Sabatini, Michela Silvestri, Rosa Sale, Lucia Scarso, Anna Carla Defilippi, Francesco M. Risso, Giovanni A. Rossi

Research output: Contribution to journalArticlepeer-review

Abstract

In addition to be involved in airway remodelling observed in asthmatic patients, lung fibroblasts may directly contribute to pulmonary inflammation through the release of mediators and through the expression of surface molecules involved in cell-cell interaction. The aim of the study was to evaluate whether two cytokines involved in asthma pathogenesis, IL-4 and TNF-α, could modulate the expression of adhesion molecules (VCAM-1 and ICAM-1) and the secretion of chemokines (eotaxin and MCP-1) related to eosinophil recruitment and activation. The constitutive expression of VCAM-1 by unstimulated fibroblasts was over 2-fold lower than that of ICAM-1 (P <0.05). Significant differences were also observed in the release of chemokines by unstimulated fibroblast, the levels of eotaxin being over 17-fold lower than those of MCP-1. Stimulation of the cells with IL-4 or TNF-α induced a dose-dependent increase in VCAM-1, while ICAM-1 was overexpressed only in culture stimulated by TNF-α (P <0.05) but not in those exposed to IL-4 (P > 0.05 each comparison). In contrast, a significant increase in MCP-1 and eotaxin release was observed in the presence of TNF-α (P <0.05) but not of IL-4 (P > 0.05). These data show that two 'proinflammatory' cytokines, such as IL-4 and TNF-α, may have different and complementary effects on functions involved in the cross-talking between fibroblasts and eosinophils.

Original languageEnglish
Pages (from-to)173-178
Number of pages6
JournalImmunology Letters
Volume84
Issue number3
DOIs
Publication statusPublished - Dec 3 2002

Keywords

  • Adhesion molecules
  • Chemokines
  • Cytokines
  • Lung fibroblasts

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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