Eotaxin-2/CCL24 and eotaxin-3/CCL26 exert differential profibrogenic effects on human lung fibroblasts

Martin Kohan, Ilaria Puxeddu, Reuven Reich, Francesca Levi-Schaffer, Neville Berkman*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

Background: Eotaxin-2/CCL24 and eotaxin-3/CCL26 play an important role in eosinophil chemotaxis and activation in asthma. We previously demonstrated that eotaxin/CCL11 is profibrogenic for human lung fibroblasts. The effect of eotaxin-2/ CCL24 and eotaxin-3/CCL26 on lung fibroblasts has not yet been investigated. Objective: To evaluate whether eotaxin-2/CCL24 and eotaxin-3/CCL26 modulate fibrotic properties of lung fibroblasts. Methods: Fibroblast proliferation was evaluated by means of 3-hydroxythymidine incorporation. Collagen production was assessed by means of 3-hydroxyproline incorporation and biochemical staining. Chemotaxis was determined using Boyden chambers. Expression of α-smooth muscle actin was evaluated by means of immunostaining. Transforming growth factor β1 release was assessed using enzyme-linked immunosorbent assay. Parametric analysis of variance, followed by the Tukey-Kramer multiple comparisons test, was used to calculate statistical significance. Results: Eotaxin-2/CCL24 but not eotaxin-3/CCL26 stimulated human lung fibroblast proliferation and collagen synthesis. In contrast, eotaxin-3/CCL26 but not eotaxin-2/CCL24 promoted fibroblast migration. Neither eotaxin-2/CCL24 nor eotaxin-3/ CCL26 induced the expression of α-smooth muscle actin or transforming growth factor β1 from lung fibroblasts. Conclusions: Eotaxin-2/CCL24 and eotaxin-3/CCL26 have differential profibrogenic effects on human lung fibroblasts. These CC chemokines may, therefore, contribute to airway remodeling in asthma.

Original languageAmerican English
Pages (from-to)66-72
Number of pages7
JournalAnnals of Allergy, Asthma and Immunology
Volume104
Issue number1
DOIs
StatePublished - Jan 2010

Bibliographical note

Funding Information:
Funding Sources: This study was supported by grant 5878–1 from the Chief Scientist Office of the Ministry of Health, Israel , and by the Israel Lung Association, Tel Aviv .

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