Induction of eotaxin production by interleukin‐4, interleukin‐13 and lipopolysaccharide by nasal fibroblasts

• M. Nonaka

• R. Pawankar

• A. Fukumoto

• N. Ogihara

• A. Sakanushi

• T. Yagi

Abstract

Background There is growing evidence that eotaxin is a key mediator in the development of tissue eosinophilia. Fibroblasts are a major source of eotaxin. The severity of diseases with eosinophilic inflammation like nasal polyposis, atopic dermatitis and asthma, where Th2‐type cytokines (IL‐4 and IL‐13) and TGF‐β are expressed locally, was shown to correlate with bacterial factors such as lipopolysaccharide (LPS) rather than allergen. Objective We examined eotaxin production by nasal fibroblasts stimulated with IL‐4 or IL‐13 alone or in combination with LPS, and the effect of TGF‐β 1 on it. Moreover, we compared the magnitude of eotaxin produced by nasal fibroblasts with that produced by lung or skin fibroblasts. Methods Fibroblast lines were established from human biopsy tissue. The expression of eotaxin mRNA was evaluated by RT‐PCR. The amount of eotaxin in the supernatants was measured by ELISA. Results IL‐4, but not IL‐13, synergized with LPS to produce eotaxin in a dose‐ and time‐dependent manner. Sequential treatment of nasal fibroblasts with IL‐4 and LPS did not have any effect. But when IL‐4 and LPS were added together, synergy for eotaxin production was observed. Moreover, this synergy was observed in nasal and skin fibroblasts, but not in lung fibroblasts. The production of eotaxin by IL‐4 and LPS was modulated by TGF‐β 1 . Conclusion These results suggest that a co‐stimulus like LPS is necessary for IL‐4 to make a strong induction of eotaxin in eosinophilic inflammations such as nasal polyposis. Modulation by TGF‐β 1 may have important implications for the development of eosinophilic inflammation.

Journal

• Clinical & Experimental Allergy

  Clinical & Experimental Allergy 34 (5), 804-811, 2004-05

  Wiley

Keywords

• Immunology
• Immunology and Allergy

Details

• CRID: 1360292621329478400
• NII Article ID: 30014612943
• DOI: 10.1111/j.1365-2222.2004.1954.x
• ISSN: 13652222
• ISSN: 09547894
• Web Site: https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-2222.2004.1954.x
• Web Site: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2222.2004.1954.x
• Data Source:
  • Crossref
  • CiNii Articles