Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells

Komiya, Akiko; Nagase, Hiroyuki; Yamada, Hirokazu; Sekiya, Takashi; Yamaguchi, Masao; Sugiyama, Yasuyuki; Hanai, Nobuo; Furuya, Akiko; Ohta, Ken; Matsushima, Kouji; Yoshie, Osamu; Yamamoto, Kazuhiko; Hirai, Koichi

doi:10.1016/j.cellimm.2003.10.001

Cited by 120 publications

(83 citation statements)

References 35 publications

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“…Similar differences in the reactivity of paired cultures of human nasal and bronchial epithelial cells were also observed by other authors [26,29]. We confirmed the earlier observations of many authors that CCL26 was the main eotaxin detected in cultures of human bronchial epithelial cells stimulated with IL-4 or IL-13 [30,31]. Some of the PCR and ELISA results for CCL26 expression are inconsistent.…”

Section: Discussionsupporting

confidence: 76%

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Paplińska-Goryca

Nejman-Gryz

Chazan

et al. 2013

Cellular and Molecular Biology Letters

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Airway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.

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Section: Discussionsupporting

confidence: 76%

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Paplińska-Goryca

Nejman-Gryz

Chazan

et al. 2013

Cellular and Molecular Biology Letters

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“…HUVEC are capable of liberating various chemokines in response to diverse stimuli (33)(34)(35). Therefore, it should be noted that HUVEC-derived chemokines might disturb the chemotactic gradient and thereby affect the TEM results.…”

Section: Discussionmentioning

confidence: 99%

Transendothelial Migration of Human Basophils

Iikura

Ebisawa

Yamaguchi

et al. 2004

The Journal of Immunology

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During allergic reactions, basophils migrate from the blood compartment to inflammatory sites, where they act as effector cells in concert with eosinophils. Because transendothelial migration (TEM) represents an essential step for extravasation of cells, for the first time we have studied basophil TEM using HUVEC. Treatment of HUVEC with IL-1β significantly enhanced basophil TEM, which was further potentiated by the presence of a CCR3-specific ligand, eotaxin/CCL11. In addition to CCR3 ligands, MCP-1/CCL2 was also active on basophil TEM. Although stromal cell-derived factor-1/CXCL12, a CXCR4 ligand, failed to induce TEM in freshly isolated basophils, it caused strong TEM in 24-h cultured cells. IL-3 enhanced basophil TEM by increasing the chemokinetic response. Spontaneous TEM across activated HUVEC was inhibited by treatment of cells with anti-CD18 mAb, but not with anti-CD29 mAb, and also by treatment of HUVEC with anti-ICAM-1 mAb. Anti-VCAM-1 mAb alone failed to inhibit TEM, but showed an additive inhibitory effect in combination with anti-ICAM-1 mAb. In contrast, eotaxin- and IL-3-mediated TEM was significantly inhibited by anti-CD29 mAb as well as anti-CD18 mAb. These results indicate that β2 integrins play the primary role in basophil TEM, but β1 integrins are also involved, especially in TEM of cytokine/chemokine-stimulated basophils. In conclusion, the regulatory profile of basophil TEM is very similar to that reported for eosinophils. Our results thus support the previous argument for a close relationship between basophils and eosinophils and suggest that the in vivo kinetics of these two cell types are similar.

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“…Eotaxin-1 is mainly produced by epithelial and mesenchymal cells, including fibroblast and smooth muscle in the airway (Ying et al 1999;Miyamasu et al 2000;Moore et al 2002). However, a large amount of eotaxin-2 is produced by peripheral blood monocytes while eotaxin-1 is not detected in the supernatants of monocytes (Komiya et al 2003). The plasma level of eotaxin-2 (248.2 ± 16.2 pg/ml) is 10 times higher than that of eotaxin-1 (26.2 ± 1.1 pg/ ml) in asthmatics of our study (data not shown).…”

Section: Subjectmentioning

confidence: 99%

Association of eotaxin-2 gene polymorphisms with plasma eotaxin-2 concentration

et al. 2005

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Chemokine (C-C motif) ligand 24 (CCL24, eotaxin-2) is a CC chemokine that recruits and activates cells bearing the CC chemokine receptor 3, which play a major role in asthma. Previously, we observed a significant association between a single nucleotide polymorphism (SNP) in eotaxin-2 (CCL24+1272A fi G) and a lower risk of asthma. Consequently, this study has followed up on those genetic effects by evaluating the association between the SNP and plasma eotaxin-2 concentration in 172 asthmatics and 135 normal controls. Asthmatics had significantly higher plasma eotaxin-2 levels than did normal controls (P=0.02). The SNP (CCL24+1272A fi G) and two haplotypes (ht2 and ht6) were strongly associated with plasma eotaxin-2 levels in asthmatics (CCL24+1272A fi G: P=0.006, ht2: P=0.006, and ht6: P=0.002). The CCL24+ 1272A fi G allele and the ht2 and ht6 haplotypes showed a gene-dose effect on the plasma eotaxin-2 levels in asthmatics (P=0.005-0.032). In conclusion, the susceptibility of patients with asthma to high eotaxin-2 production may be due to genetic effects of the CCL24+1272A fi G polymorphism, ht2 and ht6 haplotypes.

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Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells

Cited by 120 publications

References 35 publications

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

Transendothelial Migration of Human Basophils

Association of eotaxin-2 gene polymorphisms with plasma eotaxin-2 concentration

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