Eosinophil Cationic Protein Stimulates TGF-β1 Release by Human Lung Fibroblasts In Vitro

Zagai, Ulrika; Dadfar, Elham; Lundahl, Joachim; Venge, Per; Sköld, C. Magnus

doi:10.1007/s10753-007-9032-4

Cited by 51 publications

(52 citation statements)

References 27 publications

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“…Our experiment was performed with ECP stimulation at a dose below 1 µg/mL (i.e., 100 ng/mL). Our observation that there was no significant change in TGF-β1 release from NHDF by ECP stimulation is not in conflict with the report of Zagai et al 8 In conclusion, ECP is not cytotoxic but enhances the growth of NHDF. The results of array analyses indicated that CNTF, NAP-2, and NT-3 were significantly upregulated in NHDF with ECP stimulation compared with unstimulated controls.…”

Section: Figurecontrasting

confidence: 73%

“…8 However, their experiments were performed with ECP stimulation at doses of 1 -10 µg/mL. Significant elevation of TGF-β1 release was observed with ECP stimulation at concentrations > 5 µg/mL, and was not observed at 1 µg/mL.…”

Section: Figurementioning

confidence: 99%

“…However, little information is available regarding cytokine expression of human fibroblasts stimulated by ECP. One study showed that ECP stimulates transforming growth factor (TGF)-β1 release by human lung fibroblasts in vitro, 8 although the cytokine production profile from fibroblasts stimulated by ECP has not been determined in detail.…”

Section: Introductionmentioning

confidence: 99%

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Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

Sato

Soga²,

Yamaguchi

et al. 2013

Asian Pac J Allergy Immunol

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Summa ryBackground: Eosinophil cationic protein (ECP) was reported previously to be involved in allergic inflammation with cytotoxic activity. On the other hand, recent studies showed that ECP did not induce cell death but inhibited the growth of cancer-derived cells. Our previous study indicated that human ECP enhanced differentiation of rat neonatal cardiomyocytes and stress fiber formation in Balb/c 3T3 mouse fibroblasts, while the effects of human ECP on human fibroblasts are unknown.Objective: The present study was performed to determine the effects of human ECP on cytokine expression in human fibroblasts by protein array. Methods:The effects of recombinant human ECP (rhECP) on normal human dermal fibroblasts (NHDF) were examined by assaying cell growth. Furthermore, cytokine expression of NHDF stimulated by ECP, which could influence cell growth, was evaluated by protein array.Results: ECP was not cytotoxic but enhanced the growth of NHDF. The peak rhECP concentration that enhanced the cell counts by 1.56-fold was 100 ng/mL, which was significantly different from cultures without ECP stimulation (ANOVA/ Scheffe's test, P < 0.05). Array analyses indicated that ciliary neurotrophic factor (CNTF), neutrophilactivating peptide (NAP)-2, and neurotrophin (NT)-3 were significantly upregulated in NHDF stimulated with 100 ng/mL ECP compared to those without stimulation. Conclusion

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Section: Figurecontrasting

confidence: 73%

Section: Figurementioning

confidence: 99%

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Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

Sato

Soga²,

Yamaguchi

et al. 2013

Asian Pac J Allergy Immunol

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“…Also, the infected subjects carrying the G-allele (ECP 97arg ) displayed a higher frequency of peri-portal fibrosis, suggesting a role for ECP, and in particular ECP with arginine at position 97, in the development of fibrosis. The involvement of ECP in fibrotic process was suggested in previous studies; incubation of fibroblasts in the presence of ECP results in an enhanced proteoglycan production by the fibroblasts (22), and also, ECP has been shown to augment fibroblast-mediated collagen-gel contraction in vitro (23) and to promote migration of fibroblasts (24) and TGF-␤ production (25). Activated eosinophils in the lung of asthmatics are proposed to release granule proteins such as ECP, leading to remodeling and epithelial damage (26).…”

Section: E Osinophil Cationic Protein (Ecp)mentioning

confidence: 83%

The Coding ECP 434(G>C) Gene Polymorphism Determines the Cytotoxicity of ECP but Has Minor Effects on Fibroblast-Mediated Gel Contraction and No Effect on RNase Activity

Rubin

Zagai

Blom

et al. 2009

The Journal of Immunology

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Eosinophil cationic protein (ECP) is a secretory protein of the eosinophil granulocyte, a cell involved in innate immunity. Functional studies have implicated ECP in numerous processes, such as tissue remodeling in allergic inflammation and cytotoxicity toward a variety of pathogens. Recent genetic studies have suggested that the ECP 434(G>C) polymorphism resulting in an arg97thr substitution would alter the function of ECP in vivo. Functional (in vitro) studies of ECP up until now have either been conducted with native preparations containing an unknown mixture of the ECP97arg and ECP97thr variants, or with recombinant proteins. Therefore, we have now for the first time extracted the native ECP97arg and ECP97thr variants from healthy blood donors and tested them functionally in vitro. Our results show that the arg97thr shift dramatically alters the cytotoxic capacity of ECP in vitro; the tested ECP97arg variants were cytotoxic toward the small-cell lung cancer cell line NCI-H69, whereas ECP97thr was noncytotoxic. RNase activity was unaffected by the arg97thr substitution. Both ECP97arg and ECP97thr stimulated fibroblast-mediated collagen gel contraction, an experimental model, which depicts wound healing, in a dose-dependent manner. In conclusion, our results demonstrate that the ECP 434(G>C) gene polymorphism affects the functional properties of native ECP, but also that there is a dissociation between different biological activities; the arg97thr substitution impairs the cytotoxic potential of ECP but less the gel contraction and not at all the RNase activity.

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“…A decrease in the number of eosinophils in the airway wall, especially around the glands, may also contribute to mucus hypersecretion. Eosinophils are a major cellular source of TGF-b [34] and BARALDO et al [35] showed that impaired TGF-b signalling is associated with bronchial gland enlargement. Therefore, a lower number of eosinophils around the bronchial glands may lead to bronchial gland enlargement and a subsequent rise in mucus in the airway lumen, due to a decreased local TGF-b availability.…”

Section: Discussionmentioning

confidence: 99%

Chronic bronchitis sub-phenotype within COPD: inflammation in sputum and biopsies

Snoeck-Stroband

Lapperre²,

Gosman³

et al. 2007

Eur Respir J

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The presence of chronic bronchitis predicts a more rapid decline of forced expiratory volume in one second (FEV1) in patients with chronic obstructive pulmonary disease (COPD). The hallmark of COPD is airway inflammation. It was hypothesised that COPD patients with chronic bronchitis are characterised by a distinct inflammatory cell profile, as measured in bronchial biopsies and sputum.From 114 COPD patients (male/female ratio 99/15, mean¡SD age 62¡8 yrs, current smoking 63%, post-bronchodilator FEV1 63¡9% predicted, no steroids), with and without chronic bronchitis, inflammatory cell counts in bronchial biopsies and induced sputum were measured. Analysis was carried out by logistic regression.COPD patients with chronic bronchitis had lower eosinophil counts in biopsies and higher percentages of sputum eosinophils than patients without those symptoms, which remained after adjustment for smoking and sex. Patients with chronic bronchitis also showed higher percentages of macrophages and lower percentages of neutrophils in sputum, which could be explained by differences in smoking and sex.It was concluded that chronic bronchitis reflects an inflammatory sub-phenotype among patients with chronic obstructive pulmonary disease. The present results indicate a preferential distribution of eosinophils towards the airway lumen in patients with chronic bronchitis. This may have implications for anti-inflammatory treatment of chronic obstructive pulmonary disease patients with chronic bronchitis.

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Eosinophil Cationic Protein Stimulates TGF-β1 Release by Human Lung Fibroblasts In Vitro

Cited by 51 publications

References 27 publications

Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

The Coding ECP 434(G>C) Gene Polymorphism Determines the Cytotoxicity of ECP but Has Minor Effects on Fibroblast-Mediated Gel Contraction and No Effect on RNase Activity

Chronic bronchitis sub-phenotype within COPD: inflammation in sputum and biopsies

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Eosinophil Cationic Protein Stimulates TGF-β1 Release by Human Lung Fibroblasts In Vitro

Cited by 51 publications

References 27 publications

Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

The Coding ECP 434(G&gt;C) Gene Polymorphism Determines the Cytotoxicity of ECP but Has Minor Effects on Fibroblast-Mediated Gel Contraction and No Effect on RNase Activity

Chronic bronchitis sub-phenotype within COPD: inflammation in sputum and biopsies

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The Coding ECP 434(G>C) Gene Polymorphism Determines the Cytotoxicity of ECP but Has Minor Effects on Fibroblast-Mediated Gel Contraction and No Effect on RNase Activity