Monitoring the Allergic Inflammation

Venge, Per

doi:10.1007/978-4-431-98349-1_25

Cited by 41 publications

(51 citation statements)

References 118 publications

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“…In addition, important extracellular deposits of ECP are found in tissues undergoing eosinophilic inflammation and they correlate well with tissue damage as it happens, for example, in the case of bronchial asthma or in the intestinal mucosa as is the case in Crohns disease [7]. ECP levels in body fluids are currently used as marker of eosinophil activity and turnover, and correlate well with tissue damage [8]. After intraventricular injection into guinea pigs and rabbits, ECP causes the Gordon phenomenon that is characterized by cerebellar Purkinje cell degeneration [9].…”

Section: Introductionmentioning

confidence: 97%

The cytotoxicity of eosinophil cationic protein/ribonuclease 3 on eukaryotic cell lines takes place through its aggregation on the cell membrane

Navarro

Aleu

Jiménez

et al. 2007

Cell. Mol. Life Sci.

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Human eosinophil cationic protein (ECP)/ ribonuclease 3 (RNase 3) is a protein secreted from the secondary granules of activated eosinophils. Specific properties of ECP contribute to its cytotoxic activities associated with defense mechanisms. In this work the ECP cytotoxic activity on eukaryotic cell lines is analyzed. The ECP effects begin with its binding and aggregation to the cell surface, altering the cell membrane permeability and modifying the cell ionic equilibrium. No internalization of the protein is observed. These signals induce cell-specific morphological and biochemical changes such as chromatin condensation, reversion of membrane asymmetry, reactive oxygen species production and activation of caspase-3-like activity and, eventually, cell death. However, the ribonuclease activity component of ECP is not involved in this process as no RNA degradation is observed. In summary, the cytotoxic effect of ECP is attained through a mechanism different from that of other cytotoxic RNases and may be related with the ECP accumulation associated with the inflammatory processes, in which eosinophils are present.

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Section: Introductionmentioning

confidence: 97%

The cytotoxicity of eosinophil cationic protein/ribonuclease 3 on eukaryotic cell lines takes place through its aggregation on the cell membrane

Navarro

Aleu

Jiménez

et al. 2007

Cell. Mol. Life Sci.

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“…In this regard ECP seems to be of particular interest since it is one of the most potent proteins. Thus, ECP has been demonstrated to be involved not only in the specific defense against parasites but also in the inflammatory reaction in general [4]. High concentrations of ECP are measured in a variety of body fluids (serum, sputum, bronchoalveolar lavage) in asthmatics and in other inflammatory and fibrotic disorders [2], indicating a role for the eosinophil and its mediators in the remodeling process.…”

Section: Introductionmentioning

confidence: 98%

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

et al. 2007

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Eosinophilic inflammation and airway remodeling are features of asthma. Eosinophil cationic protein (ECP) is released by activated eosinophils and transforming growth factor (TGF)-beta(1) has major functions in the fibrotic process. We therefore hypothesized that ECP stimulates TGF-beta(1) release by human lung fibroblasts. Fibroblasts in monolayer displayed a constitutive release of TGF-beta(1), which increased in presence of ECP (436 +/- 60 vs. 365 +/- 48 pg/ml at 48 h; P < 0.01). mRNA expression of TGF-beta(1) was almost twofold in ECP-stimulated fibroblasts. ECP in three-dimensional cultures stimulated both TGF-beta(1) release (180 +/- 61 vs. 137 +/- 54 pg/ml; P < 0.01) and fibroblast-mediated collagen gel contraction (28 vs. 39% of initial gel area at 48 h; P < 0.001). ECP stimulates TGF-beta(1)-release by human lung fibroblasts, suggesting a potential mechanism for eosinophils in the fibrotic response. This may be an important mechanism by which ECP promotes remodeling of extra cellular matrix leading to airway fibrosis in asthmatics.

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“…Dysregulation of pro-and anti-inflammatory mediators is characteristic of chronic inflammation in allergic disorders. The signs and symptoms of allergy are the result of activation of regulatory T cells (Robinson et al 2004), consecutive activation/recruitment of Th2-pathway, and special activity of IgE antibodysecreting B cells, mast cells, and eosinophils (Venge 2003). In the Th2-pathway, interleukin-5 (IL-5) is involved in eosinophil differentiation and migration from bone marrow, survival, and activation (Denburg et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Examination of seasonal difference in serum interleukin-17 and interleukin-5 concentrations in ragweed-sensitized children

Špehar¹,

Zovko

Šegulja

et al. 2011

Aerobiologia

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Dysregulation of inflammatory mediators is characteristic for chronic inflammation in allergy. The aim was to determine the values of serum IL-17 and IL-5 in ragweed-sensitized children. The study included children analyzed during the ragweed pollen season compared to children analyzed out of season. Serum total IgE, specific IgE, and eosinophil cationic protein (ECP) were determined by fluoroimmunoassay while the concentrations of IL-5 and IL-17 were determined by flow cytometry. Patients evaluated during the pollen season, have higher values of total and specific IgE, eosinophil and neutrophil count than patients studied outside the pollen season. There was no statistically significant seasonal and out of season differences for the concentration of IL-17, IL-5, and ECP. Natural exposure to ragweed pollen allergen was not crucial for the induction of increased IL-17 and IL-5 synthesis, and factors other than allergen exposure should be investigated, especially in longitudinal studies of patients.

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Monitoring the Allergic Inflammation

Cited by 41 publications

References 118 publications

The cytotoxicity of eosinophil cationic protein/ribonuclease 3 on eukaryotic cell lines takes place through its aggregation on the cell membrane

The cytotoxicity of eosinophil cationic protein/ribonuclease 3 on eukaryotic cell lines takes place through its aggregation on the cell membrane

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

Examination of seasonal difference in serum interleukin-17 and interleukin-5 concentrations in ragweed-sensitized children

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