Maria Ferraro

INO - Istituto Nazionale di Ottica, Florens, Tuscany, Italy

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Publications (55)220.56 Total impact


  • No preview · Article · Sep 2015 · European Respiratory Journal

  • No preview · Article · Sep 2015 · European Respiratory Journal

  • No preview · Article · Sep 2015 · European Respiratory Journal

  • No preview · Article · Sep 2015 · European Respiratory Journal
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    ABSTRACT: Toll-like receptor 4 (TLR4) signaling requires a number of accessory proteins to initiate a signal. MD-2 is one of the accessory proteins with a relevant role in lipopolysaccharide responses. Although cigarette smoke increases TLR4 expression, TLR4 signaling is altered in smokers and in smokers COPD patients. The main aims of this study were to explore whether MD2 is altered in large and small airways of COPD and of smokers without COPD. The expression of MD2 ex vivo was assessed by immunohistochemistry in surgical specimens from current smokers COPD (s-COPD; n = 14), smokers without COPD (S; n = 7), and from non-smoker non-COPD subjects (C; n = 11. The in vitro effects of cigarette smoke extracts on the MD2 expression in a human bronchial epithelial cell line (16-HBE) were also assessed by flow cytometry. MD2 is reduced in the epithelium and in the submucosa in large airways but not in the epithelium and in the submucosa in small airways of smokers and of s-COPD. The expression of MD2 in the submucosa of the large airways is significantly higher in comparison to the submucosa of the small airways in all the studied groups. In vitro, cigarette smoke is able to increase TLR4 but it reduces MD2 in a dose-dependent manner in bronchial epithelial cells. Cigarette smoke may alter innate immune responses reducing the expression of the MD2, a molecule with an important role in TLR4 signaling.
    No preview · Article · Jun 2015 · Molecular and Cellular Biochemistry
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    ABSTRACT: Smoking is strongly associated with diseases such as lung cancer and chronic obstructive pulmonary disease (COPD). Lung fibroblasts are crucial for the integrity of alveolar structure by producing extracellular matrix proteins which are required for attachment, structure, and function of alveolar epithelial cells. Despite the well-known association between cigarette smoke exposure and pulmonary and cardiovascular diseases, many questions remain regarding the mechanisms by which smoking induces diseases. The aim of this study is to detect differentially expressed proteins in human foetal lung cells (HFL-1) after 5 and 10% doses of cigarette smoke extract (CSE) exposure, combining two-dimensional electrophoresis (2DE) and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). In order to evaluate cellular ability to recover as well as lasting damages, we analysed the proteomic pattern 24 hours after the CSE removal (release). Eleven proteins had significant changes in the various experimental points. Among these, 7 were up-regulated after CSE-treatments and 4 were down-regulated. Some spots seemed to be modified permanently or in a transient manner, in fact they returned to baseline levels after CSE-removal (normalisation after CSE release) and others were modified by selective CSE concentrations or only after release. MS identified, differentially expressed proteins are involved in stress response, mitochondrial activity, and aging. These findings may improve our understanding about molecular mechanisms underlying CSE caused damages and they may also integrate the comprehension of cigarette smoke effects on human health. KEY WORDS: cigarette smoke, proteomic analysis, fibroblasts.
    No preview · Article · Apr 2015 · Molecular BioSystems
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    ABSTRACT: Reduced innate immunity responses as well as reduced T regulatory activities characterise bronchial asthma. In this study the effect of budesonide on the expression of TLR4 and TLR2 in T regulatory lymphocyte sub-population was assessed. TLR4 and TLR2 expression in total peripheral blood mononuclear cells (PBMC), in CD4+/CD25+ and in CD4+/CD25-was evaluated, by flow cytometric analysis, in mild intermittent asthmatics (n=14) and in controls (n=11). The in vitro effects of budesonide in modulating: TLR4 and TLR2 expression in controls and in asthmatics; IL-10 expression and cytokine release (IL-6 and TNF-α selected by a multiplex assay) in asthmatics were also explored. TLR4 and TLR2 were reduced in total PBMC from asthmatics in comparison to PBMC from controls. CD4+CD25+ cells expressed at higher extent TLR2 and TLR4 in comparison to CD4+CD25-cells. Budesonide was able to increase the expression of TLR4, TLR2 and IL-10 in CD4+/CD25highly+ cells from asthmatics. TLR4 ligand, LPS induced Foxp3 expression. Budesonide was also able to reduce the release of IL-6 and TNF-α by PBMC of asthmatics. Budesonide potentiates the activity of Treg by increasing TLR4, TLR2 and IL-10 expression. This event is associated to the decreased release of IL-6 and ΤΝF-α in PBMC treated with budesonide. These findings shed light on new mechanisms by which corticosteroids, drugs widely used for the clinical management of bronchial asthma, control T lymphocyte activation. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · Feb 2015 · Pulmonary Pharmacology & Therapeutics
  • C D'anna · D Cigna · G Costanzo · M Ferraro · L Siena · P Vitulo · M Gjomarkaj · E Pace
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    ABSTRACT: Lung fibroblasts are crucial for the integrity of alveolar structure. Cigarette smoking, the major risk factor for chronic obstructive pulmonary disease, impairs the repair functions of lung fibroblasts. The study simultaneously assessed for the first time cell cycle, p53, p21, p38, ERK 1/2 and IL-8. Primary foetal lung fibroblasts (HFL-1) and primary lung fibroblasts from former (n=5) and current (n=5) smokers with/without cigarette smoke extracts (CSE) and inhibitors of p38 and ERK1/2 were studied for cell cycle events and for marker expression by flow-cytometry, western-blot analysis and ELISA. CSE exposure did not induce caspase 3 cleavage or DNA laddering but reduced S phase, and increased G1 and G2/M in HFL-1. Furthermore CSE increased: p53 and p21 expression; p38 and ERK 1/2 pathway activation; IL-8 release. Inhibitors of p38 and ERK 1/2 reversed the effects of CSE on cell cycle and on IL-8 release. ERK 1/2 inhibitor was able to reverse the effects of CSE on p21 expression. Primary lung fibroblasts from current smokers had higher ERK 1/2 activation in comparison to normal primary fibroblasts and higher percentage of cells in G1 phase and lower percentage of cells in S phase in comparison to former smokers fibroblasts. Cigarette smoke may affect the reparative potential of lung fibroblasts altering the expression of p53 and p21 and the progression of the cell cycle to S phase. All these events are promoted by the activation of pro-inflammatory pathways. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jan 2015 · Life Sciences
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    ABSTRACT: Background Nanomedicine studies have showed a great potential for drug delivery into the lung. In this manuscript nanostructured lipid carriers (NLC) containing Fluticasone propionate (FP) were prepared and their biocompatibility and effects in a human bronchial epithelial cell line (16-HBE) stimulated with cigarette smoke extracts (CSE) were tested.ResultsBiocompatibility studies showed that the NLC did not induce cell necrosis or apoptosis. Moreover, it was confirmed that CSE increased intracellular ROS production and TLR4 expression in bronchial epithelial cells and that FP-loaded NLC were more effective than free drug in modulating these processes. Finally, the nanoparticles increased GSH levels improving cell protection against oxidative stress.Conclusions The present study shows that NLC may be considered a promising strategy to improve corticosteroid mediated effects in cellular models associated to corticosteroid resistance. The NLC containing FP can be considered good systems for dosage forms useful for increasing the effectiveness of fluticasone decreasing its side effects.
    Full-text · Article · Nov 2014 · Journal of Nanobiotechnology
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    ABSTRACT: Leptin is involved in the lung epithelial homeostasis. Its role in the nasal tract is largely unknown. Allergic rhinitis (AR) is induced by the allergen exposure leading to consequential structural abnormalities in the nasal epithelium. Topical corticosteroids are recommended as first-line therapy in AR. Parietaria pollen is one of the most important allergenic sources in the southern Europe. In vitro, in human nasal epithelial cell line RPMI 2650, we aimed to determine whether allergen stimulation acts on leptin/leptin receptor pathway and how fluticasone furoate (FF) influences this pathway. The effects of the major allergen recombinant Par j 1 (rPar j 1), of FF, of leptin, and of TGF-β1 on cell proliferation, on leptin/leptin receptor expression and modulation (by clonogenic test, by RT-q-RT-PCR, by immunocytochemistry and by flow-cytometry), and on STAT-3 activation (assessing nuclear translocation by western blot analysis) were assessed. We found that rPar j 1 and TGF-β1 significantly decreased cell proliferation and down-regulated the leptin/leptin receptor pathway, whereas FF and leptin reverted them, both alone and in combination. Furthermore, rPar j 1 reduced, while leptin and FF increased STAT-3 activation. In conclusion, FF and leptin itself are able to preserve nasal epithelial homeostasis restoring the leptin/leptin receptor pathway altered by rPar j 1 exposure.
    No preview · Article · Jul 2014 · Molecular and Cellular Biochemistry
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    ABSTRACT: Airway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored. Mini-BALs, but not sera, from smokers show reduced concentrations of IL-33. The expression of IL-33 was increased also in bronchial epithelium from smokers. 20% CSE reduced IL-33 release but increased the mRNA for IL-33 by real time PCR and the intracellular expression of IL-33 in bronchial epithelial cells as confirmed by flow cytometry, immunocytochemistry and by western blot analysis. The effect of CSE on IL-33 expression was also observed in primary bronchial epithelial cells. IL-33 expression was mainly concentrated within the cytoplasm of the cells. LPS, an agonist of TLR4, reduced IL-33 expression, and an inhibitor of TLR4 increased the intracellular expression of IL-33. In conclusion, the release of IL-33 is tightly controlled and, in smokers, an altered activation of TLR4 may lead to an increased intracellular expression of IL-33 with a limited IL-33 release.
    No preview · Article · Jun 2014 · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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    ABSTRACT: Airway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored. Mini-BALs, but not sera, from smokers show reduced concentrations of IL-33. The expression of IL-33 was increased also in bronchial epithelium from smokers. 20% CSE reduced IL-33 release but increased the mRNA for IL-33 by real time PCR and the intracellular expression of IL-33 in bronchial epithelial cells as confirmed by flow cytometry, immunocytochemistry and western blot analysis. The effect of CSE on IL-33 expression was also observed in primary bronchial epithelial cells. IL-33 expression was mainly concentrated within the cytoplasm of the cells. LPS, an agonist of TLR4, reduced IL-33 expression, and an inhibitor of TLR4 increased the intracellular expression of IL-33. In conclusion, the release of IL-33 is tightly controlled and, in smokers, an altered activation of TLR4 may lead to an increased intracellular expression of IL-33 with a limited IL-33 release.
    No preview · Article · Jan 2014 · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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    ABSTRACT: Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters Toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown.The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4) M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.
    No preview · Article · Nov 2013 · Toxicology in Vitro
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    ABSTRACT: Gemcitabine is a chemotherapy agent commonly used in the treatment of NSCLC which has been demonstrated to induce apoptosis in NSCLC cells by increasing functionally active Fas expression. The aim of this study was to evaluate the Fas/FasL system involvement in gemcitabine-induced lung cancer cell killing. NSCLC H292 cells were cultured in presence or absence of gemcitabine. FasL mRNA and protein were evaluated by real-time PCR, and by western blot and flow cytometry, respectively. Apoptosis of FasL expressing cells was evaluated by flow cytometry, and caspase-8 and-3 activation by western blot and by a colorimetric assay. Cytotoxicity of LAK cells and malignant pleural fluid (PF) lymphocytes against H292 cells was analyzed in presence or absence of the neutralizing anti-Fas ZB4 antibody, by flow cytometry. Gemcitabine increased FasL mRNA and total protein expression, the percentage of H292 cells bearing membrane-bound FasL (mFasL) and of mFasL positive apoptotic H292 cells, as well as caspase-8 and-3 cleavage. Moreover, gemcitabine increased CH11-induced caspase-8 and-3 cleavage and proteolytic activity. Cytotoxicity of LAK cells and PF lymphocytes was increased against gemcitabine-treated H292 cells and was partially inhibited by ZB4 antibody. These results demonstrate that gemcitabine: 1) induces an up-regulation of FasL in lung cancer cells triggering cell apoptosis via an autocrine/paracrine loop; 2) induces a Fas-dependent apoptosis mediated by caspase-8 and-3 activation; 3) enhances the sensitivity of lung cancer cells to cytotoxic activity of LAK cells and malignant PF lymphocytes, partially via Fas/FasL pathway. Our data strongly suggest an active involvement of Fas/FasL system in gemcitabine-induced lung cancer cell killing. This article is protected by copyright. All rights reserved.
    No preview · Article · Oct 2013 · Immunology
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    ABSTRACT: Cigarette smoke represents the major risk factor for chronic obstructive pulmonary disease (COPD). Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Carbocysteine, an anti-oxidant and mucolytic agent, is effective in reducing the severity and the rate of exacerbations in COPD patients. The effects of carbocysteine on TLR4 expression and on the TLR4 activation downstream events are largely unknown. This study was aimed to explore whether carbocysteine, in a human bronchial epithelial cell line (16-HBE), counteracted some pro-inflammatory CSE-mediated effects. In particular, TLR4 expression, LPS binding, p21 (a senescence marker), IL-8 mRNA and release in CSE-stimulated 16-HBE as well as actin reorganization in neutrophils cultured with supernatants from bronchial epithelial cells which were stimulated with CSE and/or carbocysteine were assessed. TLR4 expression, LPS binding, and p21 expression were assessed by flow cytometry, IL-8 mRNA by Real Time PCR and IL-8 release by ELISA. Actin reorganization, a prerequisite for cell migration, was determined using Atto 488 phalloidin in neutrophils by flow cytometry and fluorescence microscopy. CSE increased: 1) TLR4, LPS binding and p21 expression; 2) IL-8 mRNA and IL-8 release due to IL-1 stimulation; 3) neutrophil migration. Carbocysteine in CSE stimulated bronchial epithelial cells, reduced: 1) TLR4, LPS binding and p21; 2) IL-8 mRNA and IL-8 release due to IL-1 stimulation; 3) neutrophil chemotactic migration. In conclusion, the present study provides compelling evidences that carbocysteine may contribute to control the inflammatory and senescence processes present in smokers.
    No preview · Article · Sep 2013 · Toxicology Letters
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    ABSTRACT: Airway epithelium alterations, including squamous cell metaplasia, characterize smokers with and without chronic obstructive pulmonary disease (COPD). The p21 regulates cell apoptosis and differentiation and its role in COPD is largely unknown. AIMS: Molecules regulating apoptosis (cytoplasmic p21, caspase-3), cell cycle (nuclear p21), proliferation (ki67/PCNA), and metaplasia (survivin) in central airways from Smokers (S), Smokers-COPD (s-COPD) and non-smokers (Controls) were studied. The role of cigarette smoke extracts (CSE) in p21, survivin, apoptosis (caspase-3 and annexin-V binding) and proliferation was assessed in a bronchial epithelial cell line(16-HBE). METHODS AND RESULTS: Immunohistochemistry, image analysis in surgical samples and flow-cytometry and Carboxy Fluorescein Succinimidyl Ester proliferative assay in 16-HBE with/without CSE were applied. Cytoplasmic and nuclear p21, survivin, and Ki67 expression significantly increased in large airway epithelium in S and in s-COPD in comparison to Controls. Caspase-3 was similar in all the studied groups. p21 correlated with epithelial metaplasia, PCNA, and ki67 expression. CSE increased cytoplasmic p21 and survivin expression but not apoptosis and inhibited the cell proliferation in 16HBE. CONCLUSIONS: In large airway epithelium of smokers with and without COPD, the cytoplasmic p21 inhibits cell apoptosis, promotes cell proliferation and correlates with squamous cell metaplasia thus representing a potential pre-oncogenic hallmark.
    No preview · Article · Apr 2013 · Biochimica et Biophysica Acta
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    ABSTRACT: Cigarette smoke extracts (CSE) induce oxidative stress, an important feature in chronic obstructive pulmonary disease (COPD), and oxidative stress contributes to the poor clinical efficacy of corticosteroids in COPD patients. Carbocysteine, an antioxidant and mucolytic agent, is effective in reducing the severity and the rate of exacerbations in COPD patients. The effects of carbocysteine on CSE-induced oxidative stress in bronchial epithelial cells as well as the comparison of these antioxidant effects of carbocysteine with those of fluticasone propionate are unknown. The present study was aimed to assess the effects of carbocysteine (10(-4) M) in cell survival and intracellular reactive oxygen species (ROS) production (by flow cytometry) as well as total glutathione (GSH), heme oxygenase-1 (HO-1), nuclear-related factor 2 (Nrf2) expression and histone deacetylase 2 (HDAC-2) expression/activation in CSE-stimulated bronchial epithelial cells (16-HBE) and to compare these effects with those of fluticasone propionate (10(-8) M). CSE, carbocysteine or fluticasone propionate did not induce cell necrosis (propidium positive cells) or cell apoptosis (annexin V-positive/propidium-negative cells) in 16-HBE. CSE increased ROS production, nuclear Nrf2 and HO-1 in 16-HBE. Fluticasone propionate did not modify intracellular ROS production, GSH and HDCA-2 but reduced Nrf2 and HO-1 in CSE-stimulated 16-HBE. Carbocysteine reduced ROS production and increased GSH, HO-1, Nrf2 and HDAC-2 nuclear expression/activity in CSE-stimulated cells and was more effective than fluticasone propionate in modulating the CSE-mediated effects. In conclusion, the present study provides compelling evidences that the use of carbocysteine may be considered a promising strategy in diseases associated with corticosteroid resistance.
    No preview · Article · Apr 2013 · Cell Stress and Chaperones
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    ABSTRACT: Background: Chronic bronchitis (CB) is a risk factor in chronic obstructive pulmonary disease (COPD) for accelerated lung function decline and increased mortality. The lung and systemic inflammatory and immunological profile of COPD patients with CB which acutely experience respiratory failure upon a disease exacerbation is unknown. Methods: In this study, we explored the expression of Foxp3 by western blot analysis, TLR4 by immunocytochemistry and the concentrations of IP-10 and IL-8 by ELISA in the mini-bronchoalveolar lavages (mini-BAL) and in the peripheral blood of patients with respiratory failure requiring intubation and mechanical ventilation. The recruited subjects were separated into three different groups: smokers with CB and COPD (COPD, n = 18), smokers with CB but without COPD (S, n = 8) and patients without CB and without COPD (C, n = 10). Results: In mini-BAL of COPD group, Foxp3 and IP-10 were significantly reduced while TLR4 was significantly increased in comparison to C. TLR4 was also increased in mini-BAL of S. In COPD peripheral blood, Foxp3 was reduced in comparison to C but no significant differences were observed for TLR4 and for IP-10. No significant differences were observed for IL-8 concentrations in the mini-BAL and in the blood of the recruited patients. The mini-BAL TLR4 expression correlated with the Clinical Infective Pulmonary Score. Conclusions: In exacerbated COPD patients with respiratory failure, lung and systemic reduced immune regulatory events (low Foxp3 expression) and lung increased innate immunity responses (high TLR4 expression) occur. These events may contribute to the increased inflammatory events leading to respiratory failure.
    No preview · Article · Mar 2013 · COPD Journal of Chronic Obstructive Pulmonary Disease
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    ABSTRACT: LTB(4) is a neutrophil chemotactic molecule importantly involved in the inflammatory responses of Chronic Obstructive Pulmonary Disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-BALs) from smokers alter the expression of the LTB(4) receptors BLT2 and PPAR-α in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of ICAM-1 and on the binding of STAT-1 to ICAM-1 promoter as well as the adhesiveness of neutrophils to bronchial epithelial cells. CSE and mini-BALs from smokers increased BLT2 and ICAM-1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR-α expression. CSE induced the activation of STAT-1 and its binding to ICAM-1 promoter. These findings suggest that, in bronchial epithelial cells, CSE promote a prevalent induction of pro-inflammatory BLT2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism which contributes to airway neutrophilia and to tissue damage. © 2013 The Authors. Immunology © 2013 Blackwell Publishing Ltd.
    No preview · Article · Jan 2013 · Immunology
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    ABSTRACT: Celiac disease is caused by a specific immune response to antigens present in wheat gluten and related proteins of rye and barley in genetically susceptible individuals. Several studies have been conducted to define the nature and role of systemic cytokine levels in the pathophysiology of celiac disease. In order to identify the potential role of the Th17 subset in the pathogenesis of the celiac disease, we analyzed the serum levels of IL -22 in affected patients. Our data show that higher IL -22 serum levels are found in cases than in the controls, with a difference near to the limits of significance.
    No preview · Article · Jan 2013 · Review of Allergy and Clinical Immunology

Publication Stats

717 Citations
220.56 Total Impact Points

Institutions

  • 2011-2015
    • INO - Istituto Nazionale di Ottica
      Florens, Tuscany, Italy
  • 2007-2015
    • Italian National Research Council
      • • Institute of Biomedicine and Molecular Immunology "Alberto Monroy" IBIM
      • • Institute of Biophysics IBF
      Roma, Latium, Italy
  • 2011-2013
    • Institute of Immunology
      Santiago de Cali, Valle del Cauca, Colombia
  • 2004-2012
    • Università degli Studi di Palermo
      • Department of internal medicine and medical specialties (DIMIS)
      Palermo, Sicily, Italy