M Ferraro

Publications (4)22.17 Total impact

• Article: Increased expression of IL-19 in the epithelium of patients with chronic rhinosinusitis and nasal polyps.

  E Pace, V Scafidi, D Di Bona, L Siena, G Chiappara, M Ferraro, S La Grutta, S Gallina, R Speciale, A Ballacchino, C Bachert, J Bousquet, M Gjomarkaj
  [show abstract] [hide abstract]
  ABSTRACT: Chronic rhinosinusitis (CRS) is an inflammation of the nose and of the paranasal sinuses. The involvement of the respiratory epithelium in the mechanisms of CRS is poorly understood. Among proteins expressed by nasal epithelial cells in CRS, IL-19 may have key functions. We here aimed to determine the expression and regulation of IL-19. Nasal biopsies from normal subjects (n = 12), subjects with CRS but without nasal polyps (NP) (CRSsNP, n = 12) and with CRS with NP (CRSwNP, n = 15) were collected. Human Asthma Gene Array and real-time PCR were used to evaluate gene expression, western blot analysis and immunohistochemistry for protein expression. Results for IL-19 were confirmed by real-time PCR. The constitutive and stimulated (LPS, TGF β) expression of IL-19 and cell proliferation were evaluated in a nasal epithelial cell line (RPMI 2650). Human Asthma Gene Array showed an increased IL-19 gene expression in NP from patients with CRS in comparison with normal subjects. Real-time PCR confirmed the IL-19 mRNA up-regulation in patients with CRSwNP and showed an up-regulation of IL-19, at lower extent, in patients with chronic rhinosinusitis without nasal polyps (CRSsNP) in comparison with normal subjects. Western blot analysis confirmed that IL-19 is increased also at protein level in patients with CRSwNP in comparison with normal subjects. In NP, IL-19 is highly expressed in the metaplastic nasal epithelium when compared to normal or hyperplastic epithelium. LPS stimulation increased IL-19 expression, and recombinant IL-19 increased cell proliferation in nasal epithelial cells. IL-19 is overexpressed in the epithelium in CRSwNP and increases epithelial cell proliferation.
  Allergy 05/2012; 67(7):878-86. · 6.27 Impact Factor
• Article: Anti-inflammatory effects of seven years treatment with Omalizumab in severe uncontrolled asthmatics.

  E Pace, M Ferraro, A Bruno, J Bousquet, M Gjomarkaj
  Allergy 11/2010; 65(11):1495-6. · 6.27 Impact Factor
• Article: Hypoallergenic fragment of Par j 2 increases functional expression of Toll-like receptors in atopic children.

  E Pace, G Duro, S La Grutta, M Ferraro, A Bruno, J Bousquet, G Bonsignore, M Gjomarkaj
  [show abstract] [hide abstract]
  ABSTRACT: Parietaria judaica (Par j) is one of the main causes of allergy in the Mediterranean countries. The activation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) inhibits nasal inflammation of atopic children. To examine, in vivo and in vitro, the effect of recombinant Par j 2 (rPar j 2) and of its fragments (1-55 and 52-102) on atopic children. We used skin prick test for in vivo evaluations. We assessed, in vitro, in peripheral blood mononuclear cells (PBMC), the effect of rPar j 2 and of the two fragments on neutrophil chemotaxis, on CD45RO, on TLR2 and TLR4 expression, on LPS binding and on interferon (IFN)-gamma release, by a microchemotaxis chamber, by flow cytometry and by enzyme-linked immunosorbent assay, respectively. In vivo while rPar j 2 induced a positive skin reaction, 1-55 and 52-102 fragments did not. In vitro, while rPar j 2 increased both CD45RO expression and neutrophils chemotaxis in PBMC, both Par j 2 fragments did not. 1-55 fragment of Par j 2 upregulated both TLR2 and TLR4 expression and LPS binding, while the rPar j 2 and 52-102 fragment did not. Finally, 1-55 fragment of Par j 2 induced IFNgamma release, while the rPar j 2 and 52-102 fragment did not. Hypoallergenic 1-55 fragment, upregulating innate immunity receptors and increasing IFNgamma, might re-orientate, in atopics, the immune system toward a physiologic balance between Th1 and Th2 responses.
  Allergy 01/2007; 61(12):1459-66. · 6.27 Impact Factor
• Article: LTB4 is present in exudative pleural effusions and contributes actively to neutrophil recruitment in the inflamed pleural space.

  E Pace, M Profita, M Melis, A Bonanno, A Paternò, C H Mody, M Spatafora, M Ferraro, L Siena, A M Vignola, G Bonsignore, M Gjomarkaj
  [show abstract] [hide abstract]
  ABSTRACT: The pleural space is a virtual compartment between the lung and chest wall that becomes filled with fluid and inflammatory cells during a variety of respiratory diseases. Here, we study the potential role of the eicosanoid metabolite leukotriene B4 (LTB4) in disparate diseases leading to acute (pneumonia) or chronic (tuberculosis, cancer) inflammation of the pleural space. LTB4 concentrations were significantly higher in pleural fluid due to pneumonia, tuberculosis and cancer with respect to congestive heart failure and correlated with neutrophil elastase, which is used as an indication of state of activation of neutrophils in the pleural space. Moreover, pleural LTB4 was biologically active, as an anti-LTB4 antibody partially neutralized the chemotactic activity of parapneumonic, tuberculous and cancer effusions. Macrophages, neutrophils, lymphocytes, mesothelial cells and cancer cells all expressed mRNA for 5-lipoxygenase, the enzyme that initiates leukotriene synthesis leading to the production of LTB4, in exudative pleural effusions. Upon stimulation in transudative pleural effusions, pleural macrophages produced, in a time-dependent fashion, a significantly higher concentration of LTB4 than mesothelial cells. These studies demonstrate that different cell types are capable of producing LTB4 in the inflamed pleural space and that this mediator may play a crucial role in the recruitment of neutrophils into the pleural space.
  Clinical & Experimental Immunology 04/2004; 135(3):519-27. · 3.36 Impact Factor