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Dive into the research topics where Oliviero Rossi is active.

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Featured researches published by Oliviero Rossi.


Clinical & Experimental Allergy | 2006

Sublingual immunotherapy with Dermatophagoides monomeric allergoid down‐regulates allergen‐specific immunoglobulin E and increases both interferon‐γ‐ and interleukin‐10‐production

Lorenzo Cosmi; Veronica Santarlasci; Roberta Angeli; Francesco Liotta; Laura Maggi; Francesca Frosali; Oliviero Rossi; P. Falagiani; G. Riva; Sergio Romagnani; Francesco Annunziato; Enrico Maggi

Background The clinical efficacy and safety of sublingual immunotherapy (SLIT) for aeroallergens has been demonstrated in several trials, whereas the immunological changes induced by this treatment, which may account for the clinical improvement, are still unclear.


Allergy | 2010

Anti-infliximab IgE and non-IgE antibodies and induction of infusion-related severe anaphylactic reactions.

Alessandra Vultaggio; Andrea Matucci; Francesca Nencini; Sara Pratesi; Paola Parronchi; Oliviero Rossi; Sergio Romagnani; Enrico Maggi

To cite this article: Vultaggio A, Matucci A, Nencini F, Pratesi S, Parronchi P, Rossi O, Romagnani S, Maggi E. Anti‐infliximab IgE and non‐IgE antibodies and induction of infusion‐related severe anaphylactic reactions. Allergy 2010; 65: 657–661.


Clinical & Experimental Allergy | 1993

The importance of Th2‐like cells in the pathogenesis of airway allergic inflammation

M. Ricci; Oliviero Rossi; M. Bertoni; Andrea Matucci

During the last 20 years a great research efFort has been made to clarify the complex mechanisms which regulate IgE antibody production. In this regard substantial progress has been made since it was shown that IL-4 and T/B-cell interactions are essential for the induction of human TgE synthesis, whereas IFN-y plays a negative regulatory role. However., more recently it has become quite clear that the reaction of inhaled allergens with IgE specific antibodies bound to Fĉ ^Rl receptors on the surface of mast cells and basophils and the subsequent release of traditional mediators is not sufficient per se to account for the persistent histological,, pathophysiological and clinical alterations that characterize the allergic respiratory disorders. In this connection it has been reasonable to address studies on the possible involvement of other kinds of cells such as, for example,, T-cells,, and of other mediators, such as cytokines.


European Journal of Heart Failure | 2007

Tako-Tsubo-like syndrome during anaphylactic reaction

Alessandra Vultaggio; Andrea Matucci; Stefano Del Pace; Ignazio Simonetti; Paola Parronchi; Oliviero Rossi; Enrico Maggi; Gian Franco Gensini; Sergio Romagnani

Tako‐Tsubos syndrome (apical ballooning or broken heart syndrome) is a reversible left ventricular dysfunction due to apical asynergy that occurs typically after sudden emotional stress in a subject without coronary disease. It is characterized by acute onset of chest pain or dyspnoea or both and is associated with electrocardiographic changes such as ST segment elevation and/or T wave inversion. Myocardial biomarkers may be normal or slightly elevated.


Current Medical Research and Opinion | 2011

Patient-related factors in rhinitis and asthma: the satisfaction with allergy treatment survey

Giorgio Ciprandi; Cristoforo Incorvaia; Silvia Scurati; Paola Puccinelli; Silvia Soffia; Franco Frati; Oliviero Rossi

Abstract Background: Patient satisfaction with the prescribed treatments represents a crucial issue that may have clinical relevance as it may significantly affect treatment compliance. We designed an observational study to evaluate the satisfaction level concerning different pharmacological treatments for allergic rhinitis (AR) and asthma in a real-life setting. Methods: The study was conducted in 21 allergy centres homogeneously distributed in Italy. Three hundred and one patients (46.8% males; 53.2% females; mean [SD] age, 33.1 [13.8] years) with AR and/or asthma were consecutively evaluated. Diagnosis, classification, symptom severity, and satisfaction degree (assessed by a questionnaire) were the parameters considered. Results: Only 33.5% of the AR patients were satisfied with the rhinitis treatments. Only 40.7% of the asthmatic patients were satisfied with the asthma treatments. Some factors associated with treatment dissatisfaction are as follows: female gender (odds ratio [OR] 2.36; p < 0.01), co-morbidity (OR 2.39; p < 0.05), rhinitis severity (OR 1.39; p < 0.05), asthma severity (OR 2.04; p < 0.05), and antihistamine use (OR 2.53); however, the use of bronchodilators had a favourable impact (OR 0.28; p < 0.05). The relatively low number of subjects prevented performing stratification of patients by treatment classes. Conclusion: The findings of this real-life study strengthen the concept that AR is particularly troublesome and that most allergic patients suffering from both rhinitis and asthma are dissatisfied with prescribed drugs.


The Journal of Allergy and Clinical Immunology | 2017

Human circulating group 2 innate lymphoid cells can express CD154 and promote IgE production

Laura Maggi; Gianni Montaini; Alessio Mazzoni; Beatrice Rossettini; Manuela Capone; Maria Caterina Rossi; Veronica Santarlasci; Francesco Liotta; Oliviero Rossi; Oreste Gallo; Raffaele De Palma; Enrico Maggi; Lorenzo Cosmi; Sergio Romagnani; Francesco Annunziato

Background: Protection against helminths consists of adaptive responses by TH2 cells and innate responses by group 2 innate lymphoid cells (ILC2s), with these latter being well characterized in mice but less so in human subjects. Objective: We sought to characterize human circulating ILC2s and compare their functional profile with that of autologous TH2 cells. Methods: Circulating ILC2s and TH2 cells were isolated by means of fluorescence‐activated cell sorting and magnetic cell sorting and expanded in vitro. ILC2s were then stimulated with phorbol 12‐myristate 13‐acetate plus ionomycin, IL‐25 plus IL‐33 (IL‐25/IL‐33), or a mixture of Toll‐like receptor ligands to evaluate their ability to produce cytokines, express CD154, and induce IgE production by autologous B cells. Cytokines and transcription factor gene methylation were assessed. Results: ILC2s expressed GATA‐3, retinoic acid orphan receptor (RORC) 2, and ROR&agr;; were able to produce IL‐5, IL‐13, and IL‐4; and, accordingly, were characterized by demethylation of IL4, IL13, IL5, GATA3, and RORC2, whereas the IFNG, IFNG promoter, and TBX21 regions of interest were methylated. ILC2s expressed TLR1, TLR4, and TLR6, and TLR stimulation induced IL‐5 and IL‐13 production. Moreover, ILC2s expressed CD154 in response to phorbol 12‐myristate 13‐acetate plus ionomycin, IL‐25/IL‐33, or a mixture of TLR ligands. Stimulated ILC2s also induced IgM, IgG, IgA, and IgE production by B cells. Finally, circulating ILC2s from atopic patients were not different in numbers and frequency but expressed higher IL‐4 levels than those from nonatopic subjects. Conclusion: This study provides the first evidence that human ILC2s can express CD154 and stimulate the production of IgE by B lymphocytes through IL‐25/IL‐33 stimulation or TLR triggering.


Clinical and Molecular Allergy | 2015

Choosing wisely: practical considerations on treatment efficacy and safety of asthma in the elderly

Nicola Scichilone; Maria Teresa Ventura; Matteo Bonini; Fulvio Braido; Caterina Bucca; Marco Caminati; Stefano Del Giacco; Enrico Heffler; Carlo Lombardi; Andrea Matucci; Manlio Milanese; Roberto Paganelli; Giovanni Passalacqua; Vincenzo Patella; Erminia Ridolo; Giovanni Rolla; Oliviero Rossi; Domenico Schiavino; Gianenrico Senna; Gundi Steinhilber; Alessandra Vultaggio; Giorgio Walter Canonica

The prevalence of asthma in the most advanced ages is similar to that of younger ages. However, the concept that older individuals may suffer from allergic asthma has been largely denied in the past, and a common belief attributes to asthma the definition of “rare” disease. Indeed, asthma in the elderly is often underdiagnosed or diagnosed as COPD, thus leading to undertreatment of improper treatment. This is also due to the heterogeneity of clinical and functional presentations of geriatric asthma, including the partial loss of reversibility and the lower occurrence of the allergic component in this age range. The older asthmatic patients are also characterized the coexistence of comorbid conditions that, in conjunction with age-associated structural and functional changes of the lung, may contribute to complicate the management of asthma. The current review addresses the main issues related to the management of allergic asthma in the geriatric age. In particular, the paper aims at revising current pharmacological and non pharmacological treatments for allergic asthmatics of advanced ages, primarily focusing on their safety and efficacy, although most behaviors are an arbitrary extrapolation of what has been tested in young ages. In fact, age has always represented an exclusion criterion for eligibility to clinical trials. Experimental studies and real life observations specifically testing the efficacy and safety of therapeutic approaches in allergic asthma in the elderly are urgently needed.


Clinical & Experimental Allergy | 2009

Influence of total serum IgE levels on the in vitro detection of β‐lactams‐specific IgE antibodies

Alessandra Vultaggio; Andrea Matucci; G. Virgili; Oliviero Rossi; Lucia Filì; Paola Parronchi; Sergio Romagnani; Enrico Maggi

Background Allergic reactions to β‐lactams are a frequent cause of adverse drug reactions; the diagnosis is based on history, clinical examination, skin testing (prick and intradermal) and demonstration of serum‐specific IgE antibodies (Abs).


Allergy | 2004

Partial safety of the new COX‐2 inhibitor rofecoxib in NSAIDs high sensitive patients

Andrea Matucci; Paola Parronchi; Alessandra Vultaggio; Oliviero Rossi; Francesca Brugnolo; Enrico Maggi; Sergio Romagnani

References 1. Slater JE. Hypersensitivity to macrolide antibiotics. Ann Allergy 1991; 66:193–195. 2. Demoly P, Bousquet J. Epidemiology of drug allergy. Curr Opin Allergy Clin Immunol 2001;1:305–310. 3. Brockow K, Romano A, Blanca M, Ring J, Pichler W, Demoly P et al. General considerations for skin test procedures in the diagnosis of drug hypersensitivity. Allergy 2002;57:45–51. 4. Kvedariene V, Bencherioua AM, Messaad D, Godard P, Bousquet J, Demoly P et al. The accuracy of the diagnosis of suspected paracetamol (acetaminophen) hypersensitivity: results of a single-blinded trial. Clin Exp Allergy 2002;32:1366–1369. 5. Paggiaro PL, Loi AM, Toma G. Bronchial asthma and dermatitis due to spiramycin in a chick breeder. Clin Allergy 1979;9:571–574. 6. Moscato G, Naldi L, Candura F. Bronchial asthma due to spiramycin and adipic acid. Clin Allergy 1984;14:355–361. 7. Shirin H, Schapiro JM, Arber N, Pinkhas J, Sidi Y, Salomon F. Erythromycin base-induced rash and liver function disturbances. Ann Pharmacother 1992;26:1522–1523. 8. JorroG,MoralesC,Braso JV,PelaezA. Anaphylaxis to erythromycin. Ann Allergy Asthma Immunol 1996;77:456–458. 9. Igea JM, Quirce S, de la Hoz B, Fraj J, Pola J, Diez Gomez ML. Adverse cutaneous reactions due to macrolides. Ann Allergy 1991;66:216–218. 10. Barbaud A, Reichert-Penetrat S. The use of skin testing in the investigation of cutaneous adverse drug reactions. Br J Dermatol 1998;139:49–58. 11. Williams DA. Stevens-Johnson syndrome after erythromycin therapy while deployed at sea. Mil Med 2000;165:636–637. 12. Veien NK, Hattel T, Justesen O, Norholm A. Occupational contact dermatitis due to spiramycin and/or tylosin among farmers. Contact Dermatitis 1980;6:410–413. 13. Acero S, Tabar AI, Echechipia S, Alvarez MJ, Gatcia BE. Occupational allergic contact dermatitis due to airborne spiramycin. J Investig Allergol Clin Immunol 1998;8:184–185. 14. Vangala R, Cernek PK. Hypersensitivity reaction to clarithromycin. Ann Pharmacother 1996;30:300. 15. Igea JM, Lazaro M. Hypersensitivity reaction to clarithromycin. Allergy 1998;53:107–109. 16. Gavura SR, Nusinowitz S. Leukocytoclastic vasculitis associated with clarithromycin. Ann Pharmacother 1998;32:543– 545. 17. Hamamoto Y, Ohmura A, Kinoshita E, Muto M. Fixed drug eruption due to clarithromycin. Clin Exp Dermatol 2001;26:48–49. 18. Lund Kofoed M, Oxholmv A. Toxic epidermal necrolysis due to erythromycin. Contact Dermatitis 1985;13:273. 19. Trevisi P, Patrizi A, Neri I, Farina P. Toxic pustuloderma associated with azithromycin. Clin Exp Dermatol 1994;19:280–281. 20. Hubner C, Dietz A, Stremmel W, Stiehl A, Andrassy H. Macrolide-induced Churg-Strauss syndrome in a patient with atopy. Lancet 1997;350:563. 21. Schissel DJ, Singer D, David-Bajar K. Azithromycin eruption in infectious mononucleosis: a proposed mechanism of interaction. Cutis 2000;65:163–166. 22. Cascaval RI, Lancaster DJ. Hypersensitivity syndrome associated with azithromycin. Am J Med 2001;110:330–331. 23. Kruppa A, Scharffetter-Kochanek K, Krieg T, Hunzelmann N. Immediate reaction to roxithromycin and prick test cross-sensitization to erythromycin and clarithromycin. Dermatology 1998;196:335–336. 24. Borja, JM, Galindo PA, Feo F, Gomez E, Lasanta A. Maculopapular exanthema from diacetyl-midecamycin (MOM). Allergy 1998;53:1004–1005. 25. Thevenot T, Mathurin P, Martinez F, Moussalli J, Poynard T, Opolon P et al. Acute hepatitis during hypersensitivity syndrome due to midecamycin. Eur J Gastroenterol Hepatol 1997;9: 1249–1250. 26. de Vega T, Blanco S, Lopez C, Pascual E, Sanchez M, Zamarron A. Clarithromycin-induced leukocytoclastic vasculitis. Eur J Clin Microbiol Infect Dis 1993;12:563. 27. Davies RJ, Pepys J. Asthma due to inhaled chemical agents the macrolide antibiotic Spiramycin. Clin Allergy 1975;5:99–107. 28. San Pedro de Saenz B, Gomez A, Quiralte J, Florido JF, Martı̀n E, Hinojosa B. FDE to macrolides. Allergy 2002;57:55–56. 29. Gurvinder SK, Tham P, Kanwar AJ. Roxithromycin induced acute urticaria. Allergy 2002;57:262. 30. Pigatto PD, Riboldi A, Riva F, Altomare GF. Fixed drug eruption to erythromycin. Acta Derm Venereol 1984;64:272–273. 31. Florido Lopez JF, Lopez Serrano MC, Belchi Hernandez J, Estrada Rodriguez JL. Fixed eruption due to erythromycin. A case report. Allergy 1991;46: 77–78. 32. Demoly P, Benahmed S, Sahla H, Messaad D, Valembois M, Godard P. Allergy to macrolides. 21 cases. Presse Med 2000;29:294–298. 33. Lopez Serrano C, Quiralte Enriquez J, Martinez Alzamora F. Urticaria from erythromycin. Allergol Immunopathol (Madr) 1993;21:225–226. 34. Gruchalla RS. Clinical assessment of drug-induced disease. Lancet 2000;356:1505–1511. 35. Webster AW, Thompson RA. The ampicillin rash. Lymphocyte transformation by ampicillin polymer. Clin Exp Immunol 1974;18:553–564.


The Journal of Allergy and Clinical Immunology | 1987

Effect of in vitro irradiation and cell cycle-inhibitory drugs on the spontaneous human IgE synthesis in vitro*

Gian Franco Del Prete; Donata Vercelli; A Tiri; Enrico Maggi; Oliviero Rossi; Sergio Romagnani; M. Ricci

The in vitro effects of radiation, diterpine forskolin (FK), and hydrocortisone (HC) on the in vitro spontaneous IgE synthesis by peripheral blood B-lymphocytes from atopic patients were investigated. Without affecting cell viability, in vitro irradiation inhibited in a dose-dependent fashion de novo IgE synthesis in vitro by B cells from all patients examined with a mean 40% reduction of in vitro IgE product after treatment with 100 rads. In contrast, the in vitro IgE production by the U266 myeloma cell line was unaffected, even by irradiation with 1600 rads. The addition to B cell cultures from atopic patients of FK consistently resulted in a dose-dependent inhibition of the spontaneous IgE production in vitro. The addition to cultures of 10(-5) and 10(-6) molar concentrations of HC was also usually inhibitory, whereas lower HC concentrations were uneffective or even enhanced the spontaneous in vitro IgE synthesis. When 10(-6) molar concentrations of both HC and FK were combined in culture, a summation inhibitory effect on the spontaneous IgE synthesis was observed. In contrast, neither FK nor HC had inhibitory effect on the in vitro spontaneous IgE synthesis by the U266 myeloma cell line. The spontaneous in vitro IgE synthesis by B cells from patients with Hodgkins disease, demonstrating high levels of serum IgE, was strongly reduced or virtually abolished after patients underwent total nodal irradiation to prevent the spread of the disease. In addition, the in vitro spontaneous IgE synthesis by B cells from atopic patients was markedly decreased or abolished by in vivo administration of betamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)

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M. Ricci

University of Florence

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