Biomedical subjects

V Rocchi

Publications and source records attributed to V Rocchi.

At least 19 recordsLinked to original sources

PubMed2005

Inflammatory mediators and eosinophilia in atopic and non-atopic patients with nasal polyposis.

Nasal polyps are characterized by eosinophilic infiltration and presence of inflammatory mediators, such as total IgE, eosinophil cationic protein (ECP) and cytokines. The role of atopy in nasal polyp pathogenesis is still unclear. Therefore, we evaluated serum IgE levels, nasal mucus concentrations of ECP and cytokines and the number of infiltrating eosinophils in nasal tissue of polyps from atopic and non-atopic patients. Samples were obtained from a randomized population of 31 patients with nasal polyposis having endonasal sinus surgery and of 13 control subjects undergone corrective surgery of the nasal septum. On the basis of medical history of allergy, positive skin-prick tests and total IgE levels, patients with polyposis were divided in atopic (n = 13) and non-atopic (n = 18) patients. We determined levels of IgE in blood, ECP and cytokines (IL-4, IL-6, IL-8, IFN-gamma and IL-2) in nasal mucus, and number of infiltrating eosinophils in nasal tissue. The concentrations of total IgE, ECP, IL-4 and IL-8 and eosinophilia were significantly higher in all patients with nasal polyps compared with controls. Inside, all patients with nasal polyposis showed lower levels of IL-6, IFN-gamma and IL-2 compared with controls. The atopic patients showed significant differences when compared with non-atopic patients for the higher concentrations of total IgE (698.80+/-322.24 vs. 279.63+/-234.11; P < 0.0001) and IL-8 (1437.2 pg/ml+/-1250.7 vs. 605.5 pg/ml+/-481.1; P < 0.015). These findings suggest that inflammation still remains the major factor in the etiology of nasal polyposis and show different levels of inflammatory mediators into atopic and non-atopic patients.

Adult↗

PubMed2005

Anti-Sm and anti-RNP antibodies.

Among anti-nuclear antibodies, anti-Sm and anti-RNP antibodies are of the utmost importance in clinical practice. Anti-Sm antibodies are directed against 7 proteins (B/B', D1, D2, D3, E, F, G) that constitute the common core of U1, U2, U4 and U5 small nuclear ribonucleoprotein (snRNP) particles; B/B', D1 and D3 are more frequently targeted. Anti-RNP antibodies react with proteins (70 Kd, A, C) that are associated with U1 RNA and form U1snRNP. Anti-Sm and anti-RNP antibodies are directed towards both discontinuous and linear epitopes which are either contained in the protein sequence or are post-translationally modified. The assays to detect anti-Sm and anti-RNP antibodies are counterimmunoelectrophoresis (CIE), immunoblot, and ELISA, based on purified or recombinant proteins or synthetic peptides. Anti-Sm antibodies are detectable in a percentage of SLE patients comprised between 5 and 30%; they are more prevalent in blacks and because of their high specificity for SLE have been included in the serological criteria for diagnosing the disease.Anti-RNP are detectable in 25-47% of SLE patients; high titers of anti-RNP antibodies are diagnostic of mixed connective tissue disorder (MCTD). The measurement of anti-Sm and anti-RNP antibodies is more important in the diagnosis of SLE than in the follow-up of patients. However, anti-RNP antibodies are more prevalent in patients with Raynaud's phenomenon and are associated with milder renal involvement. On the contrary, anti-Sm antibodies are associated with the severity and the activity of renal involvement. The specificity of anti-Sm antibodies, together with epidemiological data, suggest that Epstein-Barr virus infection has the potential to induce anti-Sm antibodies by molecular mimicry.Anti-nuclear antibodies, a hallmark of the systemic autoimmune diseases, include several populations of antibodies with different specificities. Among them, anti-Sm and anti-RNP antibodies are of the utmost importance in clinical practice; in research, the study of the mechanisms inducing their production has opened up new perspectives and helped to elucidate the pathogenesis of autoimmune disorders.

Amino Acid Sequence↗

PubMed2004

Distribution of 3-nitrotyrosine in the nasal polyps of atopic patients.

OBJECTIVE: To investigate whether formation of nitrotyrosine in the nasal polyps of atopic patients occurs. STUDY DESIGN: A nonrandomized, retrospective, controlled qualitative and quantitative study. METHODS: Nasal polyp tissue samples were acquired from 12 atopic patients. Control fragments of nasal mucosa were taken from 10 patients undergoing corrective surgery of the nasal septum. For routine histologic examinations, hematoxylin-eosin staining was used. Low-magnification microscopy was designed to yield pathologic characteristics and high magnification to quantify the number of eosinophils in the subepithelial connective tissue. Presence of nitrotyrosine was assessed by immunohistochemical method. RESULTS: Hematoxylin-eosin staining revealed presence of numerous eosinophils in the epithelium and in the subepithelial connective tissue. All polyps were characterized by epithelial damage. Nitrotyrosine was present in the eosinophils, in the ciliated cell, and in cells of the damaged epithelium. Goblet cells, glands, and vessels were found to be negative. No significant differences concerning the localization of nitrotyrosine were recognized among the examined nasal polyps. CONCLUSIONS: Nitrotyrosine immunohistochemical staining in nasal-polyp tissues suggested the existence of progressive epithelium injury caused by peroxynitrite. Consequences of peroxynitrite formation in eosinophils remain to be precisely established. The lack of nitrotyrosine in glands and blood vessels indicated that peroxynitrite does not have a significant role in the vascular and glandular dysfunction of nasal polyps.

Adult↗

PubMed2003

Cytokine secretion in nasal mucus of normal subjects and patients with allergic rhinitis.

Allergic rhinitis is regulated by the local production and release of several cytokines. The levels of Th2 cytokines IL-4, IL-6, IL-10 and the Th1 cytokine IFN-gamma were studied in nasal mucus from 30 subjects with allergic rhinitis and 45 non-atopic healthy controls. In this study a sampling technique for collecting nasal mucus, well tolerated by the subjects and with a minimal stimulation of the mucosa, was performed. The cytokine concentrations in nasal mucus samples were detected and quantitated by a new paramagnetic particle-based immunofluorescent assay system more sensitive than the conventional ELISA techniques. The new technique showed reliable values of the measured parameters. The nasal mucus from allergic patients contained significantly higher concentrations of IL-4 (25.5 +/- 3.6 pg/ml; P < 0.001) and IL-10 (1300 +/- 190 pg/ml; P < 0.05) compared to the nasal mucus from control subjects (15.2 +/- 2.3 and 532 +/- 28 pg/ml, respectively, for IL-4 and IL-10). No significant modification in IFN-gamma levels of allergic patients was found when compared to control group (respectively, 19.9 +/- 3.3 vs. 25.7 +/- 5.1 pg/ml; P > 0.05). Moreover, the allergic patients showed lower levels of IL-6 concentrations in the nasal mucus compared to control subjects (64.8 +/- 9.1 vs. 129.0 +/- 18.1 pg/ml; P = 0.0099). These data can be interpreted by the hypothesis that in response to environmental allergens there is a preferential Th2 polarity by activated CD4+ T cells and that the cytokines IL-6 and IL-10 have, respectively, an important anti-inflammatory and counterregulatory action in the pathogenesis of allergic rhinitis.

Adolescent↗

PubMed1999

Immunological alterations in adult obsessive-compulsive disorder.

BACKGROUND: Some recent findings suggest the involvement of autoimmune mechanisms in childhood onset of obsessive-compulsive disorder (OCD), on the basis of a parallel drawn with Sydenham's chorea, a manifestation of rheumatic fever. A monoclonal antibody called D8/D17 characterizing a B-lymphocyte antigen, present in almost all patients with rheumatic fever, has been found also in children affected by OCD, Tourette syndrome, and chronic tics to a greater degree than in healthy control subjects. The few observations of disturbances of some immunologic parameters in adult OCD patients, prompted the authors to investigate and compare subsets of peripheral immunological cells for differences in adult patients with OCD and healthy control subjects. METHODS: Twenty patients suffering from OCD, with no comorbidity for other psychiatric disorders, were compared with a similar group of healthy control subjects. The immune subsets were measured by flow cytometry. RESULTS: The CD8+ lymphocytes were significantly increased and CD4+ lymphocytes significantly decreased in OCD patients, while the other cells did not differ between the two groups. No correlation was found between immunologic and clinical parameters. CONCLUSIONS: These data indicate that patients with adult OCD showed increased CD8+, i.e., suppressor T lymphocytes, and decreased CD4+, which identify helper T lymphocytes, as compared with a similar group of healthy control subjects. The findings appear peculiar to patients with OCD and are suggestive of an immunologic imbalance, which might be related to the stress deriving from the frustrating situation determined by the disorder itself.

Adolescent↗

PubMed1989

Development of parkinsonism after transient ischemic attacks.

In order to correlate the influence of cerebrovascular disorders with the appearance of parkinsonism, 115 patients aged between 32 and 84 years (mean = 65) with transient ischemic attacks were followed up for one year. They were treated with platelet antiaggregant drugs. None of them received neuroleptics, calcium antagonists or other drugs known to induce parkinsonism. During the study, 8 patients (mean = 75 years) developed parkinsonism, bilateral in all but one, who remarkably enough was the only case responding to L-dopa treatment. On comparing recorded with expected incidence, our series showed significantly greater values. Our findings suggest that cerebrovascular disorders are factors contributing to parkinsonism in the elderly.

Adult↗

PubMed1970