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Biomedical subjects

M Bagnasco

Publications and source records attributed to M Bagnasco.

At least 73 records · Page 4Linked to original sources
PubMed1995

Fibrous invasive (Riedel's) thyroiditis with critical response to steroid treatment.

The Riedel's thyroiditis is an uncommon form of chronic thyroiditis characterized by an invasive fibrosclerosis of the gland, often involving the surrounding tissues. Usually, the only possible treatment is the surgical decompression of the tissues. We describe a case of aggressive Riedel's thyroiditis with severe compression and dislocation of trachea and esophagus. The surgical approach was uneffective, while an "ex juvantibus" steroid treatment, resulted in a dramatic regression of fibrosclerosis and a complete clinical remission. This report points out the possible effectiveness of corticosteroids in the treatment of selective disorders involving increased fibrogenesis.

Adult↗
PubMed1995

Follicular thyroid cells of autoimmune thyroiditis may coexpress ICAM-1 (CD54) and its natural ligand LFA-1 (CD11a/CD18).

The leukocyte functional associated antigen-1 (LFA-1)-intercellular adhesion molecule-1 (CD11a-CD18/CD54) intercellular adhesion system plays a crucial role in several immunologic phenomena, including adhesion between lymphocytes and epithelial cells. In previous studies evidence for CD54 expression on thyroid follicular cells in Hashimoto's thyroiditis was provided. In this study we evaluated the possible expression of CD11a and CD18 antigens on thyrocytes of patients with Hashimoto's thyroiditis and on thyrocytes of patients with Graves' disease and simple goiter as controls; we used both alkaline phosphatase immunostaining and indirect immunofluorescence on cryostatic tissue sections. The results showed that LFA-1 (both CD11a and CD18) positivity on thyroid follicles may occur in glands of patients with Hashimoto's disease, with a pattern very similar to that of CD54: this was observed in five of seven specimens. Conversely, no positivity was observed in tissues from patients with Graves' disease or goiter: notably, isolated follicular cells from Graves' goiter tissues are induced in culture to express CD54, but not LFA-1. Using double-staining techniques, we were able to show that in specimens from patients with Hashimoto's disease, the same follicular structures coexpressed LFA-1 and CD54. Such a coexpression of the two ligands further emphasizes the possible role of this adhesion system in the pathogenesis of epithelial damage, through bidirectional interactions between thyroid epithelial cells and infiltrating LFA-1 or CD54-positive mononuclear cells.

Adult↗
PubMed1995

Minimal persistent inflammation is present at mucosal level in patients with asymptomatic rhinitis and mite allergy.

The natural exposure to house dust mites causes sensitization in genetically susceptible patients. Persistent exposure of sensitized patients causes chronic inflammation, and consequently, hyperreactivity, thus promoting the development of clinical features. Recently, intercellular adhesion molecule-1 (ICAM-1)/CD54 expression on epithelial cells triggered by allergen has been demonstrated and related to the inflammation caused by the allergic reaction. Therefore we evaluated the possible presence of inflammation (i.e., inflammatory cell infiltrate and ICAM-1/CD54 expression on epithelium) at conjunctival and nasal levels in patients with asymptomatic allergic rhinitis caused by mites, in their relatives living in the same environment, and in healthy volunteers. In addition, the possible relationship between inflammation and house dust mite allergen exposure was evaluated. Conjunctival and nasal scrapings of allergic subjects enrolled in the study showed many inflammatory cells. A mild ICAM-1/CD54 expression on conjunctival and nasal epithelium was detectable in allergic subjects, whereas relatives and healthy volunteers showed few inflammatory cells and no ICAM-1/CD54 expression on epithelial cells. A detectable level of house dust mite, sufficient to cause sensitization, was found in all houses. This study demonstrates a minimal persistent inflammation at conjunctival and nasal levels constantly detectable in patients without symptoms who are sensitized to mites and continuously exposed to the natural allergens.

Adolescent↗
PubMed1995

Cetirizine reduces inflammatory cell recruitment and ICAM-1 (or CD54) expression on conjunctival epithelium in both early- and late-phase reactions after allergen-specific challenge.

BACKGROUND: Allergen-specific conjunctival challenge (ASCC) is a safe and reproducible experimental model of allergic conjunctivitis and a useful tool in the evaluation of effectiveness and possible mechanisms of action of drugs commonly used in the treatment of allergic diseases. OBJECTIVE: The protective effect of cetirizine on inflammatory changes after ASCC was assessed in 12 patients with rhinoconjunctivitis caused by Parietaria judaica in a double-blind study. METHODS: After a screening ASCC was performed, patients were randomized into two treatment groups; each patient was given cetirizine (oral tablets) 10 mg twice daily, or matching placebo for 3 1/2 days in off-pollen season. Clinical evaluation (itching, hyperemia, lacrimation, and swelling of eyelids) and cytologic assessment (number of inflammatory cells in conjunctival scraping and evaluation of intercellular adhesion molecule-1 (ICAM-1)/CD54 expression on epithelial cells) were performed at baseline, 30 minutes (i.e., early-phase reaction [EPR]), 6 hours, and 24 hours (i.e., late-phase reaction [LPR]) after ASCC, before and after treatment. RESULTS: The EPR clinical events and the EPR total number of inflammatory cells were significantly reduced by cetirizine compared with placebo. The LPR clinical events and inflammatory cell recruitment were reduced by cetirizine in a similar manner. Both eosinophil and neutrophil numbers were decreased by active drug in EPR and LPR. Furthermore, ICAM-1/CD54 expression was significantly reduced by cetirizine in both the EPR and LPR compared with placebo. CONCLUSIONS: This study shows that cetirizine has a protective effect on clinical and cellular EPR and LPR events (including ICAM-1/CD54 expression on epithelium) induced by ASCC.

Adolescent↗
PubMed1995

Biotransformation of genotoxic agents in marine sponges. Mechanisms and modulation.

Marine sponges do not appear to suffer from neoplastic diseases, in spite of possible high exposures resulting from their nature as sessile bottom filter feeders which pump large volumes of sea water. The assessment of several parameters related to the biotransformation of mutagens/carcinogens showed that the metabolic machinery of sponge medulla cells is mainly oriented towards detoxification, with some differences depending on species (Geodia cydonium or Tethya aurantium). Glutathione (GSH) levels were unexpectedly high in these cells, especially in Geodia, in which the concentration of this tripeptide was more than twice that measured in liver preparations from untreated rats, at least when related to the protein content. The oxidoreductive enzyme activities involved in the glutathione cycle were balanced in such a way as to favour a high GSH: oxidized glutathione (GSSG) ratio. GSH S-transferase activity was conversely rather low, compared to that of rat liver, and the dehydrogenases involved in the hexose monophosphate shunt were high in Tethya but low in Geodia. The metabolism of mutagens was investigated by using the Salmonella typhimurium his- strains TA100, TA98 and YG1024. Sponge S12 fractions failed to activate aflatoxin B1, benzo[a]pyrene and the two heterocyclic amines 3-amino-1-methyl-5H-pyrido[4,3-b]indole and 2-amino-3,4-dimethyl-imidazo[4,5-f]quinoline. Although far less efficiently than untreated rat liver S12 fractions, Geodia and especially Tethya preparations weakly activated the three aromatic amines 2-acetyl-aminofluorene, 2-aminofluorene and 2-aminoanthracene. On the other hand, sponge S12 fractions were remarkably efficient in decreasing the mutagenic potency of the direct-acting mutagens 4-nitroquinoline 1-oxide and sodium dichromate.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Acetylaminofluorene↗
PubMed1994

Chemoprevention of carcinogen-DNA adducts and chronic degenerative diseases.

Molecular dosimetry techniques were exploited in order to assess the efficacy of experimental chemoprevention assays and to evaluate the involvement of DNA alterations, not only in cancer but also in other chronic degenerative diseases. In agreement with other protective effects previously observed in the same animal models, the thiol N-acetylcysteine (NAC) totally prevented or significantly reduced the formation of carcinogen-DNA adducts in three experimental systems in rats. Thus, as assessed by 32P postlabeling, supplement of the diet with NAC decreased both deoxyguanosine-C8-aminofluorene adducts (butanol enrichment) and deoxyguanosine-N2-acetylaminofluorene adducts (nuclease P1 enrichment) formed in rat liver following dietary administration of 2-acetylaminofluorene for 3 weeks. DNA adducts were detected by synchronous fluorescence spectrophotometry in rat liver, lung, heart, and testis following a daily i.t. instillation of benzo(a)pyrene for 3 consecutive days. The whole-body exposure of rats to mainstream cigarette smoke for 40 consecutive days resulted in the appearance of DNA adducts in heart, lung, and aorta, whereas no adduct was detected by synchronous fluorescence spectrophotometry in liver, brain, and testis. Multiple DNA adducts in the aorta were also measured by 32P postlabeling. Administration of NAC by gavage inhibited the formation of DNA adducts in all organs of rats treated with benzo(a)pyrene or exposed to cigarette smoke. It is of interest that a single chemopreventive agent can display a broad-spectrum protective ability. The selective localization of DNA adducts in different organs depends on pharmacokinetics, metabolic capacity, DNA repair efficiency, and cell proliferation rate. Whereas inhibition by NAC of DNA adducts in testis can be correlated with its demonstrated ability to prevent dominant lethal mutations, we raise the hypothesis that DNA adducts in lung, heart, and aorta may be pathogenetically associated with lung cancer, cardiomyopathies, and arteriosclerosis, respectively. In order to explore the involvement of molecular and biochemical alterations in human arteriosclerosis, we started an extensive collaborative project and report here preliminary data showing the presence of DNA adducts in aorta smooth muscle cells obtained from arteriosclerotic patients.

2-Acetylaminofluorene↗
PubMed1994

Evidence of intercellular adhesion molecule-1 expression on nasal epithelial cells in acute rhinoconjunctivitis caused by pollen exposure.

Rhinoconjunctivitis caused by pollen allergy is characterized by typical signs and symptoms and mucosal infiltration by inflammatory cells during pollen season. It has been recently demonstrated that the adhesion molecule system is deeply involved in cell-to-cell interaction during inflammatory response consequent to allergic reactions. The aim of this study was to evaluate the expression of intercellular adhesion molecule-1 (ICAM-1 or CD54) on nasal epithelial cells, before and during natural seasonal exposure, in 10 allergic patients (Parietaria judaica-sensitized) and in 10 healthy volunteers, correlating this parameter with clinical and cytologic involvement. Nasal epithelial cells of allergic subjects showed a significant expression of CD54 during pollen season (p < 0.001). On the contrary, no CD54 expression was observed out of pollen season. In healthy volunteers no CD54 expression was observed both before and during pollen season. Cytologic evaluation demonstrated an infiltration by eosinophils (mainly activated [EG2+]), (p < 0.001), neutrophils (p < 0.001), and metachromatic cells (p < 0.001) during pollen season only in allergic subjects. Therefore results indicate that seasonal allergic rhinitis is characterized by an infiltration of inflammatory cells correlated with CD54 expression on nasal epithelial cells. This phenomenon is specific, being restricted only to allergic patients during pollen season.

Acute Disease↗
PubMed1994

Genotoxicity of mercury compounds. A review.

This article reviews literature data concerning the genotoxicity of 29 mercury-containing agents, including laboratory compounds as well as ingredients of preparations used as fungicides, dyes, disinfectants and drugs. A variety of genetic end-points were investigated in bacteria, yeasts, moulds, plants, insects, cultured cells from fishes, rodents or humans, aquatic organisms, amphibians, mammalia and exposed humans. The overall evaluation is quite complex. Mercury compounds failed to induce point mutations in bacteria but often exerted clastogenic effects in eukaryotes, especially by binding SH groups and acting as spindle inhibitors, thereby causing c-mitosis and consequently aneuploidy and/or polyploidy. Inorganic mercury compounds were also found to induce the generation of reactive oxygen species and glutathione depletion in cultured mammalian cells. Although different mercury compounds tended to produce qualitatively comparable genetic effects, which suggests the involvement of a common toxic entity, methylmercury derivatives and other ionizable organomercury compounds were more active in short-term tests than either non-ionizable mercury compounds (e.g., dimethylmercury) or inorganic mercury salts (e.g., mercuric chloride). The results of cytogenetic monitoring in peripheral blood lymphocytes of individuals exposed to elemental mercury or mercury compounds from accidental, occupational or alimentary sources were either negative or borderline or uncertain as to the actual role played by mercury in some positive findings. Both genotoxic and non-genotoxic mechanisms may contribute to the renal carcinogenicity of mercury, which so far has been convincingly demonstrated only in male rodents treated with methylmercury chloride.

Animals↗
PubMed1994

Effects of conjunctival hyperosmolar challenge in allergic subjects and normal controls.

Nonspecific hyperreactivity to a number of physical, chemical and pharmacological agents in a common characteristics of allergic subjects, which is strictly related to the inflammatory events consequent to an allergic reaction. Hyperosmolar stimulus has previously been shown to cause an inflammatory response inducing mast cell activation and subsequent mediator release. We investigated the clinical and cytological events following conjunctival challenge using a hyperosmolar agent (i.e. glucose solution) in patients with allergy due to pollen, in patients with allergy due to mites and in healthy individuals in order to investigate the possible existence of 'conjunctival hyperreactivity', similar to the well-known nasal and bronchial nonspecific hyperreactivity in allergic patients. Hyperosmolar stimulus was able to produce an immediate inflammatory response evidenced by clinical symptomatology, inflammatory cell infiltrate and CD54 expression on conjunctival epithelium in all allergic subjects and healthy volunteers. House dust mite-sensitive subjects, but not pollen-sensitive subjects studied out of pollen season, showed conjunctival hyperreactivity as shown by histamine challenge, in that they required lower glucose concentrations to elicit the conjunctival reaction. This is probably related to an underlying although mild, inflammation.

Adolescent↗
PubMed1994

Allergen-specific challenge induces intercellular adhesion molecule 1 (ICAM-1 or CD54) on nasal epithelial cells in allergic subjects. Relationships with early and late inflammatory phenomena.

Intercellular adhesion molecule 1 (ICAM-1 or CD54) expression on epithelial cells (EC) has been demonstrated to play a role in the local molecular events of inflammation following allergen-specific conjunctival challenge. In the light of these observations, we evaluated the possible expression of ICAM-1 on nasal EC after allergen-specific challenge. Three groups of subjects were studied: (1) 14 symptomless patients sensitized to mites, (2) 15 symptomless patients sensitized to pollen, and (3) 10 healthy volunteers as controls. The study was performed during winter. At baseline we found that both pollinosic and healthy subjects did not express CD54 on epithelial cells, whereas mite-sensitive patients showed a mild expression (possibly caused by a persistent natural allergen exposure). In addition, clinical and cellular responses were induced by lower allergen dosages in mite-sensitive patients compared with pollen-sensitive patients. CD54 was detectable in all the allergic patients but not in the control subjects 30 min after challenge. At 6 h all patients showed a marked inflammatory infiltration and CD54 persistence on EC: such an infiltration was more relevant in patients developing clinical late-phase reaction (LPR). Finally, 24 h after challenge EC CD54 expression persisted, as well as a cellular infiltrate mainly caused by eosinophils (the latter being more pronounced in mite-sensitive individuals). CD54 should be regarded as an early and sensitive marker of inflammation in both LPR-positive and LPR-negative patients. A cellular inflammatory infiltrate was detectable in both LPR-positive and LPR-negative subjects, although relevant differences in eosinophil counts were observed between the two groups. The study emphasizes the importance of the different events of inflammation in allergy.

Adolescent↗
PubMed1993

Signalling through CD28 T-cell activation pathway involves an inositol phospholipid-specific phospholipase C activity.

Stimulation of the human T-cell line, Jurkat, by a monoclonal antibody (mAb) directed against the CD28 molecule leads to sustained increases in intracellular levels of Ca2+ ([Ca2+]i); the initial rise in Ca2+ comes from internal stores, followed by Ca2+ entry into the cells. The CD28 molecule also appears to activate polyphosphoinositide (InsPL)-specific phospholipase C (PLC) activity in Jurkat cells, as demonstrated by PtdInsP2 breakdown, InsP3 and 1,2-diacylglycerol generation and PtdIns resynthesis. We also observed that interleukin-2 (IL2) production induced via CD28 triggering was sensitive to a selective protein kinase C inhibitor. Of the four other anti-CD28 mAbs (CD28.2, CD28.4, CD28.5, CD28.6) tested, only one (CD28.5) was unable to generate any InsPL-specific PLC or IL2 secretion. However, the cross-linking of cell-bound CD28.5 with anti-mouse Ig antibodies led to an increase in [Ca2+]i. CD28-molecule clustering in itself appears to be a sufficient signal for induction of PLC activity.

Antibodies, Monoclonal↗
PubMed1993

Presence of estrogen-binding sites on macrophage-like synoviocytes and CD8+, CD29+, CD45RO+ T lymphocytes in normal and rheumatoid synovium.

OBJECTIVE: To study the presence of estrogen-binding sites (EBS) in the synovial tissues of male and female patients with rheumatoid arthritis (RA) and in age- and sex-matched healthy controls. METHODS: Both type 1 (high affinity, low binding capacity) and type 2 (reduced affinity, higher binding capacity) EBS were investigated in both soluble and nuclear fractions of homogenized synovial tissue samples by a dextran-coated charcoal method. To determine what type of synovial cell was positive for EBS, cryosections of synovial tissues were immunostained with a specific monoclonal anti-estrogen receptor antibody (anti-ER MAb) using both immunofluorescence and immunoperoxidase techniques. Double immunostaining with the anti-ER MAb and with specific MAb to detect different macrophage antigens (Ber-MAC3, MAC387, CD68) and CD8+ T cell subsets (CD29+, CD45RO+ and CD29-, CD45RO-) was performed. RESULTS: Higher affinity EBS were found mostly in nuclear cell fractions of either RA or control synovial tissues (28 of the 33). These EBS were present to a lesser extent in soluble cell fractions (11 of the 33). Immunostaining showed the estrogen receptor-positive cells to be the macrophage-like synoviocytes and the CD8+, CD29+ T cells both in RA and in control synovial tissues. Higher nuclear content of EBS was consistent with more intense nuclear staining of synoviocytes and T cells. CONCLUSION: It is conceivable that the immunomodulatory activity exerted by estrogens is at least partly mediated through their interaction with EBS that are present on macrophage-like synoviocytes, functioning as antigen-processing and antigen-presenting cells, and on antigen-experienced (memory) CD8+ T lymphocytes (CD29+, CD45RO+).

Adult↗
PubMed1993

Protective effects of deflazacort on allergen-specific conjunctival challenge.

The protective effects of deflazacort, (a new heterocyclic glucocorticoid and derivative of prednisolone, with calcium and glucose-sparing effects) on the inflammatory reaction following an allergen-specific conjunctival provocation test (CPT) were assessed in a double-blind study, in 24 patients suffering from rhinoconjunctivitis due to Parietaria judaica. After an initial screening CPT, patients were randomized to four treatment groups, to receive deflazacort, 6, 30 or 60 mg, once daily or placebo, for 3 days, during the low-pollen season. Clinical evaluations (itching, hyperaemia, lacrimation and eyelid swelling), cytological assessment (number of inflammatory cells, i.e. neutrophils, eosinophils and lymphocytes, sampled by conjunctival scraping) and immunocytochemical evaluation of CD54 (intercellular adhesion molecular-1 [ICAM-1]) expression on epithelial cells were performed after CPT, at baseline, after 30 minutes (early-phase reaction [EPR]) and after 6 and 24 hours (late-phase reaction [LPR]), before and after treatment. Neither the nature or severity of clinical events nor the total number of inflammatory cells during the EPR changed during treatment with deflazacort. The severity of the clinical events during the LPR were significantly reduced by deflazacort, 30 and 60 mg/day P < 0.01) compared to the placebo-treated group. The total number of inflammatory cells during the LPR was also significantly reduced by deflazacort, 30 and 60 mg/day (P < 0.01) compared to the placebo-treated group. CD54 expression was significantly reduced by deflazacort, 30 and 60 mg/day both during the EPR (P < 0.01) and LPR (P < 0.01) compared to the placebo-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗
PubMed1993

Allergic subjects express intercellular adhesion molecule--1 (ICAM-1 or CD54) on epithelial cells of conjunctiva after allergen challenge.

BACKGROUND: Allergic inflammation can be experimentally reproduced in vivo in humans, by means of the conjunctival provocation test with allergen. The allergen stimulation triggers an early clinical response and an almost simultaneous cellular infiltrate. Among the factors that can contribute to the local cellular recruitment, we postulate a possible early involvement of CD54 in the development of inflammation caused by the allergic reaction. METHODS: We used a sensitive immunocytochemical immunoenzymatic alkaline phosphatase-monoclonal antialkaline phosphatase technique to detect the possible expression of CD54 molecule on epithelial cells of conjunctiva in 15 allergic subjects and in 15 healthy individuals in basal conditions and after allergen challenge (Parietaria judaica) during the off-pollen season. RESULTS: At baseline all studied individuals did not evidence CD54 expression on epithelial cells; 30 minutes after allergen challenge, all the allergic individuals showed a marked expression of CD54 on conjunctival epithelium, whereas none of healthy subjects showed any CD54 expression. First, CD54 expression on conjunctival epithelium after specific provocation test appeared as a specific phenomenon occurring only in sensitized subjects; moreover, it is an immediate event concomitant with the local inflammatory infiltrate. Therefore conjunctival epithelium unexpectedly appeared to be more than a bystander in the allergic reaction; it may be perceived as an active participant interacting with the inflammatory infiltrate. CONCLUSIONS: These findings indicate that CD54 may play a central role in the allergic inflammation and strongly support the concept that maneuvers designed to interact with the adhesion machinery expressed on inflammatory cells and epithelium may be a helpful therapeutic approach.

Adult↗