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Biomedical subjects

M Matucci-Cerinic

Publications and source records attributed to M Matucci-Cerinic.

At least 55 records · Page 3Linked to original sources
PubMed1997

Neuropeptides of the autonomic nervous system in Sjögren's syndrome.

OBJECTIVE: To assess the activity level of the autonomic nervous system in Sjögren's syndrome (SS) and to correlate this with stress. METHODS: Patients with SS (n = 12) and healthy controls (n = 10) were analysed for the content of vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) in their stimulated saliva by radioimmunoassays and for stress by the use of a modified Jenkins Activity Survey (JAS). RESULTS: The data are expressed as median (interquartile range). Salivary VIP output (pg/min) and NPY output (pg/min) were high in SS compared with healthy controls (30.0 (15.6, 36.6) versus 12.3 (9.2, 24.0), p = 0.045, 4.8 (0.6, 24.1) versus 0.7 (0.0, 2.4), p = 0.038, respectively). Patients experienced only a little, but not significantly, more stress than the healthy controls (stress index -2.8 (-7.7, 6.9) versus -5.2 (-12.9, 2.7), p > 0.05). Stress in general was associated with high salivary VIP concentrations (r = 0.41, p = 0.05). CONCLUSIONS: These findings show that adequately processed saliva (containing aprotinin and EDTA as neuropeptidase inhibitors) contains measurable amounts of marker peptides of the autonomic nervous system. Secondly, VIP concentration but not output may be affected by stress, which may act by decreasing watery salivary flow. In patients with SS, VIP and NPY outputs are increased. This may indicate increased leakage into saliva or efforts to compensate for the diminished salivary flow, or both.

Adult↗
PubMed1996

Lack of sympathetic involvement in dermatitis confined to the median nerve territory. A case report.

Both decreased and increased sympathetic nerve activity has been suggested as a possible underlying mechanism in inflammatory skin lesions. Modulation of sympathetic function has been proposed in the treatment of dermatitis. This case report describes the investigation strategy and normal findings in a case of dermatitis strictly confined to the median nerve territory, illustrating the need for specific tests of sympathetic function when pharmacological as well as physical sympatho-modulatory therapies are considered.

Eczema↗
PubMed1995

Somatostatin-induced modulation of inflammation in experimental arthritis.

OBJECTIVE: To study the antiinflammatory effect of different doses of intraarticular somatostatin in experimental arthritis in rabbits. METHODS: Chronic arthritis was induced by a single injection of fibrin into the knee joint of rabbits previously sensitized to this antigen. The effects of sequential intraarticular injections of somatostatin into the rabbit knee, at doses of 500, 750, and 1,000 micrograms, were monitored by measuring knee joint circumferences and hematologic parameters. The measurements were compared with those obtained following use of triamcinolone acetonide and placebo. At the end of the experiments, the knee joints were examined histologically. RESULTS: Somatostatin treatment induced a statistically significant and dose-related reduction of knee joint swelling. This effect was shorter than that produced by triamcinolone acetonide; however, the antiinflammatory activity elicited by successive doses of triamcinolone acetonide declined both in extent and duration, while the effects of somatostatin remained unchanged at each successive treatment. Histopathologic observations showed that both somatostatin and triamcinolone acetonide reduced the inflammatory signs in the joint structures, although triamcinolone acetonide appeared to be more effective. CONCLUSION: These findings suggest that somatostatin exerts an antiinflammatory effect in this model of experimental arthritis and may represent a valid and safer alternative to corticosteroids for intraarticular therapy of arthritis.

Animals↗
PubMed1995

Auranofin and its combination with LTB4 influences ATP level and migration of human polymorphonuclear cells in vitro.

Auranofin (AF), an orally administered antirheumatic drug, reduces the ATP level of PMN cells in vitro in a dose-dependent manner and provokes various effects on PMN migration. Under the experimental conditions, AF in concentrations between 10(-8) M and 10(-3) M produced a statistically significant (P < 0.05) dose-related reduction in ATP level, which ranged from 89% of the control value with 10(-8) M AF to 46.8% of the control with 10(-3) M AF. On the other hand, the combination of AF and the chemoattractant LTB4 (1 ng/ml) shows agonistic effects on the intracellular ATP level. AF at 10(-5) M significantly increases the ATP (33%; P < 0.03). In general migration of PMN cells is stimulated by 10(-7) M AF [chemotactic index (CI) = 1.26], but inhibited by 10(-5) M (CI = 0.65), 10(-4) M (CI = 0.09) and 10(-3) M AF (CI = 0.01). These effects were statistically significant at P < 0.05. In the presence of LTB4 (1 ng/ml), which resulted in an average CI of 2.9, AF also inhibits the chemotactic effect of the chemoattractant, with the CI being significantly reduced at 10(-6) M AF (CI = 2.3) and 10(-4) M AF (CI = 0.05). In the latter case the effect was also confirmed by the leading-front technique. AF at 10(-6) M is a level that could be reached in the blood after continuous therapy regimens, and these results are therefore of practical interest. They expand our knowledge of the effects of AF on PMN cells, whereby reducing effects on intracellular ATP were observed with AF alone and stimulating effects in combination with LTB4. With low AF concentrations, the reduction of the ATP level is only a part of its action that seems to be independent of its effect on cell migration and chemotaxis.

Adenosine Triphosphate↗
PubMed1995

The central role of the endothelium in the pathogenesis of vasculitides.

The pathogenesis of vasculitides is poorly understood. A growing body of evidence indicates that endothelium injury is a fundamental step in the development of all types of vasculitides. In the recent years, it has become evident that endothelial cell is responsible for a multiplicity of functions such as several immunological activities and the control of the vascular tone. The alteration of endothelium may result in metabolic and biologic disorders leading to pathologic changes. Even though the importance of endothelial cell is now demonstrated, the pathophysiological mechanisms able to induce the vascular damage are still not completely defined. In the next years, the better knowledge of the physiology of the endothelium might lead to a more appropriate therapy of vasculitis.

Endothelium, Vascular↗
PubMed1994

Increased collagen synthesis in skin fibroblasts from patients with primary hypertrophic osteoarthropathy. Evidence for trans-activational regulation of collagen transcription.

OBJECTIVE: To investigate collagen synthesis in skin fibroblasts from patients with primary hypertrophic osteoarthropathy (HOA), a disorder characterized clinically by skin thickening. METHODS: Collagenase-digestible protein, messenger RNA (mRNA) levels, and transcriptional activity of the alpha 1(I) procollagen gene were assessed in skin-derived fibroblast lines. RESULTS: Compared with fibroblasts from uninvolved skin, fibroblasts from involved skin had elevated levels of collagen synthesis and alpha 1(I) procollagen mRNA, and increased transcriptional activity of the alpha 1(I) procollagen promoter. CONCLUSION: Abnormalities of collagen synthesis in fibroblasts from patients with primary HOA can be accounted for, at least in part, by a trans-activated up-regulation of collagen transcription.

Aged↗
PubMed1994

High free and latent collagenase activity in psoriatic arthritis synovial fluids.

Collagenase activity has been studied intensively in SF from OA and RA patients. Less is known about collagenolytic activity in PsA SF. Therefore we examined collagenolytic activity in crude and trypsin treated SF as well as the alpha 1-antitrypsin and alpha 2-macroglobulin concentrations in 50 patients suffering from OA (n = 13), RA (n = 17), and PsA (n = 20). Free collagenolytic activity was low in the crude OA SF (1.80 +/- 1.35 micrograms released collagen/min/ml SF) and almost equally low in RA SF (2.35 +/- 1.80 micrograms released collagen/min/ml SF; P > 0.3). The PsA SF, however, exhibited a significantly higher free collagenolytic activity (5.63 +/- 5.69 micrograms released collagen/min/ml SF; P < 0.05 in comparison to OA and RA SF). The treatment of the SF with trypsin further activated collagenolytic activity in each group (OA 2.17 +/- 1.35 micrograms released collagen/min/ml SF; RA 6.48 +/- 6.73 micrograms released collagen/min/ml SF; PsA 11.24 +/- 5.02 micrograms released collagen/min/ml SF) and yielded significant differences between OA and RA, OA and PsA, and RA and PsA SF (P < 0.05). Concomitantly with the collagenolytic activity, the alpha 1-antitrypsin and alpha 2-macroglobulin concentrations of the SF were measured. In SF from patients with PsA (172.9 +/- 69.4 mg/100 ml) and RA (190.6 +/- 64.7 mg/100 ml) the alpha 1-antitrypsin was significantly higher than in those from OA SF (106.1 +/- 39.2 mg/100 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Neutral endopeptidase (3.4.24.11) in plasma and synovial fluid of patients with rheumatoid arthritis. A marker of disease activity or a regulator of pain and inflammation?

In recent years the role of the peripheral nervous system has been focused on the pathogenesis of rheumatoid arthritis (RA). In particular, substance P (SP), released by the sensory terminals, has been demonstrated to be involved in cartilage breakdown [13]. The aim of our work was to study the levels of SP and its peptidases, neutral endopeptidase (3.4.24.11) (NEP) and angiotensin-converting enzyme (ACE), in the synovial fluid and plasma of 30 patients with RA and 14 patients with osteoarthritis (OA). ACE and NEP were determined with a fluorimetric assay and SP with a radioimmunoassay (RIA) method. ACE levels were normal in the plasma of patients with RA and OA (6.1 +/- 1.9 and 6.7 +/- 1.4 pmol/ml/min, respectively); we found no differences in the values, of ACE between RA and OA synovial fluid (5.7 +/- 4.2 and 5.5 +/- 4.1 pmol/ml/min, respectively). NEP levels were significantly increased in plasma (139.3 +/- 36 pmol/ml/min) and synovial fluid (133.8 +/- 32 pmol/ml/min) of patients with RA when compared to patients with OA (73.4 +/- 22 in plasma and 15.2 +/- 10.8 pmol/ml/min in synovial fluid) and healthy controls (89.7 +/- 14 pmol/ml/min in plasma). In synovial fluid, SP was significantly higher in RA patients (43.1 +/- 16.6 pg/ml) than in OA patients (12 +/- 13.1 pg/ml), while plasma levels did not show any difference (RA: 14.4 +/- 10.2; OA: 13.6 +/- 10.6; healthy subjects: 11.3 +/- 3.9 pg/ml). The only relationship detected in controls and in OA was among plasma NEP and ESR (P < 0.05) and synovial fluid NEP (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Capsaicin stimulates the migration of human polymorphonuclear cells (PMN) in vitro.

Capsaicin, a homovanillic acid derivative in plants, has distinct pharmacological effects in vivo, e.g. it depletes primary afferent neurons of substance P and other tachykinins. The effect of capsaicin on the migration of human neutrophils was tested in concentrations ranging from 10(-8) M to 10(-3) M. In comparison to the control 10(-8) M capsaicin significantly enhanced the migration of PMN cells (CI 1.29; 2P < 0.009) and a peak migration activity was detected with 10(-6) M (CI 1.32; 2P < 0.01). With higher concentrations of capsaicin the CI was not significantly changed. These results show that capsaicin, a plant derived neurotoxin, exhibits a migration modifying activity on human neutrophils through a direct mechanism not mediated by neuropeptides. In addition capsaicin (10(-7) and 10(-5) M) did not affect the luminol-dependent chemiluminescence and therefore does not contribute to a superoxide anion generation in human PMN.

Adenosine Triphosphate↗
PubMed1993

Mesoglycan treatment restores defective fibrinolytic potential in cutaneous necrotizing venulitis.

BACKGROUND: Cutaneous necrotizing venulitis (CNV) is a clinical disorder associated with segmental inflammation and fibrinoid necrosis of the dermal venules. It usually presents clinically as palpable purpura, even sometimes as nodules, bullae, ulcers, and urticarial lesions. This form, when showing as leukocytoclastic vasculitis is apparently characterized by the tissue deposition of circulating immune complexes and by reduced cutaneous (CFA) and plasma (PFA) fibrinolytic activity due to reduced release of plasminogen activator (PA) from the venular endotheliocytes. Reduced CFA and PFA cause large amounts of fibrin deposits in both intra- and perivascular areas, which are able to magnify and self perpetuate the inflammatory processes following immune complex deposition. METHODS: We have studied both the PFA and CFA potential (the maximum amount of PA released in the skin after certain stimuli) and the deposits of immunoglobulins, C3, and fibrin related antigen, before and after intradermal injection of histamine (a substance able to provoke endothelial release of PA), in three subjects affected by CNV before and 20 days after 10 mg/kg/day I.M. treatment with the fibrinolytic agent mesoglycan. RESULTS: Cutaneous fibrinolytic activity and CFA potential, reduced prior to treatment, was normal after treatment, while the deposits of immunoglobulins (IgA, IgG and IgM), C3, and fibrin related antigen, detected with direct immune fluorescence (DIF) showed similar findings before and after treatment. CONCLUSIONS: These data suggest that reduced CFA may play a major role in the pathogenesis of the immunologically mediated injury in CNV. The intraperivascular deposition of fibrin is favored. The fibrinolytic agent mesoglycan seems effective in restoring defective fibrinolysis in patients affected by cutaneous necrotizing venulitis, suggesting that in cases with reduced cutaneous fibrinolytic activity (or potential) the use of a fibrinolytic agent should be considered.

Adult↗
PubMed1993

[The enzymatic mechanisms involved in the pathogenesis of rheumatoid arthritis and arthrosis. The role of metalloproteases and serine proteases in the breakdown of articular cartilage].

Rheumatoid arthritis and osteoarthritis, expression, respectively, of inflammatory and degenerative articular involvement, are the most important diseases affecting joint cartilage. Proteolytic enzymes are the effectors of the articular damage: their increased production by chondrocytes and synoviocytes leads to cartilage breakdown. These enzymes, whose structure and specific activities have been defined in the recent years, carry out their action in the extracellular matrix. They are characterized by the presence of a particular element at the active site, that allows to distinguish four different families. The most studied and the best known among them are metalloproteinases, represented by several enzymes with common features, and serinoproteinases, some members of which, particularly urokinase and tissue-type plasminogen activator, are recently indicated as potential responsible for articular destruction. Activators, and inhibitors of proteinases play a fundamental role: a fine balance, that controls the mechanisms of activation and inhibition, seems to take place at transcriptional level. Any factor able to modify the cellular shape and the cytoskeleton, gives rise to lytic enzyme expression at the genomic level. With the progress of knowledges, serinoproteinases are assuming an increasing relevance, particularly the components of the fibrinolytic pathway.

Arthritis, Rheumatoid↗
PubMed1993

Sensory neuropeptides and rheumatic diseases.

Sensory peptides are involved not only in neurotransmission and neuromodulation but also in the local control of immune function, vascular tone, and cellular proliferation. It appears that different activities of these neuropeptides are mediated by specific receptors on immune and nonimmune cells. The purpose of this article is to discuss what is known of the main sensory neuropeptides and to speculate on their possible pathophysiologic role in joint (rheumatoid arthritis) and connective tissue diseases (systemic sclerosis).

Humans↗
PubMed1992

Effect of substance P and somatostatin on migration of polymorphonuclear (PMN) cells in vitro.

The effects of the two neuropeptides, substance P (SP) and somatostatin (SOM), on the migration of polymorphonuclear cells derived from 13 volunteers were investigated. The neuropeptides were applied in concentrations between 10(-12) and 10(-6) M. Only at a concentration of 10(-6) M SP did the chemotaxis of PMN cells increase slightly but statistically significantly. In contrast to SP, SOM showed a significant dose-dependent stimulation of chemotaxis, which was first traceable at 10(-10) M and increased up to 10(-6) M. Although it is uncertain whether in vivo SP and SOM contribute directly to the invasion of PMN cells into the joint cavity, the influence of these neuropeptides on PMN migration in vitro is a further indication of the neuropeptide involvement in the genesis of inflammation.

Adenosine Triphosphate↗