[Heavy chain diseases (author's transl)].
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Heavy Chain Disease↗
Biomedical subjects
M Triggiani
Publications and source records attributed to M Triggiani.
Cyclosporin A inhibits the release of histamine and peptide leukotriene C4 from human lung mast cells.
We investigated the effect of cyclosporin A (CsA) on in vitro release of chemical mediators from mast cells purified from human lung tissues. CsA (3 X 10(-2) to 1 microgram/ml) dose-dependently inhibited IgE-mediated release of histamine and peptide leukotriene C4 (LTC4) from human lung mast cells. The same concentrations of CsA also inhibited the release of histamine from lung mast cells challenged with the Ca2+ ionophore A23187. Therefore, CsA in pharmacological concentrations inhibits the IgE- and non-IgE-mediated release of inflammatory mediators from mast cells purified from human lung tissues.
Calcimycin↗
Secretory phospholipase A2: a putative mediator of airway inflammation.
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Humans↗
Histamine-induced activation of human lung macrophages.
BACKGROUND: Histamine plays a central role in the pathogenesis of allergic and inflammatory diseases by modulating vascular and airway responses. Increasing evidence suggests that histamine also regulates the function of inflammatory and immune cells. Macrophages are primarily involved in inflammatory diseases of the lung. We explored the ability of low concentrations of histamine to induce the release of proinflammatory mediators from human lung macrophages. METHODS: Macrophages purified (> 95%) from lung parenchyma by Percoll density gradients and adherence to polystyrene dishes were incubated (37 degrees C, 2-24 h) with histamine (10(-9)-10(-6) M). At the end of incubation, the release of beta-glucuronidase and IL-6 was determined. RESULTS: Histamine induced a concentration-dependent release of beta-glucuronidase and IL-6 with a maximum release after 2 and 6 h of incubation, respectively. Exocytosis induced by histamine was noncytotoxic and was Ca(2+)- and temperature-dependent. The effect of histamine was inhibited by the H(1) receptor antagonist fexofenadine but not by the H(2) antagonist ranitidine. CONCLUSIONS: These data indicate that histamine is an effective stimulus for exocytosis and cytokine production from human lung macrophages. These effects are inhibited by pharmacological concentrations of fexofenadine. Our results suggest that histamine may contribute to the long-term evolution of lung inflammation and tissue remodelling in allergic diseases by modulating the production of proinflammatory and immunoregulatory mediators by macrophages.
Cells, Cultured↗
Biochemical functions of a pool of arachidonic acid associated with triglycerides in human inflammatory cells.
The distribution of arachidonic acid (AA) within intracellular lipid pools of inflammatory cells is thought to be an important factor regulating the production of eicosanoids. We have recently identified a pool of AA associated with triglycerides (TGs) in human lung macrophages. This pool is also present in other human inflammatory cells (mast cells, eosinophils, monocytes and platelets) and it contains a percentage of total cellular AA ranging from 10 to 45%. Kinetic studies of AA incorporation have shown that TG are the first acceptor pool for exogenous AA that is subsequently transferred to phospholipid pools. During cell activation, AA is released from phospholipids; however, a large amount of AA is rapidly reincorporated into TGs. The TG pool also supplies AA to the phospholipid pools once these have been depleted during cell activation. These data suggest that TGs are not only a storage site for AA but may also be important as regulators of AA metabolism and eicosanoid biosynthesis in human inflammatory cells.
Arachidonic Acid↗
Arachidonic acid remodeling in human inflammatory cells migrating to the lung in vivo.
Recent evidence suggests that arachidonic acid (AA), the precursor of eicosanoids, is stored in various glycerolipid pools with different biochemical specificities. Upon cell activation, AA is rapidly remodeled within these glycerolipid pools. We have explored the changes in AA content and distribution in human neutrophils as they are activated in vivo in the lungs of patients with adult respiratory distress syndrome (ARDS). Neutrophils from bronchoalveolar lavage fluid of ARDS patients contained an amount of total cellular AA four times larger than that of blood (resting) neutrophils and accumulated a larger proportion of AA into a pool associated with triglycerides (TG). These biochemical changes were associated with an increased number of cytoplasmic lipid bodies and with the acquisition of the hypodense phenotype. These data indicate that the accumulation of AA into TG is a marker of cell activation and suggest a central role of the TG pool in AA metabolism in inflammatory cells activated in vivo.
Arachidonic Acid↗
Antiinflammatory effects of oxatomide.
There is increasing evidence that histamine may have wider proinflammatory and immunomodulatory activities than previously reported. It may influence several functions of lymphocytes, monocytes, basophils and macrophages, modulating the release of inflammatory mediators and cytokines. These observations have aroused interest in the pharmacology and clinical applications of histamine H1 receptor antagonists and have led to the identification of novel antiinflammatory properties for this class of drugs. Oxatomide, initially characterized as an H1 antagonist, inhibits the secretion of several mediators of inflammation from human basophils and mast cells. In vitro oxatomide inhibits the release of both preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4 and prostaglandin D2). The inhibitory effect is not restricted to basophils and mast cells but is also evident on other inflammatory cells such as the neutrophils. In this cell, oxatomide inhibits arachidonic acid mobilization, and leukotriene B4 and platelet-activating factor synthesis, presumably by reducing the activity of cytosolic phospholipase A2. These observations extend the pharmacological activities of oxatomide beyond H1 receptor antagonism and suggest that this drug influences a variety of biochemical events in human inflammatory cells. These antiinflammatory activities help to explain its beneficial effect in various allergic and inflammatory disorders, including urticaria, allergic rhinitis and bronchial asthma.
Animals↗
[Basophil count of the newborn is not useful in prediction of allergic diseases].
Basophil granulocytes and their mediators are involved in the pathogenesis of allergic inflammation. We evaluated basophil count, blood histamine content, eosinophil count and serum total IgE levels in one hundred-thirteen healthy newborns at birth. 108 children were prospectively studied with a follow-up to 18 months of age for development of topic disorders. No difference was found in newborns with biparental family history of atopy (FHA) in comparison with newborns with monoparental FHA and with newborns without FHA. Children who developed atopic disorders had neonatal basophil count higher than those who did not develop atopic symptoms (p = 0.03). No significant correlation was found between basophil and eosinophil counts (r = 0.013), between basophil count and serum total IgE levels (r = 0.012) and between basophil count and blood histamine content. Positive predictive value and sensitivity of basophil count for allergy up to 18 months of age was respectively only 33% and 27%. Our data indicate that an increased basophil count at birth is not associated with FHA and is not a good predictive marker of atopy.
Age Factors↗
Primary cardiac malignancy presenting as left atrial myxoma. Clinical and surgical considerations.
Primary heart neoplasms occur in 0.002-0.3% of autopsies: 30% are myxomas and 20-30% are malignancies, almost always sarcomas. Cardiac metastases are 10 to 40 times more frequent than primary heart cancer. We describe a case of a left atrial sarcoma erroneously diagnosed as myxomas preoperatively. Standard surgical indication for resection of cardiac myxomas is based on echocardiography. Because of the severity of cardiac malignant lesions than can mimic atrial myxomas at echocardiography, through preoperative investigation should be accomplished, best by magnetic resonance imaging. In case of suspected malignancy, total body computed tomography should be performed to avoid unnecessary cardiac operations in case of disseminated cancer. To date the only good medium and long-term results in the therapeutic management of heart sarcomas have been achieved by transplantation: the probable explanation is that criteria of surgical radicality should be those followed for soft tissue tumors located elsewhere in the organism.
Diagnosis, Differential↗
Basophil count in neonates is not suitable for atopy predictivity.
Basophil granulocytes and their mediators are involved in the pathogenesis of allergic inflammation. We evaluated basophil count, blood histamine content, eosinophil count and serum total IgE levels in one hundred-thirteen healthy newborns at birth. 102 children were prospectively studied with a follow up to 18 months of age for development of atopic disorders. No difference was found in newborns with biparental family history of atopy (FHA) in comparison with newborns with monoparental FHA and with newborns without FHA. Children who developed atopic disorders had neonatal basophil counts higher than those who did not develop atopic symptoms (p = 0.03). No significant correlation was found between basophil and eosinophil counts (rs = 0.013), between basophil count and serum total IgE levels (rs = 0.012) and between basophil count and blood histamine content. Positive predictive value and sensitivity of basophil count for allergy up to 18 months of age was only 33% and 27%, respectively. Our data indicate that an increased basophil count at birth is not associated with FHA and is not a good predictive marker of atopy.
Basophils↗