Biomedical subjects
Publications and source records attributed to M Reale.
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The lymphokines interleukin-2 and interferon alpha or gamma are synthesized and secreted by activated mononuclear cells (MC) and play a critical role in the proliferative expansion of T-lymphocyte effector cells during the immune response. The pretreatment of human peripheral blood mononuclear cells (PBMC) with antibody IgG against human interleukin-1 (IL-1) from normal rabbit serum, inhibited their natural killer (NK) activity against both myeloid (K562) and lymphoid (MOLT-4) cell lines. Percent specific lysis of tumor cells decreased by increasing the antibody anti-IL-1 dose in an almost linear fashion. When the effector cells were pretreated with human recombinant interleukin-2, human interferon alpha or gamma and indomethacin alone or in combination, the inhibitory effect of antibody against human IL-1 was almost totally reversed.
The cyclooxygenase pathway promotes formation of an endoperoxide that is the precursor of prostaglandins (PG), thromboxanes (Tx) and prostacyclins (PGI2), all of which have important biologic activities. In this study, we examined the ability of human polymorphonuclears (PMN) to synthesize TRxA2, 6-KETO-PGF1 alpha and PGE2 in response to human recombinant interleukin 1 (IL1) and tumor necrosis factor (TNF) alone and in combination. Blood was obtained from healthy donors and whole blood was centrifuged over Ficoll-Hypaque in 2% dextran for 30 min. PMNs were resuspended in Gey's buffer, exposed to the IL1 and TNF at 300 ng/ml and 0.5 ng/ml concentrations, and incubate for 30 min. at 10(6) cell/ml. Results indicate that IL1 and TNF alone have little or no effect on human neutrophils to synthesize TxA2, 6-KETO-PGF1 alpha and PGE2 production. This effect was completely inhibited by two non-steroidal anti-inflammatory drugs (i.e. indomethacin and proglumetacin).
Lipoxin A (LXA) is a novel eicosanoid, generated by the interactions of lipoxygenases, which has a variety of biological actions. When added to human polymorphonuclear leukocytes, LXA stimulated thromboxane formation which was monitored as TxB2 by radioimmunoassay. The compound augmented the formation of TxA2 stimulated by the ionophore of divalent cations (A23187). Formation of thromboxane was inhibited by two non-steroidal anti-inflammatory drugs (i.e. indomethacin and proglumetacin). Results of the present study indicate that LXA can provoke the release and transformation of endogenous arachidonic acid to thromboxane. Moreover, they suggest a relationship between lipoxin A and the formation of cyclooxygenase pathway products.
Peritoneal rat macrophages incubated with human recombinant tumour necrosis factor (hrTNF alpha) released 2-3 times more thromboxane (TxB2) than untreated macrophage controls, a result similar to that obtained by incubating them with endotoxin (ET) or calcium ionophore A23187.
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Macrophages (M phi) and polymorphonuclear leukocytes (PMNs) are cell types that interact with bacterial endotoxin and play key roles in mediating the inflammatory reaction. We examined the ability of rat peritoneal macrophages and human PMNs to synthesize thromboxane A2 (detected as TxB2) in response to human recombinant interleukin 1 (hrIL1). TxB2 levels were measured by radioimmunoassay in the cell-free supernatant of cell suspensions after 1 hr incubation at 37 degrees C. TxB2 release by both PMNs and M phis was increased in a dose-dependent manner by hrIL1.
The DNA synthesis of lymphocytes triggered by phytohemagglutinin or phorbol-myristate-acetate is strongly reduced by the externally applied electromagnetic field (ELF). Ca2+ uptake by stimulated lymphocytes is also reduced by ELF. The effect appears to be synergistic with that of the well-known calcium blocker agent, verapamil.
The present study involves the determination of the effect of supernatants obtained from mitogen-induced lymphocytes of human tonsils and containing lymphotoxins on human peripheral blood polymorphonuclear leukocytes (PMNs). PMNs treated with supernatants from phytohemagglutinin-stimulated lymphocytes were found to increase the release of thromboxane B2, compared to normal control levels. This increase was blocked by the preincubation of PMNs with indomethacin. The production or increase in production of thromboxanes may be induced by lymphotoxins since these substances have been reported to activate phospholipase A2 in target cell membranes, which may result in release of the thromboxane precursor, arachidonic acid.
PMN's were cultivated in vitro and treated with supernatants obtained from mitogenic-induced lymphocytes of human tonsil. Cytoplasmic vacuolization increased with time and there was a lower number of neutrophilic clumps in the culture treated with a supernatant containing lymphotoxin. In addition, the PMN's released more thromboxane B2 which was inhibited by indomethacin. We conclude that the action of lymphotoxin on the target PMN's is not mediated by the production of thromboxane B2.
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Polymorphonuclear leukocytes (PMN) are capable to produce prostaglandins in vivo and in vitro, and thromboxane B2 (TXB2) which is the main metabolite of arachidonic acid in these cells. In the present work we studied, with radioimmunoassay method, the effect of calcium ionophore A23187 on PMN. This substance is capable to stimulate TXB2 release by PMN and its effect is inhibited by indomethacin.
Blastogenesis of human peripheral blood lymphocytes stimulated in vitro by non-specific mitogens (PHA, ConA, PWM) upon exposure to extremely low frequency EMF has been studied. Different frequencies of square waveforms have been used. PHA-stimulation resulted in strong inhibitions as measured by [3H]thymidine incorporation. A frequency window (3-50 Hz) within which ConA-induced blastogenesis was significantly inhibited has been individuated. The mitogenic effect of PWM was significantly affected only at 3 Hz.