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E Manfrini

Publications and source records attributed to E Manfrini.

6 recordsLinked to original sources
PubMed1995

Alcohol modulation of human normal T-cell activation, maturation, and migration.

We are interested in the characterization of the effects of alcohol on human T-cell activation, maturation, and migration, because this cell population is crucial in the initiation, regulation, and propagation of cellular immunity. We and others have described the effects of both acute and chronic exposure of human immune cells to ethanol (EtOH) in vitro. Herein, we briefly, review these reports and expand this body of literature with the inclusion of new data recently obtained in our laboratory. We confirm the blunting effects of EtOH on the production of interleukin-2 and mitogen proliferative response following T-cell mitogen stimulation, and on the expression of membrane markers of activation. We show that EtOH significantly alters the expression of the CD4 cell-associated marker of activation, CD26. We report the effect of EtOH on the expression of the homing receptor CD62L by CD4+ cells, and on their ability to adhere by a CD18-mediated process to a defined cellular substratum. Furthermore, we demonstrate the effects of EtOH and EtOH and beta-endorphin pretreatment on the activation of CD4+ lymphocytes endowed with the homing receptor CD62L.

Alcoholic Intoxication↗
PubMed1994

Steroid receptor-mediated modulation of CD4+CD62L+ cell homing. Implications for drug abusers.

Naive human T cells home to peripheral lymph nodes via the leukocyte endothelial cell adhesion molecule-1 (LECAM-1, l-selectin, CD62L, Leu8 antigen) they express. We enriched populations of CD4+CD62L+ cells (attachment of Leu8+ T cells to flasks coated with anti-mouse IgG (AIS); Leu8+ T cells, 82.3% pure (+/- 2.3%), enriched for CD4+ cells by incubation over flasks coated with anti-CD4 antibody--this 3-4-day procedure yields an 88 +/- 1.4% recovery. Cells were treated with dexamethasone in vitro for 24-48 h, and monitored by flow cytometry. We found severe toxicity by this steroid at high concentration (10(-6) M: 35% decrease in CD62L+ T cells, 22% drop specifically in CD4+CD62L+ cells), suggesting the onset of receptor-mediated apoptotic events. The toxicity was dose dependent (5% and 7% drop in CD62L+ T and CD4+CD62L+ cells, respectively, at 10(-9) M, the concentration found in plasma 10 h following the administration of 1 mg dexamethasone). One mg of dexamethasone given to normal subjects leads to a 15-20% decrease in circulating CD4+CD62L+ cells at 10 h. This tends to be correlated with a drop in the number of glucocorticoid cytosolic receptors. Thus, steroids seem to modulate CD4+CD62L+ cell homing by means of receptor-mediated mechanisms.

Adult↗
PubMed1988

Glutamate decarboxylase-immunoreactive neurons and terminals in the periaqueductal gray of the rat.

The periaqueductal gray of 5 rats was processed for immunocytochemistry using an antiserum to glutamate decarboxylase. In both colchicine-pretreated (4 rats) and untreated (1 rat) animals, glutamate decarboxylase-positive cell bodies were present in all periaqueductal gray subdivisions, especially in the dorsal and ventrolateral subdivision. The perikaryal cross-sectional area of labelled neurons was smaller than that of periaqueductal gray projecting neurons retrogradely labelled with horseradish peroxidase in separate experiments. The morphology of glutamate decarboxylase-containing neurons resembled that of small polygonal, triangular and fusiform cells described in previous Golgi studies. Glutamate decarboxylase immunoreactivity was also observed in a large number of terminal-like structures, most of which were distributed close to the somata and dendrites of both glutamate decarboxylate-positive and -negative neurons. At all rostrocaudal levels the highest concentration of these elements was observed around the aqueduct. These results suggest that two sub-populations of neurons are present in the periaqueductal gray of rats, one consisting of small-sized glutamate decarboxylase-positive neurons (intrinsic neurons) and the other of large-sized glutamate decarboxylase-negative neurons (projecting neurons). Intrinsic circuits could be present between glutamate decarboxylase-positive and -negative neurons and between glutamate decarboxylase-positive neurons.

Animals↗
PubMedDate not supplied

Cocaine blunts human CD4+ cell activation.

Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of enriched CD4+ T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections.

Antigens, CD↗