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A Bellocq

Publications and source records attributed to A Bellocq.

25 records · Page 2Linked to original sources
PubMed1996

Regulation of interleukin-10 production by beta-adrenergic agonists.

Catecholamines have been shown to inhibit some aspects of macrophage activation through a beta receptor-dependent mechanism. This study was undertaken to analyze the effects of isoproterenol, a specific beta-adrenergic agonist, on the synthesis of interleukin-10 (IL-10), a major macrophage-deactivating factor. Isoproterenol increased IL-10 release from lipopolysaccharide-(LPS)-activated mouse peritoneal macrophages in a dose-dependent manner. A significant effect was already observed with 1 microM isoproterenol, while a 4.5-fold increase was achieved with 10 microM. This increase was observed only if macrophages were exposed to isoproterenol for at least 2 h before LPS challenge. It was apparent within 0.5 h and persisted through 24 h at all the LPS concentrations used. A similar increase was observed at the IL-10 mRNA level, as judged by enzyme-linked immunosorbent assay-polymerase chain reaction. The macrophage response to isoproterenol that led to cyclic AMP accumulation was markedly inhibited by H-89, a potent inhibitor of protein kinase A. These data suggest the involvement of cyclic AMP in the regulation of IL-10 synthesis by isoproterenol. IL-10 was in turn partly responsible for a reduction in tumor necrosis factor-alpha synthesis. In vivo, the administration of oxprenolol, a beta-receptor antagonist, significantly reduced serum IL-10 levels 90 min after LPS challenge. Thus, the present study provides the first evidence that endogenous catecholamines are of critical importance in determining the magnitude of the IL-10 response in experimental endotoxemia.

Adjuvants, Immunologic↗
PubMed1994

Activation of T cells by previously activated T cells. HLA-unrestricted alternative pathway that modifies their proliferative potential.

When cultured in the presence of previously activated T cells, up to 30% of resting T cells are activated, as indicated by lymphoblastic morphology, formation of cell aggregates, expression of activation Ags (CD25 and HLA-DR), and a proliferative response. This activation occurred in the absence of accessory cells and was not HLA restricted, and the TCR repertoire of the responding cells was extremely diverse without evidence for preferential expansion of T cells expressing certain V beta families or clonal populations. The ability of activated T cells to stimulate resting T cells was a transient phenomenon, which was first detected 24 h after activation and which peaked between 48 and 96 h; the stimulation of previously resting T cells produced more lymphostimulatory activity than restimulation of recently activated cells. Both resting CD4+ and CD8+ T cells expressing TCR-alpha beta and -gamma delta responded to previously activated cells, including cells with both the naive and memory phenotypes. When T cells were activated by this pathway and recultured in the presence of Ag and accessory cells, the strong proliferative response observed at 5 to 7 days with use of fresh T cells was almost entirely absent, and this impaired Ag-induced proliferative response could not be explained by the generation of suppressor cells or the inability of these cells to respond to growth factors. These findings are compatible with the possibility that Ag-specific activation of T cells permits the subsequent Ag-independent activation of other T cells and could explain the broad TCR repertoire and impaired Ag-induced proliferation of activated T cells at sites of immune reactions.

Adult↗
PubMed1994

T cell receptor repertoire of T lymphocytes recovered from the lung and blood of patients with sarcoidosis.

We evaluated the repertoire of V beta segments used in forming the T-cell receptor of lavage and blood T lymphocytes from 11 sarcoid patients and 10 normal subjects using procedures based on quantitative polymerase chain reaction, permitting analysis of both the abundance of transcripts using each of 20 different V beta families and the diversity of the VDJC beta rearrangements within each V beta family. Blood and lung T cells from sarcoid patients had a very diverse V beta repertoire. For all V beta families but one, the abundance of the V beta transcripts fell within the mean +/- 2 SD of that observed for normal blood lymphocytes; no difference in the overall abundance was observed comparing lavage and blood T cells, and the length of VDJC beta rearrangements for a given V beta family in samples from sarcoid patients was usually quite heterogeneous. Despite the overall polyclonality, evidence for selective expansion of T cells was found, in that an increased abundance of V beta 19 transcripts was observed for sarcoid blood and/or lung T cells in eight out of 11 patients studied, and rearrangements of a single predominant length using certain (e.g., V beta 19, V beta 14), but not all, V beta families were present. Sequencing confirmed the presence of a single predominant VDJC beta rearrangement in these cases. These findings suggest that the alveolitis in sarcoidosis results from two distinct processes, a local clonal expansion of T cells associated with an apparently nonspecific accumulation of T cells with an extremely diverse V beta repertoire.

Adult↗
PubMed1993

[Pulmonary hypertension: a rare complication of hepatic cirrhosis].

Pulmonary hypertension is a rare pulmonary complication of chronic hepatic diseases. Anatomopathologic and clinic data are very similar to primary pulmonary hypertension. Although the lesions of arteriopathy are more related to portal hypertension than to hepatic lesions, the physiopathology of this morbid association is unknown.

Dyspnea↗
PubMedDate not supplied

Growth hormone and somatostatin in glomerular injury.

Among other neuropeptides and neurohormones, growth hormone (GH) and somatostatin (SRIF) have been shown to modulate the development of glomerular injury in various renal diseases. In particular, GH is implicated in the induction of glomerular hypertrophy and sclerosis in partial nephrectomy and diabetic nephropathy. While GH effects on glomerular hypertrophy are likely mediated by insulin-like growth factor I (IGF-I), GH effects on glomerular sclerosis are independent of IGF-I. Those effects rather require multiple signaling pathways functioning in series, e.g. angiotensin II binding preceding transforming growth factor beta (TGF-beta) release, or pro-inflammatory factor release preceding repair/scarring processes. In contrast with GH, SRIF administration prevents the development of glomerular lesions in experimental diabetes, partial nephrectomy and immune glomerulonephritis. Inhibitory effects of SRIF on glomerular hypotrophy may be through a decrease in GH secretion and/or IGF-I expression or through a direct blockade of glomerular cell proliferation. The mechanisms underlying the anti-inflammatory effects of SRIF are most likely a deactivation of inflammatory cells related in part to an upregulated response of these cells to glucocorticoids. Additional studies will be required to further define the role of GH and SRIF in the development of glomerular injury and, hence, to identify new targets for a therapeutic approach in glomerular diseases.

Diabetic Nephropathies↗