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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have demonstrated that hepatic dysfunction, induced by experimental biliary ligation (EBL), impairs lymphocytic responsiveness to PHA stimulation in vitro and to cellular antigens in vivo. This suppression appears to be selective for T-cell mechanisms while B-cell-mediated functions remain intact. The purpose of this study was to determine whether coexisting hepatic insufficiency could exert a protective effect on vascularized or nonvascularized allograft survival in the transplanted recipient. Female Wistar-Furth (Rtlw) 225 g rats were assigned randomly to three groups: EBL, sham operation (Sham) and normal control (NC). Fourteen days following operation animals received heterotopic cardiac or skin allografts from Buffalo (Rtlb) donors. Cardiac and skin graft survival was determined daily, rejection was confirmed histologically, and technical failures were omitted from analysis. Allograft survival was expressed as median survival time +/- SEM. Serum total bilirubin (mean +/- SEM) was significantly elevated at Day 14 in EBL animals compared to Sham and NC groups (15.1 +/- 1.0 vs 0.1 +/- 0 and 0.2 +/- 0.1 mg/dl, respectively, P less than 0.01). Median cardiac allograft survival time by Probit was 10.6 +/- 2.6 vs 5.6 +/- 0.7 and 6.0 +/- 0.9 days, respectively (P less than 0.03). Skin graft survival (mean and range) was similar in all groups. These results demonstrate that EBL in the rat suppresses T-cell function and significantly prolongs vascularized allograft survival, but not skin allograft survival across the Rtl histocompatibility barrier. The mechanism whereby coexisting hepatic dysfunction exerts a protective effect on vascularized allograft survival warrants further investigation.
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PMID:The protective effect of hepatic dysfunction on vascularized allograft survival. 329 86

Using human thymocytes and autologous thymic epithelial (TE) cells grown in vitro in long-term culture, we have found TE cells can function as accessory cells for mitogen-induced mature thymocyte activation. Tritiated thymidine incorporation, blast formation, and protein synthesis were all induced in accessory cell-depleted thymocytes by autologous TE cells in the presence of suboptimal concentrations of PHA. After 3 days of mitogen stimulation of thymocyte-TE cell cocultures in vitro, thymocyte blasts bound to TE cells and 77 +/- 4% (mean +/- SEM) of TE cells acquired expression of major histocompatibility complex (MHC) class II (DR) antigen. TE accessory cell function for thymocyte activation was dependent on the number of TE cells added to thymocyte cultures, was not dependent on TE cell division, but did require TE cell protein synthesis. In thymocyte separation experiments, the predominant cell type responding to PHA in the presence of TE cells was T6- mature (stage III) thymocytes. Thus, human TE cells are capable of providing signals that lead to mature thymocyte activation.
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PMID:Human thymic epithelial cells function as accessory cells for autologous mature thymocyte activation. 349 29

Peripheral blood from asplenic trauma patients (ASP) was analyzed for immunoglobulin concentrations, complement levels, T- and B-lymphocyte populations, and mitogen response of T cells, and compared to a similar analysis performed on the blood of normal controls (C). The interval from splenectomy to testing averaged 1,471 +/- 193 days (mean +/- SEM) in the ASP. Total lymphocyte count averaged 2,941 +/- 234 in the ASP with a T-cell count of 2,030 +/- 182 and a B cell count of 351 +/- 58. The average control lymphocyte count of 1,769 +/- 147 was significantly less than ASP (p less than 0.001) as were the T-cell count of 1,328 +/- 107 (p less than 0.005) and the B-cell count of 124 +/- 18 (p less than 0.001). Responses to PHA were diminished in ASP lymphocytes by 38% at 3 days (p less than 0.01) and by 49% at 5 days (p less than 0.001) when compared to C. Levels of IgM were significantly decreased (p = 0.05) in ASP. Levels of C3, C4, and C5 were similar in ASP and C. These data demonstrate persistent abnormalities in immune function in adult ASP without underlying lymphoreticular disorders and suggest a possible explanation for the increased septic risk in this patient group.
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PMID:Long-term depressed immune function in patients splenectomized for trauma. 349 65

TGF-beta 1 is known to modulate lymphocyte activation affecting cell proliferation and the production of cytokines and Igs. Little is known about the characteristics of T cells grown in the presence of TGF-beta 1. We have stimulated human T cells with PHA in the presence of TGF-beta 1 under serum-free conditions for 7 days and characterized the resulting cell population. TGF-beta 1 (0.0032 to 10 ng/ml) affected neither [3H]thymidine incorporation (day 4) nor cell yield (day 7) in these cultures. However, cells activated in the presence of TGF-beta 1 proliferated vigorously in secondary cultures and produced highly elevated amounts of IL-2 (12 +/- 3-fold enhancement of IL-2 production in response to CD2 plus CD28 stimulation compared with control cells, mean +/- SEM; n = 10). The enhancing effects of TGF-beta 1 were demonstrable over a wide range of concentrations (0.4 to 10 ng/ml). The increased IL-2 protein production was paralleled by a dramatic up-regulation of IL-2 mRNA. In addition, cells precultured with TGF-beta 1 responded with enhanced cluster formation in the secondary cultures. With regard to their phenotype, we observed an increased expression of the alpha E beta 7-integrin human mucosal lymphocyte-1 and of the CD2-restricted epitope CD2R, whereas the expression of CD11a was slightly decreased. In contrast, TGF-beta 1 did not influence the constitutive or activation-induced expression of CD4, CD8, CD45RA, CD45RO, CD25, CD71, CD54, CD58, CD59, and B7. We conclude that TGF-beta 1 supports the generation of human effector cells with a strongly enhanced capacity to respond to subsequent restimulation.
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PMID:TGF-beta 1 is a potent inducer of human effector T cells. 796 15

Transplantation of cellular components of the permissive peripheral nerve environment in some types of spinal cord injury holds great promise to support regrowth of axons through the site of injury. In the present study, Schwann cell grafts were positioned between transected stumps of adult rat thoracic spinal cord to test their efficacy to serve as bridges for axonal regeneration. Schwann cells were purified in culture from adult rat sciatic nerve, suspended in Matrigel: DMEM (30:70), and drawn into polymeric guidance channels 8 mm long at a density of 120 x 10(6) cells ml-1. Adult Fischer rat spinal cords were transected at the T8 cord level and the next caudal segment was removed. Each cut stump was inserted 1 mm into the channel. One month later, a bridge between the severed stumps had been formed, as determined by the gross and histological appearance and the ingrowth of propriospinal axons from both stumps. Propriospinal neurons (mean, 1064 +/- 145 SEM) situated as far away as levels C3 and S4 were labelled by retrograde tracing with Fast Blue injected into the bridge. Near the bridge midpoint there was a mean of 1990 +/- 594 myelinated axons and eight times as many nonmyelinated, ensheathed axons. Essentially no myelinated or unmyelinated axons were observed in control Matrigel-only grafts. Brainstem neurons were not retrogradely labelled from the graft, consistent with growth of immunoreactive serotonergic and noradrenergic axons only a short distance into the rostral end of the graft, not far enough to reach the tracer placed at the graft midpoint. Anterograde tracing with PHA-L introduced rostral to the graft demonstrated that axons extended the length of the graft but essentially did not leave the graft. This study demonstrates that Schwann cell grafts serve as bridges that support (1) regrowth of both ascending and descending axons across a gap in the adult rat spinal cord and (2) limited regrowth of serotonergic and noradrenergic fibers from the rostral stump. Regrowth of monoaminergic fibres into grafts was not seen in an earlier study of similar grafts placed inside distally capped rather than open-ended channels. Additional intervention will be required to foster growth of the regenerated axons from the graft into the distal cord tissue.
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PMID:Bridging Schwann cell transplants promote axonal regeneration from both the rostral and caudal stumps of transected adult rat spinal cord. 915 24

We evaluated the levels of inositolmono-(IP1), di(IP2), tri-(IP3) and tetraphosphates (IP4) in human neutrophils (N) stimulated with gamma interferon (IFN-gamma) (200 microliters from a pool of cell culture supernatant obtained from 1 x 10(7) PHA-primed peripheral blood mononuclear cells (30-60 min at 37 degrees C, 5% CO2)) in the presence of in the absence of interleukin 10 (IL-10) (10 micrograms/10 microliters). The results, reported as mean +/- SEM cpm, showed that IFN-gamma induced a significant increase only in the IP3 level (N + medium = 1,413 +/- 172 and N + IFN-gamma = 8,875 +/- 832). However, this activation mediated by IFN-gamma was blocked partially in the presence of IL-10 (N + IFN-gamma + IL-10 = 2,430 +/- 239) (P < 0.05). Interleukin 10 alone did not induce significant alterations in the content of IP1 (1,203 +/- 123), IP2 (1,880 +/- 163), IP3 (938 +/- 102) or IP4 (2,403 +/- 345) when compared to the respective controls in the absence of IL-10 (IP1 = 1,625 +/- 132; IP2 = 1,343 +/- 149; P3 = 1,413 +/- 172 and IP4 = 3,281 +/- 234). We also demonstrated the inhibitory effect of IL-10 of chemoluminescence generation by human neutrophils during phagocytosis of opsonized particles (OZ). Chemoluminescence generation was enhanced by IFN-gamma (N = OZ = 42.8 +/- 3.9 and N + OZ + IFN-gamma = 66.5 +/- 4.3) and this effect was reduced by IL-10 (N + OZ + IFN-gamma + IL-10 = 37.6 +/- 5.1). These data suggest that IL-10 modulates the neutrophil response and may be important for the development of new treatments of inflammatory injury.
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PMID:Effect of gamma interferon and interleukin 10 on phosphoinositol turnover by human neutrophils in vitro. 918 Nov 14

To investigate the effect of ex vivo hyperthermia (HT) and 137Cs-irradiation on micronucleus (MN) production in cytokinesis-blocked lymphocytes, we obtained the peripheral blood samples from the same cancer patients (n=6) before and during fractionated partial-body radiotherapy (xRT). The whole blood cultures were heated at 43.5 degrees C for 60 min, followed by 137Cs irradiation (0-4 Gy). The control cultures from the same patients were incubated at 37 degreesC after being exposed to radiation. The lymphocytes were then stimulated with PHA. Cytochalasin B was applied at 44 h, and lymphocytes were harvested at 72 h. MN frequency was determined on Giemsa-stained slides. We found that in patients before xRT, HT (43.5 degrees C) significantly increased the MN yield (mean+/-SEM) in unirradiated lymphocytes from 15.6+/-2.8 (37 degrees C) to 39.7+/-10.9. Further, in patients either before or during xRT, when the lymphocytes were treated with HT (43.5 degrees C) and combined with ex vivo irradiation, the MN yield (Y) could be estimated by a linear equation Y=C+alphaD. Our findings indicate that as measured by the MN production in cytokinesis-blocked lymphocytes, HT alone at 43.5 degrees C++ induced DNA damage. Moreover, it enhanced the radiation-induced cytogenetic damage. Therefore, the application of HT may impair the T-cell function in cancer patients who are receiving radiotherapy. 1998 Elsevier Science B.V.
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PMID:Effect of ex vivo hyperthermia on radiation-induced micronuclei in lymphocytes of cancer patients before and during radiotherapy. 972 37

The delta opioid receptors (DORs) modulate T cell proliferation, IL-2 production, chemotaxis, and intracellular signaling. Moreover, in DOR-transfected Jurkat cells, delta opioids have been shown to suppress HIV-1 p24 Ag expression. These observations led us to characterize the expression of DORs by human peripheral blood T cells and to determine whether a specific DOR agonist, benzamide,4-([2,5-dimethyl-4-(2-propenyl)-1-piperazinyl](3-methoxyphenyl)methyl]-N,-,(2S[1(S*),2alpha,5beta])-(9Cl) (SNC-80), can suppress p24 Ag expression by HIV-1-infected CD4+ T cells obtained from normal donors. By immunofluorescence flow cytometry, PHA stimulated the expression of DOR from 1.94 +/- 0.70 (mean +/- SEM) to 20.70 +/- 1.88% of the PBMC population by 48 h (p < 0.0001). DOR expression was approximately 40% of both the PHA-stimulated CD4+ and CD8+ T cell subsets, and virtually all DORs were found on these subsets. To determine whether activated DORs suppress HIV-1 expression, PBMC were prestimulated with PHA, and then CD4+ T cells were purified, pretreated with SNC-80, and infected with HIV-1. In a concentration-dependent manner, SNC-80 inhibited production of p24 Ag. SNC-80 10(-10) M maximally suppressed (approximately 50%) both lymphocytotropic (HIV-1 MN) and monocytotropic (SF162) strains; higher concentrations were less effective. Naltrindole, a selective DOR antagonist, abolished the inhibitory effects of SNC-80. Kinetic studies indicated that 24-h pre- or postincubation with SNC-80, relative to infection with HIV-1, eliminated its suppressive effects. Thus, stimulating the DORs expressed by activated CD4+ T cells significantly suppressed the expression of HIV-1. These findings suggest that opioid immunomodulation directed at host T cells may be adjunctive to standard antiviral approaches to HIV-1 infection.
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PMID:Immunofluorescence detection of delta opioid receptors (DOR) on human peripheral blood CD4+ T cells and DOR-dependent suppression of HIV-1 expression. 1144 Nov 21

Bovine seminal-ribonuclease (BS-RNase) is a member of the 'ribonucleases with special biological actions' family since it possesses specific anti-tumour, anti-spermatogenic and embryotoxic activities and exerts an immunosuppressive effect on T lymphocytes. In previous studies it was demonstrated that BS-RNase induced apoptosis in proliferating, malignant and normal cells and that telomerase activity loss also caused apoptotic death in neoplastic cells. Since an obvious relationship between cell proliferation and telomerase activity exists, the aim of this work was to study if the pro-apoptotic cytotoxic action exerted by BS-RNase on proliferating malignant cells (HT29) and proliferating normal cells (PHA-stimulated lymphocytes) could be linked to a possible BS-RNase effect on telomerase activity. In BS-RNase-treated HT29 cells (Na-butyrate-differentiated or not) and human lymphocytes (proliferating or not), we investigated cell vitality (MTT method) and morphology (SEM), BS-RNase localization (immunofluorescence), telomerase activity (TRAP-ELISA method), hTR mRNA expression (RT-PCR), and hTERT levels (western blot). While no BS-RNase effect was detectable on not proliferating cells, a clear relationship was noticed between the diminished number of vital elements of both proliferating cell populations after treatment (48 h and 72 h for HT29 and PHA-stimulated lymphocytes, respectively) with 50 microg/ml BS-RNase and the decrease of their telomerase activity. At the same time, we found that hTR levels, the RNA subunit of telomerase, in proliferation-inhibited BS-RNase-treated cells were diminished. Moreover, by immunofluorescence technique, we detected BS-RNase in the HT29 cell nucleolus after 3-h treatment. Therefore, as hTR has been recently proven to co-fractionate with nucleoli, we hypothesize that a BS-RNase direct action on the telomerase hTR subunit could be a possible mechanism of action by which BS-RNase exerts its pro-apoptotic effects only on proliferating cells.
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PMID:Bovine seminal ribonuclease is cytotoxic for both malignant and normal telomerase-positive cells. 1614 25

A SBR was used in this study for investigating the influence of carbon source on EBPR metabolism and microorganism communities when feeding with acetate and propionate. The SBR was operated with a cycle time of 8 h and each cycle consisted of 4 min feeding, 2 h anaerobic period, 5 h aerobic period, 35 min setting, 15 min decanting and 6 min waiting. The COD of influent was kept at 300 mg/L during the experiment. Acetate and propionate were used as the sole carbon source for operation of 60 days, respectively. The phosphorus release/ COD consumption in the end of anaerobic phase were 0.35 and 0.27 when acetate and propionate were used as the carbon source, respectively. The PHA composition was different when different carbon source was dosed. PHB accounted for 92.6% in the end of anaerobic phase but the value for PHV was only 7.4% when acetate was selected as the carbon source. No PH2MV was detected during this process. The compositions of PHA were PHB (10.2%), PHV (35.8%) and PH2MV (54.0%) in the end of anaerobic cycle when propionate was used as the sole carbon source. There was variation of microorganism communities during this process for the results of DGGE combined with SEM micrographs and PHA staining. Coccus morphotype PAOs were accumulated in acetate-fed phase and rod morphotype PAOs were accumulated in propionate-fed stage. Different PAOs were accumulated and the metabolic pathways were different when different carbon sources were used, but good EBPR could be achieved during all these conditions.
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PMID:[Influence of carbon source on EBPR metabolism and microorganism communities]. 1977 97


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