摘要:

AbstractPrevious findings have shown that lipopolysaccharide (LPS)-activated human monocytes express cytokines (CKs) on their membrane. Furthermore, those associated to membrane products such as tumor necrosis factor (TNF)-αand interleukin (IL)-1 have been demonstrated to exert many biological activities. In this paper, evidence is provided that human polymorphonuclear cells (PMN) exhibited an increased phagocytic capacity following incubation with either lipid A (LA)-activated autologous monocytes or supernatants recovered from LA-stimulated mononuclear cell cultures. In order to investigate the possible role of monocyte membrane-associated TNF-α, IL-1αand IL-1βin the modulation of PMN activity, in a separate series of experiments LA-activated monocytes or LA-activated supernatants were pretreated with anti-recombinant human (Rhu) TNFα, anti-Rhu IL-1αand anti-Rhu IL-1βmonoclonal antibodies (MoAbs), respectively. Such an approach gave rise to an abrogation of monocyte-mediated triggering effect on PMN functional capacity.Taken together, these data suggest that activated monocytes can upregulate PMN phagocytosis by a cell-to-cell contact mechanism, likely related to membrane-associated CKs.

ISSN:0892-3973    

DOI:10.3109/08923979209005398

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effects of acute and chronic zidovudine (AZT) administration on immunologic test responses of mice were studied. The effects of AZT administration combined with morphine or methadone treatment, were also studied separately comparing the effects of each drug.We noted that AZT-treatment did not modify the T-lymphocyte subsets (L3T4/LyT2rate), whereas morphine-treatment and AZT plus morphine treatment decreased the percentage of T helper cells.Acute and chronic AZT-treatment increased Natural Killer cell (NK) activity and also recovered the decreased NK cell activity produced by morphine-treatment.AZT-treatment, morphine-treatment, AZT plus morphine treatment and AZT plus methadone treatment strongly depressed the phagocytic physiological activity of Polymorphonuclear leukocytes (PMNs).Another evidence of immunologic responsiveness against AZT was the reduction of the mitogenic and antigenic response of lymphocytes.These results suggest a negative role of AZT-treatment especially on phagocytic activity and confirms a depressive effect of morphine-treatment on several immune functions studied. Furthermore, there is no indication of additive or synergistic toxic effects of AZT, morphine and methadone on the immune functions above that seen with each of these drugs when tested alone.

ISSN:0892-3973    

DOI:10.3109/08923979209005399

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractABSTRCTSEffects of Bu-Zhong-Yi-Qi-Tang (Japanese name : Hochu-ekki-to) on the resistance againstListeria monocytogeneswere observed in ICR mice orally administered this medicine daily for 10 days. Survival rates were increased by the pretreatment in mice inoculated i.v. with bacteria 1 day after the last administration and in mice inoculated i.p. 4 days after the last administration. After an i.v. inoculation ofL. monocytogenes, the numbers of bacteria in the spleen and liver increased gradually to kill mice by day 5 in untreated group but the bacterial numbers increased slightly by day 3 and decreased from day 3 to day 8 in Hochu-ekki-to pretreated group. After an i.p. inoculation, the number of bacteria in the peritoneal cavity decreased very rapidly within 6h in Hochu-ekki-to treated group compared to that in untreated group. After the administration, number of polymorphonuclear cells increased in the peripheral blood, peritoneal cavity and spleen. In treated mice, macrophages increased in number in the peritoneal cavity and the spleen but decreased in the peripheral blood. Peritoneal macrophages from treated mice showed an enhanced activity to killL. monocytogenes in vitrowithin 60 min after ingestion of bacteria. Hochu-ekki-to may augment the host defense againstL. monocytogenesthrough the activation of macrophage series during an early phase of infection.

ISSN:0892-3973    

DOI:10.3109/08923979209005400

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effects of oral administration of antitumor polysaccharide SPR-901 (RBS), anα-1,3 branchedα-1,6 glucan, on concanavalin A (Con A)-induced interleukin 2 (IL-2) production of splenocytes were studied. The augmentation effect on Con A-induced IL-2 production was evident when more than 30 mg/kg of SPR-901 was administered orally to mice. On the other hand, oral administration of B512 dextran, an analogousα-1,6 glucan, did not show any augmentation effects on IL-2 production. The augmentation effect of SPR-901 on IL-2 production seemed to be mediated mainly by macrophages stimulated with SPR-901.

ISSN:0892-3973    

DOI:10.3109/08923979209005401

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractSeveral studies outline the imbalance of phagocyte functions in chronic obstructive pulmonary disease (COPD). In this regard, here, we have assessed either monocyte- and polymorphonuclear cell (PMN)-mediated chemotactic, phagocytic and killing capacities or PMN-triggered metabolic pathway in a group of COPD patients before and at different times after thymostimulin administration. Before therapy, an increase of O2-generation and a decrease of myeloperoxidase release were found in these individuals when compared to controls. Moreover, a reduction of either PMN-mediated chemotaxis and killing or monocyte chemotactic capacities was observed. By contrast, no differences were seen in terms of p-glucuronidase release, monocyte-mediated killing and PMN or monocyte phagocytic function. During a one-year monitoring following immunotherapy, O2- production and myeloperoxidase activity fell within normal values, while phagocyte functional capacities were unaffected by such a treatment. Furthermore, COPD subjects exhibited a significant improvement of their clinical status as assessed during a one-year follow-up.All together, these findings suggest a potential role for thymostimulin in the treatment of COPD patients.

ISSN:0892-3973    

DOI:10.3109/08923979209005402

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractStudies were carried out on the ability of some anesthetic agents (Propofol, Dormicum, Ketalar and Penthotal) to induce the release of cytokines by human monocytes and lymphocytes in vitro. All anesthetic agents tested at hematic concentrations reached during anesthetic administration cause an increase in the production of Tumor necrosis factor (TNF) from human monocytes; the increase is 4–5 times greater than controls. The greatest Interleukin - 1α(IL-1α) production increase was induced by Propofol. The release of Interleukin -6 (IL–6) is notably increased by Ketalar (about 10 times greater than controls). In the presence of different anesthetic agents, human lymphocytes release Interleukin -4 (IL-4) and Interferonγ- (IFN-γ). Penthotal and Ketalar increase IL-4 production which appears quite high compared to that obtained with Con A used as standard challenge. Propofol induce IL-4 release which is about the same as that seen with Con A. IFN-γis released in high quantities by lymphocytes treated with Propofol. Dormicum, Ketalar and Penthotal induce non-significant increase of IFN-γrelease. The results concern the choice of anesthetic, in relation to its action on host immune response. This aspect is particularly interesting in immunocompromised host.

ISSN:0892-3973    

DOI:10.3109/08923979209005403

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractSerum tumor necrosis factor (TNF) levels in 33 patients with inflammatory bowel disease (IBD) were measured by using a sensitive enzyme immunoassay. Four of five Crohn's diseases (CD) and nine of twenty eight ulcerative colitis (UC) had elevated levels of serum TNF. In active CD or UC, a greater fraction of patients studied had significantly increased serum TNF levels (3/3 for CD and 8/11 for UC). Production of TNF by peripheral blood monocytes when stimulated by lipopolysaccharide was also increased in these patients and correlated with their serum TNF levels. These rusults suggest that TNF may have some pathoetiological meaning in IBD.

ISSN:0892-3973    

DOI:10.3109/08923979209005404

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractVery little is known regarding the effects of nicotine, the most pharmacologically active component of tobacco products, on T lymphocyte activity or interleukin production. Therefore, rats were implanted subcutaneously with osmotic mini-pumps containing either physiological saline, nicotine (1.5 mg/kg/day) or a high dose of nicotine (4.5 mg/kg/day) for a period of 14 days. The ability of the splenic T lymphocytes to respond to the polyclonal T lymphocyte mitogens, Concanavalin A (ConA) or phytohemagglutinin (PHA), and the ability of mitogen stimulated splenic T lymphocytes to produce interleukin 2 (IL2) were determined. Treatment with nicotine suppressed, in a dose dependent fashion, the ability of splenic T lymphocytes to respond to mitogen, but dramatically enhanced the ability of mitogen stimulated lymphocytes to generate IL2.

ISSN:0892-3973    

DOI:10.3109/08923979209005405

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractWe examined the effect of famotidine, a histamine-type 2 receptor antagonist, on the immunocompetent cells. The number of DR(+)cells were significantly decreased in patients with systemic lupus erythematosus (P<0.05) by parenteral administration of famotidine (40 mg/days for 4 weeks). However, total lymphocyte number and monocyte number did not change. Immunoglobulin levels of patients with rheumatoid arthritis and normal male did not change. Furthermore, phytohemmaggulutinin induced lymphocyte proliferation was increased by addition of famotidine (10 ng/ml). Nonetheless, famotidine did not have raitogenic function itself to lymphocyte and did not affect IL-2 product ion.

ISSN:0892-3973    

DOI:10.3109/08923979209005406

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractNeoplastic Jurkat cells were submitted to a PHA stimulation test after a preincubation in maternal or nulliparous serum (10% dilution). The Il2R expression was significantly downregulated among maternal serum treated cells.Retroplacental serum was significantly more inhibitive than peripheral maternal serum (P<0,01). The maternal IgG fractions and mostly the retroplacental IgG fraction proved to contain a factor mainly responsible for the I12R expression inhibitive property.The molecular mechanism of this phenomenon was further studied. It was shown that H7 (acting as a protein kinase inhibitor) could not influence the Il2R modulation. E.G.T.A., a calcium chelator, was not able to interfere with the inhibitive influence of maternal serum. It was suggested that the maternal serum mediated inhibition of the IL2R expression is not influenced by the hydrolysis of membrane bound phosphatidyl inositol.In contrast, pertussis toxin markedly enhanced, in a dose dependent way, the suppressive influence of maternal serum as compared to nulliparous serum. At low concentrations, pertussis toxin lost its stimulating property and retained its ability to ADP ribosylate the alpha subunit of G proteins inducing a release of adenyl-cyclase mediating cAMP synthesis.This mechanism has been further studied by the addition of dbc AMP or dbc GMP to Jurkat cells preparations stimulated by PHA. dbc AMP, in a dose-related way, induced a downregulation of the IL2R expression of stimulated neoplastic cells preincubated in nulliparous or maternal serum, dbc GMP did not influence the IL2R expression in the same experimental conditions. The maternal serum mediated cells showed the most pronounced IL2R inhibition. Finally, it was shown that the cAMP synthesis by PHA stimulated Jurkat cells was upregulated in a dose dependent way, after a previous cellular incubation in progressive concentrations of maternal serum. In contrast, among nulliparous serum pretreated cells, cAMP synthesis remained significantly lower, after a lectin stimulation, as compared to the cAMP production derived from retroplacental serum treated and stimulated cells.Taken together, these experiments suggest that the maternal serum dependent suppression of the IL2R expression is related to a protein G stimulation followed by an enhanced cAMP synthesis.

ISSN:0892-3973    

DOI:10.3109/08923979209005407

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor