Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human blood monocytes isolated by centrifugal elutriation from healthy donors were tested for ability to produce membrane-associated IL-1 in response to activation stimuli such as various types of interferons (alpha, beta and gamma) and/or synthetic des-methyl muramyl dipeptide (norMDP). When monocytes were treated with norMDP or lipopolysaccharide (LPS) for 16 hr, they released IL-1 into their culture supernatant. When these activated monocytes were fixed with paraformaldehyde (PFA), they stimulated blastogenic responses of C3H/HeJ mouse thymocytes to PHA, suggesting that membrane-associated IL-1 could be induced by norMDP or LPS. Membrane-associated IL-1 was also found to be induced by the synergistic actions of suboptimal concentrations of rIFN-gamma and nor MDP, but not of rIFN-alpha A or rIFN-beta with norMDP. A specific anti-IL-1 alpha antiserum completely inhibited membrane-associated IL-1 activity, but did not affect the thymocyte-stimulating activity of fixed monocytes. IL-1 alpha was detected by fluorescence staining using the anti-IL-1 alpha antiserum on monocytes fixed after gamma IFN-gamma and norMDP. These results suggest that IFN-gamma may be important in expression of membrane-bound IL-1 alpha by the human blood monocytes responsible for regulation of immune responses in vivo.
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PMID:Induction of membrane-associated interleukin 1 alpha (IL-1 alpha) by synergistic activation of human blood monocytes with interferon gamma and muramyl dipeptide analog. 248 23

The role of the monocyte in human cytomegalovirus (HCMV)-induced immunosuppression was examined by assessing the ability of the virus to directly suppress various monocyte accessory cell functions. Both patient-derived and laboratory-adapted strains of HCMV were capable of impairing antigen-presenting functions of purified human monocytes. In seven of 12 virus-infected samples, there was a significant decrease (P less than 0.05) in the ability of HCMV-infected monocytes to present tetanus toxoid to autologous lymphocytes compared with mock-infected controls; similar results were obtained with Candida albicans and mumps. In contrast, the response to PHA was impaired in only one of eight HCMV-infected samples. The increased expression of MHC class II Ia antigens (HLA-DQ and HLA-DR) by monocytes after stimulation by interferon-gamma was impaired in approximately one-third of the 43 virus-infected samples tested. Interleukin-1 (IL-1) production after incubation with the stimulating antigens, however, was unaffected. Attempts to augment immuno-suppression by co-stimulation of monocytes with lipopolysaccharide (LPS), heat-killed Escherichia coli or Listeria monocytogenes were not successful; however, dramatically increased levels of immunosuppression was obtained with HCMV preparations containing mycoplasma. Thus, although HCMV is capable of directly perturbing monocyte accessory cell functions, the variability and partial suppression observed suggests that infection of monocytes by HCMV alone is not sufficient to produce the levels of immune hyporesponsiveness observed in HCMV-infected patients.
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PMID:Suppression of monocyte functions by human cytomegalovirus. 253 90

The results of cytogenetic studies are reported in 89 patients with B-cell CLL. LPS (E. coli lipopolysaccharide), PWM (pokeweed mitogen), PHA (phytohaemagglutinin), EBV (Epstein-Barr virus), TPA (phorbol 12-myristate 13-acetate), and LA (leucoagglutinin) were used as mitogens. Mitoses were obtained from 78 cases. Clonal aberrations could be demonstrated in 26 cases. Trisomy 12 was the most frequent finding (8 cases) and was sole abnormality in 4 cases. Chromosomes #14, #17, and #11 were involved in structural aberrations in 5, 7, and 7 cases respectively, but a t(11;14)(q13;q32) was the only structural aberration seen more than once. The median observation time was 47 months (range 1-87). The presence of clonal abnormalities did not influence survival significantly, either when calculated from diagnosis or from cytogenetic analysis. Patients with more than one aberration, however, had a significantly shorter survival than patients with normal mitoses only (p less than 0.05). The survival of 8 patients with trisomy 12 (in 4 as sole abnormality) was not different from that of patients with normal mitoses only.
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PMID:B-cell chronic lymphocytic leukaemia: clonal chromosome abnormalities and prognosis in 89 cases. 261 12

It is well documented that endotoxin can have immunosuppressive effects on lymphocytes and induce the production and secretion of monokines which act on the lymphocytes. To delineate the interaction between macrophages and lymphocytes more clearly, 0.15 mg of lipopolysaccharide (LPS) (E. coli 0111:B4) was injected into Hartley guinea pigs intraperitoneally twice a day for 7 days (saline for control group). Seven days after the last injection, spleens were taken and lymphocyte proliferation was determined in the presence and absence of macrophages. When macrophages were present, there was a significant suppression of lymphocyte proliferation when PHA and PWM were used as mitogens. There was no suppression of proliferation when the macrophages were removed. Splenic macrophages were also cultured in the presence and absence of LPS and their supernatants analyzed for PGE2 and TXB2. There was no significant difference between the endotoxin and control groups for PGE2 or TXB2 production in the presence and absence of LPS. However, the endotoxin group had significant decreases in serum levels of C3 postinjection of endotoxin which could indicate C3 degradation by LPS. Taken together these results give further evidence that macrophage products in addition to PGE2 can inhibit lymphocyte proliferation. C3 degradation products could possibly stimulate macrophages to produce inhibitors of lymphocyte proliferation or induce suppressor cells.
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PMID:The immunosuppressive effects of the in vivo administration of endotoxin as influenced by macrophages. 266 1

On stimulation with lipopolysaccharide (LPS), normal human macrophages (M phi) and endothelial cells (EC) produced factors which inhibited interleukin 2 (IL-2)-dependent lymphocyte proliferation and PHA plus interleukin 1 (IL-1)-dependent mouse thymocyte proliferation but not IL-1-dependent human fibroblast proliferation, suggesting that they were inhibitors of the IL-2 response. In addition, these factors inhibited the production of IL-2 by normal human peripheral blood mononuclear cells (PBMC). The factors also inhibited PBMC proliferation in response to PHA and concanavalin (Con A) but did not inhibit the proliferation of EC, U937 cells, or Epstein-Barr virus-transformed B cells. On Sephadex G200 gel filtration, the inhibitory factors from both M phi and EC were detected almost entirely in a 130- to 150-kDa fraction, but active material was also detected in a 15- to 20-kDa fraction. On isoelectric chromatofocusing of the 130- to 150-kDa fraction, inhibitory activity was associated with fractions eluted at three isoelectric points, pH 7.0, 5.4, and 4.8. The isoelectric fractions isolated from M phi and EC showed similar patterns of inhibition. When 130- to 150-kDa fractions from Sephadex G200 of the M phi and EC supernatants were treated with an antibody against a macrophage-derived suppressor factor produced by the human monocytic leukemia cell line THP-1, the activity of both fractions was neutralized. The above findings suggest that normal M phi and EC secrete an identical or closely related inhibitor of IL-2 synthesis and IL-2 response, and this inhibitor regulates these IL-2-related functions by a suppressive action on the T lymphocyte.
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PMID:T cell inhibitor secreted by macrophages and endothelial cells. 267 71

A number of mitogens was used in 21 chronic B-lymphocytic leukaemia patients. Thymidine uptake assays were performed to evaluate cell stimulation. Phytohemagglutinin and phorbol-myristate 13 acetate were found to be the most efficient on cell proliferation. Abnormal clones were found 7 times with PMA, 4 times with PHA, twice with pokeweed, but in no case with lipopolysaccharide or proteine-A. The efficiency of PHA as a B-cell activator is likely to be due to T cell mediation.
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PMID:Use of various mitogens and cell stimulation index in 21 patients with chronic lymphocytic leukaemia. 281 75

We studied the function of monocyte-mediated suppression in the proliferative responses of depressed T-cells of patients with advanced lung cancer, with both local (Stage III) and extrapulmonary metastasis (Stage IV). The mononuclear cells of 13 non-treated patients showed a significant drop in proliferation upon stimulation with suboptimum, optimum and supraoptimum doses with regards to normal controls (p less than 0.001). On treating T-cells with indomethacin, lymphoblastic transformation increased in both groups (patients and controls), but was significantly greater in the patient group (p less than 0.001). The lipopolysaccharide (LPS) exerted an inhibitory effect on the suppressor cells of normal individuals, yet failed to do so in the case of patients treated either with or without indomethacin. The stimulation of the patients mononuclear cells with PWM failed to increase proliferation, and was not affected by either indomethacin of LPS. Our conclusions are as follows: Patients with lung cancer present a drop in mononuclear cell proliferation when stimulated with PHA; This phenomenon may be due to an exacerbation of the immune systems suppressor function; One of the suppressor mechanisms is prostaglandin-dependent and mediated by monocytes; The B-cells have no relevant functions.
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PMID:Mechanism of suppression of the depressed lymphocyte response in lung cancer patients. 293 Oct 10

A study was made of the nature of secondary immuno-deficiency, peculiarities of disordered function of regulatory T-lymphocytes (helpers and suppressors), and their interrelationships in different clinical variants of chronic glomerulonephritis (CGN). Altogether 94 CGN patients were examined, of them 34 were with urinary syndrome and 60 with nephrotic syndrome. With relation to a clinical variant of disease the absolute amount of T-lymphocytes was significantly lowered, the amount and function of B-lymphocytes showed a tendency to an increase. Function of nonspecific Concanavalin A-induced T-suppressors using PHA as a mitogenic indicator (T-T-suppression) was insignificantly raised, and when lipopolysaccharide (T-B-suppression) was used it was considerably suppressed. T-lymphocyte helper activity in CGN patients was on an increase.
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PMID:[Characterization of secondary immune deficiency in patients with chronic glomerulonephritis]. 296 Nov

The effects of ultraviolet-B radiation (UV-B) on accessory function of human blood adherent mononuclear cells (ADH) for antigen and mitogen-induced responses, and production by ADH of the amplifying cytokine interleukin 1 (IL-1) were examined. Responder lymphocytes were rendered accessory cell dependent by treatment of nonadherent cells with OKIal+complement. UV-B depressed accessory function of ADH in a dose-dependent manner. UV-B at 5 mJ/cm2 decreased accessory function of 2 x 10(4) ADH for tetanus toxoid-induced responses (measured as incorporation of 3H-thymidine) by 84% (P less than 0.001, n = 6) and phytohaemagglutinin-induced responses 91% (P less than 0.001, n = 4). UV-B also decreased accessory activity of peripheral blood mononuclear cells but not Epstein-Barr virus-transformed B cells for a PPD-reactive T cell line. Viability was approximately 90% 0-72 h after exposure of ADH to 5 mJ/cm2 of UV-B. Interleukin 1 (IL-1) activity of supernatants of ADH was assayed on C3H/HeJ mouse thymocytes. Pretreatment of ADH with 5 mJ/cm2 UV-B decreased lipopolysaccharide-stimulated IL-1 activity from 169 +/- 34 (mean U/ml +/- s.e.) to 4 +/- 1 (P less than 0.01, n = 4). Lysates of UV-B irradiated. LPS-stimulated ADH had no discernible IL-1 activity. Addition of IL-1 partially restored accessory activity of UV-B irradiated ADH for lymphocyte responses to TT. Exposure of ADH to TT or PHA for 30 min before irradiation blocked the inhibitory effect of UV-B on accessory activity. Thus, low doses of UV-B are deleterious to accessory function and to production of IL-1 by ADH. Interference with production of cytokines and with initial interactions of accessory cells with antigen and mitogen may be critical to the effects of UV-B on immunoregulatory function of ADH.
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PMID:Deleterious effect of ultraviolet-B radiation on accessory function of human blood adherent mononuclear cells. 296 88

The present studies were performed to determine the effects of severe protein deficiency and subsequent injection of thymosin fraction 5 (TF5) on T and B cell functions. BALB/c mice, 4 weeks old, were fed a normal protein (21%), a low protein (4%) or a protein free (0%) diet and then injected with TF5 or buffer (PBS). A significant increase was observed in the PHA (phytohemagglutinin) and LPS (lipopolysaccharide) induced mitogenesis with increasing age of the well-nourished, PBS injected animals. The severely protein malnourished mice, PBS injected and the well nourished mice, injected with TF5 had smaller increases in both B and T cell mitogenesis with increasing age. TF5 injection of the malnourished mice increased PHA and LPS mitogenesis nearly to the levels of the well-nourished mice. The protein malnourished mice consistently had higher serum corticosteroid levels than controls. No changes in serum corticosteroids were observed with TF5 injection of controls, but there was a significant decrease in the corticosteroid levels of the severely malnourished with TF5 injection. Cytoxicity assays of T cell function, antibody dependent cellular cytoxicity and cytoxicity to mouse thymona tumor cells, in mice fed moderately protein deficient diets showed suppression compared to controls fed 20% protein. TF5 injection partially and temporarily increased these functions in the malnourished mice.
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PMID:Thymosin fraction 5: effects on T cell functions in mice immunosuppressed by severe dietary protein deficiency. 309 92


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