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)

Peripheral blood monocytes from human immunodeficiency virus (HIV)-infected individuals or AIDS-related complex/AIDS patients ex vivo exhibit distinct alterations in some but not all immune functions. In studies presented here, monocytes from healthy donors were infected with HIV 1 in vitro and co-cultures with autologous uninfected T lymphocytes were set up. The monocyte/macrophage (M phi)-dependent T cell function was determined by measurement of proliferative and secretory [interleukin (IL)2, interferon-gamma] responses to lectin (phytohemagglutinin), mitogen (anti-CD3 monoclonal antibody), or recall antigen (tetanus toxoid, tuberculin). Accessory function of M phi was normal after HIV infection when optimal amounts (10%-20%) were added to the T lymphocytes. However, HIV infection of M phi significantly decreased T cell proliferative responses and secretion of IL2 when supplemented at limited dilution (0.5%-5%), although interferon-gamma production was not affected. Whereas the lipopolysaccharide-triggered M phi production of IL1 was not impaired by HIV 1 infection, there was a significant decrease in this response when anti-CD3 monoclonal antibody or tetanus toxoid were used to trigger the peripheral blood mononuclear cells. The impairment of proliferation of T lymphocytes in the presence of HIV 1-infected M phi could be overcome by addition of exogenous IL 1. Taken together, these data clearly show that the mononuclear phagocyte-dependent enhancement of stimulated T cell proliferation and lymphokine secretion is decreased when the restricted numbers of monocytes/M phi are HIV 1 infected. There are, therefore, two possible roles of M phi in HIV infection and progression to disease. First, as a reservoir and vehicle for dissemination of the virus, and second, as an immune cell whose essential functions are impaired by infection.
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PMID:Decreased accessory cell function of macrophages after infection with human immunodeficiency virus type 1 in vitro. 225 85

Tumor necrosis factors alpha and beta (TNF-alpha and TNF-beta) are multifaceted polypeptide cytokines which may mediate some of the significant changes in cellular homeostasis which accompany the invasion of the mammalian host by viruses, bacteria, and parasites. Although it is well established that bacterial lipopolysaccharide is a potent inducer of TNF-alpha, there is still very little known of the types of agents which can trigger the production of TNFs in mononuclear leukocytes. Using an enzyme-linked immunosorbent assay for measuring TNF-alpha and TNF-beta, we examined the capacity of various T-lymphocyte and beta-lymphocyte mitogens as well as microbial components to stimulate production of these cytokines in culture. The mitogens phytohemagglutinin, concanavalin A, and pokeweed mitogen induced production of both TNF-alpha and TNF-beta, while whole-killed Staphylococcus aureus and Bordetella pertussis, like lipopolysaccharide, were potent inducers of TNF-alpha but failed to stimulate TNF-beta production. TNF-alpha production was detectable within 1 h after stimulation, while TNF-beta production was not detected until after 8 h of culture. The bacterial products tetanus toxoid, purified protein derivative, pertussis filamentous hemagglutinin, and pertussis toxin were all able to induce TNF-alpha and TNF-beta production. Disrupted (frozen-thawed) Plasmodium falciparum-infected erythrocytes were also potent inducers of TNF-alpha and TNF-beta. The results demonstrated that a wide variety of microbial components are inducers of TNF-alpha. Some may not only be more effective than lipopolysaccharide but can also induce TNF-beta production. Furthermore, evidence is presented showing that TNF-beta but not TNF-alpha production correlates with lymphoproliferation.
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PMID:Production of tumor necrosis factors alpha and beta by human mononuclear leukocytes stimulated with mitogens, bacteria, and malarial parasites. 225 24

The potential for immunizing against gonadotropins without using Freund's complete adjuvant was explored in bonnet monkeys by using tetanus toxoid (TT) as carrier and Salmonella lipopolysaccharide (LPS) as adjuvant. Pure hCG beta subunit and or sheep LH beta subunit was coupled with TT by employing N-succinimidyl-pyridyl-dithio-propionate reagent. Fertile female bonnet monkeys were injected with 50 mcg gonadotropin equivalent monthly. 1 mg sodium phthalyl derivative of LPS was added to the 1st injection. Animals with low titers were also given a booster on Day 145 with Leiras adjuvant. 3 of 5 monkeys immunized with ovine beta-LH subunit bonded to TT had strong responses, and 2 produced high antibody titers after a booster with Leiras adjuvant. A 2nd group of 3 monkeys treated with both ovine beta LH and beta hCG conjugated to a common carrier, TT, showed high titers, between 750 and 1300 ng/ml, which were sustained for nearly a year. Scathard analysis indicated that the combined antigens raised antibodies of high affinity, with Ka values ranging from 5 x 109 to 6 x 1010 per M. There were no cross reactions with either human FSH or TSH. 2 of the monkeys immunized against the combined antigens remained infertile for 6 and 3 cycles respectively, or until their antibody titers fell to 35 and 5 Monkeys in the 1st group also were infertile for several cycles before their antibody levels fell below 120 ng/ml against hCG.
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PMID:Enhancement of antigonadotropin response to the beta-subunit of ovine luteinizing hormone by carrier conjugation and combination with the beta-subunit of human chorionic gonadotropin. 242 91

A semi-synthetic vaccine against Pseudomonas aeruginosa immunotype 3 was prepared by chemical coupling of P. aeruginosa immunotype 3 O-polysaccharide to tetanus toxoid. The O-polysaccharide was obtained by mild acid hydrolysis of immunotype 3 lipopolysaccharide, and purified by gel permeation chromatography. The purification was evaluated by high performance liquid chromatography. Additional analyses revealed a high grade of purity of the O-polysaccharide, and an at least 1000-fold reduction of endotoxic activity as compared to homologous lipopolysaccharide. O-Polysaccharide was conjugated to tetanus toxoid, using 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide as coupling reagent. Antigenic determinants of both O-polysaccharide and tetanus toxoid were retained after conjugation, as tested in a sandwich enzyme-linked immunosorbent assay. Immunization of mice revealed that O-polysaccharide was nonimmunogenic in mice, while the O-specific part of the conjugate was able to induce high levels of IgG antibodies reacting with immunotype 3 lipopolysaccharide in an enzyme-linked immunosorbent assay. By immunoblotting it was shown that the antibodies were directed to high molecular weight lipopolysaccharide only, demonstrating specificity for its O-polysaccharide moiety.
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PMID:O-polysaccharide-protein conjugates induce high levels of specific antibodies to Pseudomonas aeruginosa immunotype 3 lipopolysaccharide. 243 18

The distribution of total and antigen-specific IgA1 and IgA2 antibodies in human colostrum was determined by ELISA using subclass-specific monoclonal reagents. In 18 samples of colostrum the mean ratio of total IgA1 to IgA2 was found to be 53:47, respectively, but significant individual variations were observed. In two samples we found unusually low levels of IgA1, while IgA2 was in the normal range. IgA1 and IgA2 antibody activities were determined against the following antigens: bovine gamma-globulin and beta-lactoglobulin, tetanus toxoid, protein antigen I/II of Streptococcus mutans, influenza virus vaccine, polysaccharides of pneumococcal, meningococcal and Haemophilus influenzae type b origin, and lipopolysaccharide (LPS) from Escherichia coli K235. The IgA antibody activity directed against the polysaccharides was almost equally distributed between the two subclasses. However, antibody activity specific for protein antigens was found predominantly in the IgA1 subclass while anti-LPS activity was mostly of the IgA2 subclass.
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PMID:IgA subclasses of human colostral antibodies specific for microbial and food antigens. 247 28

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

Previous studies showed that both resting and lipopolysaccharide activated B cells were very effective accessory cells and antigen presenting cells in T cell responding to mitogens and antigens. This paper discusses the role of B cell surface IgM in antigen presentation. Splenic B cells obtained from C57BL/6 mouse were depleted of macrophages, dendritic cells and T cells. The purified B cells were prepulsed with sheep anti-mouse IgM antibody (SaM) at 4 degrees C for 60 min or with tetanus toxoid antigen (TT-Ag) at 37 degrees C for 12 h before pulsing with TT-Ag or SaM. Then B cells (2 x 10(5)/well) were used as antigen presenting cells without further addition of TT-Ag in TT-Ag primed T cells (2 x 10(5)/well, obtained from TT-Ag immunized C57BL/6 mouse lymph node) proliferation. The results showed that antigen presentation of B cells prepulsed with SaM before pulsing with TT-Ag was blocked. But if B cells were preincubated with TT-Ag before pulsing with SaM, antigen presentation of B cells was not blocked by SaM. These results have suggested that B cell surface IgM can take up antigen and can present the antigen to antigen specific T cells. It has also been revealed that B cell surface IgM by taking up antigen plays an important role in antigen presentation. Also, the biological significance of the role on B cell surface IgM in antigen presentation is discussed.
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PMID:[Role of B cell surface IgM in antigen presentation]. 279 42

We have analyzed at the clonal level (limiting dilution assay) the repertoire of lipopolysaccharide (LPS)-responsive murine B cells committed to the production of autoantibodies characteristic of systemic lupus erythematous (SLE), i.e. anti-single-stranded DNA (ssDNA), anti-double-stranded DNA, anti-Sm and rheumatoid factors (RF). Our results demonstrated that: (1) the frequency of precursor B cells producing each lupus autoantibody (approximately 1 in every 100-400 LPS-responding B cell) was similar in two non-autoimmune (C57BL/6 and BALB/c) and four SLE-prone (NZB, (NZB x NZW)F1, MRL/MpJ and BXSB/MpJ) mice despite the marked differences in autoimmune responses in the different SLE-prone mice, and (2) the relative frequency of autoantibody-secreting precursor B cells was constant throughout life, and equally distributed among activated and resting B-cell populations and among B cells from the peritoneal cavity and spleen. The lack of association of anti-ssDNA secretion with anti-Sm or RF secretion in cultures set up with a smaller number of B cells ruled out the possibility that the similar frequency of different autoantibody-secreting cell precursors is due to the poly-specificity of IgM autoantibodies. Notably, the frequencies of autoantibody-secreting precursor cells were significantly lower, approximately 4 and 10 times, than those of anti-tetanus toxoid and anti-dinitrophenyl antibody-producing precursor B cells, respectively. The similar frequency of precursor B cells producing four different lupus autoantibodies on the one hand and the considerable variation in each autoimmune response among SLE-prone mice on the other, support the hypothesis that specific stimulatory mechanisms may govern each autoimmune response in different SLE strains of mice.
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PMID:Autoantibody repertoire analysis in normal and lupus-prone mice. 280 76

In health, pulmonary alveoli are maintained free of inflammatory responses to inhaled foreign antigens. The specific role of alveolar macrophages (AM) in modulating the local cellular immune response to antigens is controversial. Immunoregulatory function and properties of AM and blood monocytes (MN) were compared. The AM were obtained by bronchoalveolar lavage of healthy volunteers, MN by adherence of peripheral blood mononuclear cells to plastic. These accessory cells were added in increasing ratios to a responder population rendered rigorously accessory cell-dependent by nylon wool adherence and depletion of cells bearing the surface Class II MHC determinant, HLA-DR. At low ratios of mononuclear phagocytes to lymphocytes (less than or equal to 1:10), MN and AM supported significant and comparable blastogenic responses to tetanus toxoid (3H-thymidine incorporation at a 1:10 ratio was 9,697 +/- 2,508 for MN and 8,969 +/- 1,454 for AM, mean cpm +/- SE, n = 9, p = NS) and other antigens. Interleukin-1 (IL-1) activity in supernatants of MN stimulated with lipopolysaccharide (LPS), 10 micrograms/ml, was 115 +/- 28 versus 67 +/- 21 U/ml in supernatants of AM (n = 9, p greater than 0.2). At suboptimal concentrations of LPS, however, MN expressed more IL-1 activity than did AM. The specific mean fluorescence intensity of surface expression of HLA-DR determinants as assessed by flow cytometry was similar for MN and AM. At the higher ratio of 1:2, MN supported 32% increased responses to tetanus toxoid compared with that at 1:5 (p less than 0.05). In contrast, AM at a ratio of 1:2 suppressed lymphocyte response by 69% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spectrum of immunoregulatory functions and properties of human alveolar macrophages. 295 14

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


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