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)

Data is presented comparing the activities of three immunosuppressive agents, cyclosphosphamide, frentizole and azathioprine in models of humoral immunity in mice. Cyclophosphamide and frentizole suppressed the primary and secondary plaque forming cell responses to sheep erythrocytes at lower doses than did azathioprine. Prolonged suppression of serum antibody titers occurred following short-term therapy with cyclophosphamide or frentizole, but not azathioprine. Azathioprine was also the least effective agent in suppressing a primary response to the T-independent antigen, trinitrophenylated lipopolysaccharide. All three agents were found to inhibit the induction and activity of suppressor cells at immunosuppressive doses.
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PMID:Comparative effects of azathioprine, cyclophosphamide and frentizole on humoral immunity in mice. 40 16

Heat-labile, rat skin-fixing antibodies were detected readily in the sera of young female mice dosed intranasally with the body fluid of Ascaris suum (ABF) and the adjuvant, Bordetella pertussis vaccine (BPV). In addition, washed cell suspensions prepared from spleen and the lymph nodes regional to the lungs were positive in an adoptive cutaneous anaphylaxis assay, an assay which may detect activities of reagins associated with mast cells rather than reaginic antibody-secreting cells. The intraperitoneal route was a poor means of inducing circulating anti-ABF reagins and an intraperitoneal injection of ABF + BPV delayed the appearance of circulating reagins in mice dosed at the same time with ABF + BPV intranasally. Hypothymic female BALB/c. nu/nu ('nude') mice failed to produce circulating reagins to ABF but an injection of normal thymocytes or cortisone-resistant thymocytes from syngeneic female mice led to higher titers of circulating reagins than found in normal female BALB/c. nu/+ littermates. Using cells from young male or female syngeneic donors and male and female BALB/c. nu/mu recpiients, evidence was obtained for a defect in the thymus of young male mice and conceivably this defect may extend to the peripheral T cell population in such mice. Cyclophosphamide pretreatment or adrenalectomy increased circulating reagin titers in normal mice dosed intranasally with ABF + BPV, and pretreatment with lipopolysaccharide intranasally markedly reduced titers of circulating anti-ABF reagins. In the discussion, emphasis is given to the hypothesis that potent allergens are T cell-stimulating, relatively persistent antigens which, when located in submucosal lymphoid sites and under conditions of limited antibody production as a result of limited recruitment of 'helper' T cells systemically, lead to the induction and sustained production of IgE by resident Bxi cells and their progeny.
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PMID:Studies on immune responses to parasite antigens in mice. II. Aspects of the T cell dependence of circulating reagin production to Ascaris suum antigens. 108 24

Fu-Zheng Jie-Du decoction (FZJD) was an adjuvant drug of anti-tumor. In the present paper, the authors studied the effects of FZJD and cyclophosphamidum (CTX) on tumor necrosis factor (TNF) production of peritoneal macrophages (PM) of normal and EMT6 solid tumor-bearing mice. The results showed that in vitro, lipopolysaccharide (LPS) could induce TNF production of PM of normal mice; in contrast; FZJD and CTX were unable to induce TNF and inhibited the LPS effect. In vivo, CTX could not influence the TNF production of PM of tumor-bearing mice but FZJD could enhance the TNF production of PM of tumor-bearing mice treated with CTX.
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PMID:[Effects of fu-zheng jie-du decoction and cyclophosphamidum on the production of tumor necrosis factor in mice]. 239 56

Cyclophosphamide injections to mice following T cell mitogen (lectins from Lens culinaris and concanavalin A) were shown to suppress (20-40-fold) thymus-dependent response to SRBC. At the same time no damage-specific and polyclonal response to thymus-independent antigen and polyclonal activator of B cells--lipopolysaccharide--has been observed. Injections of lectin and cyclophosphamide to mice prevented the onset of DTH reaction to SRBC and induction of antigen-specific DTH suppressor cells. Thus, cyclophosphamide injection after T cell mitogen leads to T-cell anergy, with B-cell activity remaining unchanged.
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PMID:[T-cell immunodeficiency in mice receiving lectin and cyclophosphamide]. 326 Nov 77

Treatment of mice with the direct-acting alkylating agent methyl methanesulfonate produced marked suppression of the humoral response to sheep erythrocytes and suppression of T cell responses to foreign antigens. These effects occurred without loss of spleen, thymus or body weight and in the absence of peripheral blood, splenic or bone marrow cytotoxicity. In comparison, exposure to urethan decreased spleen weights, number and viability of spleen cells, and numbers of circulating lymphocytes. Significant suppression of T cell mitogen responsiveness was observed at all dose levels of urethan. Thymus weights, proliferative responses to the B cell mitogen lipopolysaccharide and delayed hypersensitivity responses were decreased at the highest urethan dose. Cyclophosphamide treatment significantly depressed thymic weight, lymphoproliferative responses of T and B cells, antibody production and delayed hypersensitivity responses. These results suggest differential sensitivity in components of the host defense system to weak carcinogens.
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PMID:Alteration of immune function in mice following carcinogen exposure. 355 66

We have compared four assays to detect hemopoietic stromal damage induced by various cytostatic agents in young (4-week old) and adult (12-week old) mice. These assays included: (a) quantitation of the hemopoietic stem cell content of subcutaneously implanted spleens and femurs, (b) quantitation of fibroblastic colony-forming units per femur and spleen, (c) quantitation of the growth of normal hemopoietic progenitor cells in irradiated cytostatic drug-treated mice, and (d) measurement of splenic hemopoietic stem cell accumulation in response to bacterial lipopolysaccharide-induced hemopoietic stress. Busulfan caused a short- and long-term hemopoietic stromal defect. However, the four assays used showed different kinetics and severity of the stromal damage. Cyclophosphamide treatment resulted in a short-term stromal damage which was repaired within one week to three months, depending on the assay used. Methotrexate and vincristine did not cause long-term stromal damage as measured by the four assays used, whereas a short-term splenic stromal damage was detected using the subcutaneous implantation technique. No significant differences in stromal sensitivity to drug treatment were observed between young and adult mice. The presented data suggest that the four assays used to study stromal integrity measure different components of the hemopoietic microenvironment, and indicate that the use of a single assay may well lead to erroneous interpretations.
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PMID:Long-term effects of cytostatic agents on the hemopoietic stroma: a comparison of four different assays. 366 11

Thymus-derived (T) and bone marrow-derived (B) lymphocytes were isolated from human peripheral blood and cultured with various mitogens and antigens. Purified protein derivative of tuberculin stimulated both purified T and B cells from patients with positive skin reactivity to purified protein derivative but did not stimulate nonimmune lymphocytes. Similarly, both T and B lymphocytes from patients with periodontal disease were stimulated to proliferate when incubated with dental plaque, whereas cells from normal individuals without gingivitis were unresponsive. In contrast, one component of plaque, bacterial endotoxins (lipopolysaccharide), minimally stimulated B lymphocytes from both normal or gingivitis patients. T lymphocytes from patients with periodontal disease were also stimulated by plaque antigen to produce chemotactic lymphokine activity (CTX) for human monocytes. B cells purified by the EAC rosetting method nonspecifically produced CTX without concomitant blastogenesis; however, after dissociation of adherent EAC these immune B cells did not spontaneously produce CTX. Lymphokine synthesis by B cells was not dependent on concomitant blastogenesis. Dissociated B cells from periodontitis patients also produced CTX activity after stimulation with dental plaque antigen. Therefore, both T and B lymphocytes, after stimulation with nonendotoxin antigenic components of plaque, proliferated and produced lymphokines, which are presumed to contribute to the pathogenesis of periodontal disease.
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PMID:Blastogenesis and lymphokine synthesis by T and B lymphocytes from patients with periodontal disease. 454 44

This study shows that bone marrow-derived lymphocytes of guinea pigs if appropriately activated produce a monocyte chemotactic factor (MNL CTX). Activation of B lymphocytes to produce a chemotactic lymphokine occurs subsequent to interactions with a variety of membrane-associated receptors. Polymeric B-cell mitogens with multiple binding sites, polymerized flagellin and lipopolysaccharide, initiated mediator synthesis. Furthermore, interaction of antigen-antibody complexes or aggregated gamma globulin with the Fc receptor and binding of antigen-antibody-complement complexes at the C3 receptor can effectively facilitate mediator production in the absence of a significant proliferative response. Additionally, intact anti-immunoglobulin but not its Fab fragments activated the B cells. An anti-Fab effectively converted the inactive Fab-bound B cells into producers of MNL CTX, suggesting that the basic mechanism of activation depended upon cross-linking of receptors. Thus, interaction of B-cell surface receptors such as Fc, Ig, and C3 sites with mitogenic as well as nonmitogenic molecules capable of bridging the receptors appears to trigger B-cell mediator production.
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PMID:Induction of guinea pig B-cell lymphokine synthesis by mitogenic and nonmitogenic signals to Fc, Ig, and C3 receptors. 461 80

Cellular and humoral parameters of the polyclonal stimulation of lymphocytes induced by a single injection of bacterial lipopolysaccharide were determined in 6-11 week-old C57B1/6 mice at various periods of time. The study of cellular parameters on day 5 in 8-10 week-old mice appears to be suitable to quantify the induced polyclonal stimulation. Cyclophosphamide was shown to inhibit it, particularly when the drug was given the day or one day after the injection of lipopolysaccharide, and a dose dependent effect was observed. This model may be useful for the selection, and the immunopharmacological study, of drugs able to modulate a polyclonal stimulation of B lymphocytes.
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PMID:An in vivo model for the experimental selection and pharmacological study of drugs able to modulate polyclonal activation of B lymphocytes. 621 Feb 58

Cyclophosphamide (CPA) is known to exert greater toxic effects of B- than on T-lymphocytes in vivo. Both in vitro and in vivo CPA treatments were used to assess the possible cytogenetic basis for these observations. First, male C57BL/6 mouse lymphocytes were stimulated to divide in vitro with either phytohemagglutinin (T-cell mitogen) or lipopolysaccharide (B-cell mitogen), and were then treated with CPA (0.05 to 1.0 mM) and 5-bromo-2'-deoxyuridine (2 microM) at 24 hr. Cultures were harvested at 60 hr following a 4-hr treatment with demecolcine (1.35 microM). CPA caused concentration-related increases in sister chromatid exchange (SCE) up to 3 times control frequencies; the resulting SCE induction curves for B- and T-cells were sigmoidal and equivalent. Second, mice were given a single i.p. injection of CPA (0.5, 1.0, or 5.0 mg/kg). Blood was removed 24 hr later and cultured without additional CPA, as described above. Dose-related increases in SCE frequencies were seen for both T- and B-lymphocytes. CPA induced consistently 2.5 to 3.7 more SCEs in B-cells than in T-cells. Thus, B- and T-lymphocytes exhibited an equal sensitivity to CPA in vitro, but B-cells were more susceptible to the genotoxic effects in vivo.
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PMID:Sister chromatid exchange induction in mouse B- and T-lymphocytes exposed to cyclophosphamide in vitro and in vivo. 660 9


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