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)

Interleukin-2 (IL-2), originally described as a growth factor required for sustained proliferation of T cells in vitro is a glycoprotein hormone of known structure which appears to be important for the generation of immune responses in vivo. As well as T lymphocytes, B lymphocytes and large granular lymphocytes with natural killer activity (NK cells) can also respond to IL-2. The action of IL-2 seemed to be limited specifically to lymphocytes, however, and the term 'T-lymphocytotrophic hormone' was used. Here we provide evidence that human monocytes display a substantially increased cytotoxic activity as a direct and rapid response to human recombinant IL-2 but not to human recombinant glycosylated interferon-gamma (IFN-gamma) or lipopolysaccharide. Our results reveal a previously unknown function of IL-2 and suggest its possible involvement in monocyte-T cell interactions.
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PMID:Recombinant interleukin-2 directly augments the cytotoxicity of human monocytes. 310 Sep 57

Regulation of the production of the biologically active vitamin D3 sterol 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] by cultured pulmonary alveolar macrophages (PAM) obtained from 6 patients with pulmonary sarcoidosis and from 9 normal subjects was studied. The sarcoid cells, all collected from patients with normal calcium metabolism, synthesized 1,25-(OH)2-[3H]D3 from the substrate 25-hydroxyvitamin [3H]D3 (25OH-[3H]D3), whereas in vitro incubation with recombinant human interferon-gamma (IFN gamma) or lipopolysaccharide (LPS) was required for induction of synthesis of the hormone by normal PAM. Exogenous 1,25-(OH)2D3 (10-100 nmol/L) decreased endogenous hormone production by normal PAM by approximately 45%. The relative inhibitory effect of 1,25-(OH)2D3 was less pronounced in sarcoid PAM, in which 10-100 nmol/L 1,25-(OH)2D3 inhibited 250HD3-1-hydroxylase by approximately 25%. An accompanying induction of the 250HD3-24-hydroxylase, which is typical for renal cells, was found at low levels in only 3 of 10 experiments; in this regard, no differences between sarcoid and normal PAM were apparent. PTH or forskolin did not influence 250HD3 metabolism by PAM. 1,25-(OH)2D3 production by sarcoid PAM was enhanced by lipopolysaccharide and IFN gamma. Likewise, recombinant human interleukin-2 stimulated 1,25-(OH)2D3 production by sarcoid PAM, suggesting a possible role for both IFN gamma and interleukin-2 in the induction of 1,25-(OH)2D3 synthesis by sarcoid PAM in vivo. Recombinant human IFN alpha, IFN beta, and granulocyte-macrophage colony-stimulating factor had little effect. Dexamethasone and chloroquine, which have in vivo antihypercalcemic activity in sarcoidosis, both inhibited 1,25-(OH)2D3 synthesis by sarcoid PAM; chloroquine simultaneously stimulated the 24-hydroxylase. Our studies suggest that the 250HD3-metabolizing system in PAM is in some respects different from renal metabolism of 250HD3.
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PMID:Regulation of 1,25-dihydroxyvitamin D3 production by cultured alveolar macrophages from normal human donors and from patients with pulmonary sarcoidosis. 311 53

A class of interleukin-2-dependent T-cell clones, isolated from a murine fetal thymus, was previously shown to suppress the induction of cytotoxic responses to alloantigens (H.-S. Teh, M. Ho, and W. R. McMaster, J. Immunol. 135:1582-1588, 1985). In that article, the immunosuppressive properties of these T-cell clones were shown to be a direct consequence of infection by Mycoplasma hyorhinis. Suppression of cytotoxic responses was mediated by both the mycoplasmas and a 200-kilodalton factor present in supernatants of infected cultures. This factor was sensitive to proteases but was resistant to heating to 60 degrees C for 1 h and to incubation on ice at pH 2 or pH 14 for 4 h. The production of suppressor factor in infected cultures was independent of the viability or the protein synthesis capability of the mammalian cells, suggesting that it was produced by M. hyorhinis. The factor was most suppressive when it was added during the early stages of the cytotoxic response. Its suppressive effects on cytotoxic responses were not reversed by the addition of an excess of recombinant interleukin-2. This factor also suppressed mitogenic responses to lipopolysaccharide. However, it is not a growth inhibitor since it did not affect the proliferation of tumor cell lines. A simple method for detecting M. hyorhinis in the infected T-cell clones and for eliminating it is described.
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PMID:Suppression of cytotoxic responses by a supernatant factor derived from Mycoplasma hyorhinis-infected mammalian cell lines. 325 4

Abnormalities of lymphocyte proliferation in chronic hepatitis B virus infection are well documented, although the underlying mechanisms are poorly understood. To determine whether these defects may be secondary to disordered lymphokine production, we have simultaneously assayed interleukin-1 and interleukin-2 production in 31 chronic carriers of the hepatitis B virus. Supernatants from mononuclear cells cultured both in the presence and absence of lipopolysaccharide contained significantly increased quantities of interleukin-1 activity in patients compared with normal controls (p less than 0.01). Lysates of monocytes from patients also contained more interleukin-1 than those of controls (p less than 0.05) in the presence of lipopolysaccharide or silica, or both. These results indicate that interleukin-1 production is markedly elevated in patients with chronic hepatitis B virus infection, whereas in contrast, interleukin-2 production was found to be reduced in these patients (p less than 0.01). As one of the biological properties of interleukin-1 is to stimulate fibroblasts to produce collagen, the relationship between fibrosis in the liver biopsy specimen and interleukin production was examined. There was a highly significant correlation (p less than 0.001) between interleukin-1 production and the severity of fibrosis, suggesting that this lymphokine may be closely related to the development of cirrhosis in such patients.
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PMID:Interleukin-1 and interleukin-2 activity in chronic hepatitis B virus infection. 325 34

Interleukin-1 (IL-1) exhibits multiple biological properties on various tissues by modulating immunologic, inflammatory, metabolic, and neurologic functions. Considerable attention has focussed on the measurement of IL-1 activity. We reported a simple, sensitive, and specific bioassay for IL-1 using human melanoma A375 subclone which is highly sensitive for the cell growth inhibitory activity of IL-1. This bioassay method is allows detection of as low as 10pg of IL-1 beta/ml or 30pg of IL-1 alpha/ml. Since this A375 subclone cell dose not respond to prostaglandin E2 plant lectins, lipopolysaccharide, and cytokines such as interleukin-2, interleukin-6, tumor necrosis factor, interferon or colony-stimulating factor, it is an extremely useful and rapid method for the measurement of IL-1 activity in a variety of experimental and clinical conditions. The assay method was used in the presence of antisera to IL-1 beta to discriminate two species of IL-1, IL-1 alpha and IL-1 beta, produced in human peripheral mononuclear cells.
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PMID:A simple, sensitive bioassay for the detection of interleukin-1 using human melanoma A375 cell line. 326 84

We have performed a biochemical characterization of B cell stimulatory factors (BSF) produced by Con A-stimulated mouse spleen cells that stimulate growth of lipopolysaccharide (LPS)-preactivated B cells (designated BSF-LPS). Two biochemically distinct forms of BSF-LPS were identified in preparative isoelectric focusing, one acidic form having a pI of 3.9-4.4 and a more basic form with a pI 5.2-5.9. The biochemical heterogeneity of the BSF-LPS activity from Con A-stimulated spleen cells was further demonstrated by ion exchange chromatographies using a fast protein liquid chromatography (FPLC) system. The acidic and the basic forms of BSF-LPS could be totally separated from each other and both are distinct from interleukin-2 (IL-2). Moreover, extending the characterization of the BSF-LPS, together with the use of various murine assay systems for BSF, we could formally exclude that IL-4 or IL-5 accounted for the BSF-LPS activities. In summary, our data provide evidence for the existence of heterogeneous BSF-LPS which maintain growth of LPS-preactivated B cell blasts, and show that these factors can be distinguished from the other lymphokines which have been involved in the control of the cell growth of murine B lymphocytes.
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PMID:Biochemical characterization of B cell stimulatory factors for lipopolysaccharide-preactivated B cell blasts: distinction from other known lymphokines. 326 68

This study was undertaken to compare and assess the relative contribution by IL-2 and IL-1 to the maturation into antibody-forming cells (AFC) of normal, mitogen-activated, proliferating B cells. Antigen affinity-enriched B cells were cultured under conditions at which T cells and macrophages are limiting. B cells were induced to proliferate upon stimulation with lipopolysaccharide (LPS), but not to mature into AFC. Maturation into AFC of LPS-stimulated B cells required the presence of recombinant interleukin-2 (IL-2). B cells stimulated with IL-2 alone were neither induced to proliferate nor to differentiate into AFC. Recombinant interleukin-1 (IL-1), in the presence of LPS, failed to induce the B cells to differentiate into AFC. However, IL-1 strongly synergized with IL-2 in further enhancing the AFC response. Although it has been known for some time that IL-2 and IL-1 contribute to the B cell response, our results indicate that these lymphokines primarily control the maturation of proliferating B cells into AFC.
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PMID:The role of recombinant IL-2 and IL-1 in murine B cell differentiation. 326 69

The rat hepatoma cell line MH1C1 has been characterized to show a stimulated secretion of C-reactive protein in response to both leukocyte supernatant and a purified human interleukin-1 preparation. The time-dependency and dose-response relationship of CRP secretion were comparable to and somewhat more sensitive than the effects of leukocyte supernatant and purified human interleukin-1 on the proliferative rate of murine thymocytes; the proliferative rate of the hepatoma cell line MH1C1 was unchanged under these conditions. Agents which affect the thymocyte bioassay response to interleukin-1 namely interleukin-2, lipopolysaccharide, concanavalin A and phytohemagglutinin showed no effect on the C-reactive protein release of the MH1C1 cell line. These data strongly support the suitability of this cell line for the in vitro study of the hepatic acute phase stimulus-secretion response.
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PMID:The use of the rat hepatoma cell line MH1C1 to investigate the stimulus-secretion response of hepatic acute phase proteins. 326 28

Ribosomal preparations from Klebsiella pneumoniae, Haemophilus influenzae, Streptococcus pyogenes, and Streptococcus pneumoniae were investigated with respect to their activating capacity towards murine lymphoid cells. The proliferation of BALB/c spleen cells was induced in a dose-dependent fashion (from 1 to 100 micrograms/ml) by ribosomes of K. pneumoniae, H. influenzae, and S. pyogenes with a peak activity at 48 or 72 hr of culture. The majority of the blast cells induced by these ribosomal preparations were positive for surface-immunoglobulin (S-Ig) and negative for Thy 1.2. Furthermore, K. pneumoniae, H. influenzae, and S. pyogenes ribosomes induced the synthesis of IgM and some IgA. Cell proliferation and induction of IgM production were also demonstrated with the 3 ribosomal preparations using spleen cells from athymic nude (nu+/nu+) mice, Lyb-5-defective CBA/N spleen cells, B cell-enriched and T cell-depleted BALB/c spleen cell suspensions, as well as spleen cells from the Ips gene-deficient C3H/HeJ strain. Cell culture supernatants contained specific anti-ribosome IgM antibodies. Antibodies of other specificities (anti-sheep erythrocytes) were also demonstrated in supernatants from K. pneumoniae-stimulated cultures. Evidence against a possible role of contamination of K. pneumoniae and H. influenzae ribosomes by lipopolysaccharide- or lipid A-associated proteins in this effect is discussed. Ribosomes from S. pneumoniae did not induce 3H-thymidine incorporation nor Ig production. None of the 4 ribosomal preparations was found to stimulate T cell blastogenesis or to induce interleukin-2 production by naive BALB/c spleen cells. Finally, ribosomes from H. influenzae, S. pyogenes, S. pneumoniae but not those of K. pneumoniae stimulated interleukin-1 production by adherent spleen cells, from BALB/c mice.
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PMID:Induction of murine B cell proliferation and immunoglobulin synthesis by some bacterial ribosomes. 326 81

To evaluate the role of zinc status in immune system dysfunction in diabetic animals, the interleukin-2 production and the lymphocyte mitogenic response to phytohaemagglutinin, concanavalin A and lipopolysaccharide were measured in streptozotocin-induced diabetic rats, diabetic rats treated with insulin and their non-diabetic controls maintained on low zinc, normal zinc and high zinc diets for 3 weeks. Unstimulated lymphocyte proliferation was significantly lower in diabetic rats compared to nondiabetic control rats maintained on normal zinc diet (1505 +/- 318 vs 3447 +/- 497 cpm) (p less than 0.005) or low zinc diet (546 +/- 191 vs 4011 +/- 628 cpm) (p less than 0.005). High zinc diet attenuated the difference between the diabetic rats (2404 +/- 833 cpm) and control rats (3929 +/- 713 cpm). Insulinised diabetic rats were similar to control rats. Phytohaemagglutinin-stimulated lymphocyte proliferation was not significantly altered with dietary zinc changes, but diabetic rats on low zinc diet had significantly lower (p less than 0.025) values compared to control rats on the same diet (41470 +/- 7874 vs 72308 +/- 8895 cpm). Insulinisation did not normalise phytohemaegglutinin-stimulated lymphocyte proliferation (40711 +/- 3666 cpm). Similarly, cells from diabetic rats on low zinc diet, unlike their controls, failed to respond to concanavalin A stimulation. Compared to control rats the diabetic rats on either low or normal zinc diets had lower lipopolysaccharide-stimulated lymphocyte proliferation. High zinc diet or insulinisation normalised mitogenic response of lymphocytes to lipopolysaccharide. Unlike the diabetic rats alterations in dietary zinc intake did not significantly affect the lymphocyte proliferation in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of zinc status on the immune function of diabetic rats. 326 57


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