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)

Evidence is presented that the ferritin-inhibitable, Ia+ monocyte progenitor in murine marrow requires two signals for stimulation of clonal proliferation. Escherichia coli K235 lipopolysaccharide (LPS) at 0.1 ng/ml enhanced macrophage colony formation by 25 to 70% in murine marrow cultures stimulated with colony-stimulating factor (CSF-1). The progenitors which responded to LPS and CSF-1 represented a distinct subpopulation. Pretreatment of marrow cells with complement plus anti-Ia, anti-H2, anti-asialo GM1, and anti-Mac-1 antibodies specifically depleted the two-signal-requiring progenitors. In addition, the same progenitors were depleted by preincubation with hydroxyurea, indicating that these cells were in cell cycle when removed from the marrow. When compared with the quiescent progenitors, the Ia+, cycling cells were more sensitive to the antiproliferative effects of interferon alpha/beta but were more resistant to inhibition by E prostaglandins. Pretreatment with T cell-specific antibodies and complement specifically enhanced cloning of quiescent progenitors without affecting cloning of the Ia+, cycling subpopulation. Moreover, rat liver ferritin at 10(-8) to 10(-10) M specifically inhibited clonal proliferation of the Ia+ progenitors. Finally, the requirement for LPS as the additional stimulant could be replaced by the addition of haplotype-specific anti-Ia antibody to CSF-stimulated cultures. In contrast to LPS, anti-IA was competitive with inhibitory ferritin in clonal proliferation of the Ia+ progenitors. The significance of these observations in regulation of monocytopoiesis is discussed.
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PMID:Characterization of a two-signal-dependent, Ia+ mononuclear phagocyte progenitor subpopulation that is sensitive to inhibition by ferritin. 345 88

A stromal cell line, GY30, was cloned from mouse bone marrow adherent cell layers. In culture, GY30 cells sustain the production of granulocyte-macrophage progenitor cells (GM-CFU) but fail to support the survival of pluripotential stem cells (CFU-S). GY30 cells secrete two growth factor activities distinct from interleukin-3 (IL-3), IL-2, and macrophage colony-stimulating factor (M-CSF) but functionally similar to GM-CSF and G-CSF. The production of both CSFs is increased 70- to 200-fold by treating GY30 cells with lipopolysaccharide or IL-1. RNA blot analysis reveals the presence of GM-CSF and G-CSF transcripts and demonstrates that IL-1 regulates the production of both factors at the mRNA level. Further, these studies show that the GM-CSF secreted by GY30 cells is structurally similar to the GM-CSF produced by activated T cells.
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PMID:Control of hemopoiesis by a bone marrow stromal cell clone: lipopolysaccharide- and interleukin-1-inducible production of colony-stimulating factors. 349 27

T cell activation is widely believed to depend on interleukin 1 (IL 1) provided by antigen (Ag)-presenting cells (APC). Because IL 1 is not a constitutive product of APC, we examined the features of its production during the interaction of murine T cell clones and APC. We observed that IL 1 was detectable in supernatants of most myoglobin-specific T cell clones grown with APC and Ag. Two of these T cell clones induced exceptionally high levels of IL 1 in their supernatants, and these same clones demonstrated the unusual restriction to I-Ek, which is a low responder type for sperm whale myoglobin. One of these clones was characterized additionally as to the mechanism of IL 1 induction. This clone rapidly stimulated IL 1 production in the APC population (detectable at 4 hr of co-culture) or in macrophages (M phi) or a M phi-like cell line. IL 1 induction was Ag dependent and H-2 restricted. Induction was radioresistant, both on the part of the T cell and of the IL 1 producer. The IL 1-induction process was attributable to a lymphokine produced by the T cell clone. This lymphokine was distinct from IFN-gamma, TNF and CSF-1 and may account for a principal mechanism of T----APC signalling. The induced IL 1 was the same in size, co-mitogenicity, and pyrogenicity as lipopolysaccharide-induced IL 1.
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PMID:IL 1 induction by murine T cell clones: detection of an IL 1-inducing lymphokine. 349 59

An interleukin 1 alpha (IL-1 alpha) cDNA probe and an IL-1 responsive T-cell clone (D10.G4; half-maximal stimulation, 0.1-1 pM) have been used to study the production of IL-1 by primary murine cell populations, particularly macrophages and dendritic cells. Spleen and peritoneal macrophages produced IL-1 mRNA and released biologically active IL-1 when challenged with lipopolysaccharide (LPS). Induction of IL-1 was evident over a dose range of 0.01-10 micrograms of LPS per ml, and maximal mRNA levels were maintained from 4 to 20 hr. Several other stimuli did not induce IL-1 in cultured macrophages, including phorbol 12-myristate 13-acetate, gamma-interferon, Con A, macrophage colony-stimulating factor, IL-3, cachectin, and activated T cells. Activated T cells could markedly reduce the response of peritoneal macrophages to LPS. When other cell types were compared with macrophages, keratinocytes had high levels of IL-1 mRNA, apparently in response to endogenous LPS. However B and T lymphocytes did not yield detectable IL-1 during proliferative responses to LPS and Con A, respectively, while dendritic cells produced little or no IL-1 when challenged with a battery of stimuli. Therefore, IL-1 may not be required for the potent accessory function of dendritic cells in lymphocyte mitogenesis. The results indicate that macrophages and dendritic cells have different secretory capacities. The macrophage is the principal leukocyte that synthesizes IL-1, and select stimuli increase and decrease the levels of macrophage IL-1 mRNA.
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PMID:Induction of murine interleukin 1: stimuli and responsive primary cells. 349 97

Continuous intraperitoneal infusion of a macrophage colony-stimulating factor (M-CSF or CSF-1) for 6 d resulted in a 2.3-fold increase in the frequency of progenitor cells (CFUc) of macrophages in femoral marrow in C3H/HeN mice but there was no significant increase in the number of blood leukocytes in these animals. Infusion of bacterial lipopolysaccharide (LPS) also increased femoral macrophage CFUc frequency to the same extent as the above. Furthermore, the effect of the M-CSF preparation was much less pronounced in LPS-resistant C3H/HeJ mice than in LPS-sensitive C3H/HeN mice. The results show that the effect of M-CSF on bone marrow CFUc is marginal, even when it is administered in large amounts in the animals.
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PMID:Increase in macrophage progenitor cell number in femoral marrow of mice after continuous infusion or repeated injections of a macrophage colony-stimulating factor. 350 Oct 11

Purified murine colony-stimulating factors (CSF) recombinant interleukin 3 (IL-3), natural CSF-1, and recombinant granulocyte-macrophage (GM) CSF were assessed in vivo for their effects on BDF1 mouse bone marrow and spleen granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells in untreated mice and in mice pretreated with purified iron-saturated human lactoferrin (LF). The CSF and LF preparations did not contain detectable endotoxin (less than 0.1 ng). Mice pretreated with LF were more sensitive to the effects of CSF. In mice pretreated with LF, 2,000 U IL-3 or 20,000 U CSF-1 significantly enhanced the cycling status and absolute numbers of all progenitors, whereas 20,000 U GM-CSF significantly increased the cycling status of CFU-GM and CFU-GEMM, but had no effect on cycling of BFU-E or on numbers of any of the progenitors. The effects of CSF in mice pretreated with LF were not mimicked by 0.1-100 ng E. coli lipopolysaccharide.
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PMID:Comparative effects in vivo of recombinant murine interleukin 3, natural murine colony-stimulating factor-1, and recombinant murine granulocyte-macrophage colony-stimulating factor on myelopoiesis in mice. 354 76

The ability of the mononuclear phagocyte-specific colony-stimulating factor, CSF-1, to down-regulate its receptor on peritoneal exudate macrophages (PEM) was examined. Because of the essentially irreversible binding of CSF-1 to its receptor at 2 degrees C, unoccupied cell surface receptors could be measured by rapidly cooling PEM to 2 degrees C and determining the amount of 125I-CSF-1 bound at this temperature. On incubation with 125I-CSF-1 at 37 degrees C more receptors were lost than could be accounted for by 125I-CSF-1 binding. This receptor loss, apparently caused by CSF-1 itself, was shown to be due in large part to the presence of contaminating lipopolysaccharide (LPS), which at 10 ng/ml was by itself able to cause complete loss of the CSF-1 receptors. LPS also induced loss of the insulin receptor by PEM. LPS did not cause apparent CSF-1 receptor loss by binding to the receptor or by stimulating the release of CSF-1 or substances which compete for the binding of 125I-CSF-1 to the receptor. However, LPS did stimulate release of factors by LPS responsive (C3H/HeN) PEM which caused CSF-1 receptor loss by LPS non-responsive (C3H/HeJ) PEM. In the absence of LPS induced effects, incubation of 125I-CSF-1 with PEM at 37 degrees C resulted in down-regulation of the CSF-1 receptors. The number of CSF-1 receptor sites down-regulated corresponded to the number of CSF-1 molecules that were cell-associated plus the number that were intracellularly degraded and released.
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PMID:Modulation of receptors for the colony-stimulating factor, CSF-1, by bacterial lipopolysaccharide and CSF-1. 609 75

Among various immunomodulating agents examined, OK-432 (Streptococcus pyogenes cell bodies), BCG (bacillus Calmette-Guerin) and LPS (lipopolysaccharide) were effective in enhancing the production of granulocyte/macrophage colony-stimulating factor (GM-CSF) in the cultures of mouse spleen cells. Control non-stimulated spleen cell cultures accumulated GM-CSF activity maximally on day 3 and lost it subsequently within a few days. On the other hand, a large amount of GM-CSF activity could be detected in the medium until day 9 when OK-432 was added in the culture at the start of incubation. The GM-CSF obtained from OK-432 or LPS stimulated cultures and the GM-CSF obtained from the control non-stimulated culture eluted from an Ultro-gel AcA 34 column at a similar position and inactivated similarly at 80 degrees C. However, these three GM-CSFs behaved in slightly different manners upon isoelectrofocusing. These results suggest that the GM-CSFs produced in increasing amounts by the stimulated spleen cells are similar to that produced by the control non-stimulated cells, but slightly different from one another in the extent of sialylation according to the difference of the stimulant.
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PMID:Effect of various immunomodulators on the production of granulocyte/macrophage colony-stimulating factor (GM-CSF) in mouse spleen cell cultures. 660 23

Addition of lipopolysaccharide (LPS) to the culture of mouse myeloid stem cells (CFUc) increased the incidence of compact colonies and decreased that of dispersed ones in the presence of colony-stimulating factor (CSF-1) which had not such an effect by itself even in high concentrations. Although colony morphology was thus changed, nearly all colonies were composed of monocytes. The incidence of compact colonies increased with the increase of LPS concentration but plateaued at about 50%. Bone marrow cells of LPS-tolerant mice responded to LPS in vitro to a slightly decreased extent. The activity of LPS was decreased by alkaline or acid hydrolysis of the LPS molecule and inhibited by polymixin B, but not by indomethacin, alpha-L-fucose, nor by alpha-methyl-D-mannoside. Other immunopotentiating substances, such as OK-432, Lentinan, and Levamisole, had no effect on the colony morphology. Both muramyl dipeptide and poly(I).poly(C) were also ineffective. Furthermore, the action of LPS was not abolished by the use of heat-inactivated serum in the culture. LPS was no longer stimulative for the induction of lysosomal enzymes in the CSF-stimulated culture, although it greatly enhanced the enzyme induction in the unstimulated culture. These results indicate that the cells of monocyte/macrophage lineage develop the capacity for migration before they become responsive to LPS, and that the LPS-responding monocytic cells can proliferate even in a state of confluence induced by LPS.
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PMID:Migration inhibitory action of bacterial lipopolysaccharide on progenitor cells of monocyte/macrophage lineage growing in culture in the presence of colony-stimulating factor (CSF-1). 698 74

To examine the in vivo role(s) of type I interferons (IFNs) and to determine the role of a component of the type I IFN receptor (IFNAR1) in mediating responses to these IFNs, we generated mice with a null mutation (-/-) in the IFNAR1 gene. Despite compelling evidence for modulation of cell proliferation and differentiation by type I IFNs, there were no gross signs of abnormal fetal development or morphological changes in adult IFNAR1-/- mice. However, abnormalities of hemopoietic cells were detected in IFNAR1 -/- mice. Elevated levels of myeloid lineage cells were detected in peripheral blood and bone marrow by staining with Mac-1 and Gr-1 antibodies. Furthermore, bone marrow macrophages from IFNAR1 -/- mice showed abnormal responses to colony-stimulating factor 1 and lipopolysaccharide. IFNAR1 -/- mice were highly susceptible to viral infection: viral titers were undetected 24 hr after infection of IFNAR1 +/+ mice but were extremely high in organs of IFNAR1 -/- mice, demonstrating that the type I IFN system is a major acute antiviral defence. In cell lines derived from IFNAR1 -/- mice, there was no signaling in response to IFN-alpha or -beta as measured by induction of 2'-5' oligoadenylate synthetase, antiviral, or antiproliferative responses. Importantly, these studies demonstrate that type I IFNs function in the development and responses of myeloid lineage cells, particularly macrophages, and that the IFNAR1 receptor component is essential for antiproliferative and antiviral responses to IFN-alpha and -beta.
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PMID:A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses. 747 80


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