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)

Peritoneal macrophages (M phi s) collected from Chlamydia psittaci 6BC-immune mice after intraperitoneal challenge with 10(6) 6BC (immune-boosted [IB] M phi s) were compared by various functional criteria with other in vivo- and in vitro-activated M phi populations. While casein-, protease peptone-, and thioglycolate (Thio)-elicited M phi s were equally susceptible to in vitro infection with 6BC, IB M phi s did not support chlamydial growth and M phi s from Mycobacterium tuberculosis BCG- or Listeria monocytogenes-sensitized mice exhibited intermediate susceptibility to infection. The resistance of IB M phi s was not due to the ingestion of fewer 6BC organisms, nor were these cells persistently infected, since chlamydiae could not be recovered from infected IB M phi s after in vitro infection, even after extended incubation times. In contrast, Thio M phi s stimulated in vitro with gamma interferon (IFN-gamma), with or without lipopolysaccharide, resulted in cells that exhibited chlamydiastatic activity which was lost shortly after IFN-gamma was removed from the culture medium. Conversely, the antichlamydial activity of IB M phi s was stable over time but not through the production of autostimulatory cytokines, as evidenced by the lack of stimulation of Thio M phi s to restrict 6BC replication in coculture experiments. IB M phi s exhibited enhanced oxidative activity, but anti-IFN-gamma antibody did not abrogate this response. IB M phi s were recovered only from immunized mice that survived an otherwise lethal 6BC intraperitoneal challenge. These cells appear to be important for development of protective immunity to chlamydiae, and evidence suggests that stimulation by cytokines other than IFN-gamma (with or without lipopolysaccharide) is required for the observed heightened in vivo activation.
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PMID:In vivo-activated mononuclear phagocytes and protective immunity to chlamydiae in mice. 313 Dec 46

While mouse peritoneal macrophages respond well to lipopolysaccharide, lung macrophages were neither activated for tumor cell cytotoxicity nor killed directly by it. The unresponsiveness of lung macrophages was ascribed to lack of expression of lipopolysaccharide-binding sites on the cell surface. It was found that in vitro treatment of lung macrophages with interferon-gamma or in vivo sensitization of them with viable BCG restored the response by expression of the lipopolysaccharide binding sites. The modes of action of interferon-gamma and BCG in expressing the binding sites on mouse lung macrophages are discussed.
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PMID:Interferon-gamma or BCG restores the responsiveness of mouse lung macrophages to lipopolysaccharide. 313 56

Murine alveolar macrophages (AM) have been shown to be inefficient at providing accessory function for initiation of the in vitro plaque-forming cell (PFC) response. In the present study AM, which were obtained either from untreated mice (resident AM) or mice injected i.v. with BCG (activated AM) potently suppressed the PFC response of spleen cells from animals previously primed with sheep erythrocytes (SRBC). Addition of AM at a concentration of 10% with respect to spleen cells resulted in greater than 90% suppression of the PFC response. In order to determine if inefficient antigen presentation was associated with AM-mediated suppression, the role of IL-1 and Ia antigen was studied. Addition of exogenous recombinant IL-1 (rIL-1) stimulated the PFC response in control cultures, but had no effect on AM-mediated suppression. Resident AM could be activated with lipopolysaccharide or antigen to produce significant levels of IL-1. Membrane-bound IL-1, thought to be important in the presentation of particulate antigens, was detected on glutaraldehyde-fixed resident AM and was significantly elevated in BCG-activated macrophages. The frequency of cell surface Ia antigen expression was low in resident AM (4%), but could be increased (35%) after in vivo activation with BCG. Recombinant interferon-gamma (IFN-gamma), known to enhance expression of Ia antigen and production of IL-1, had no effect on AM-mediated suppression when used either to pretreat AM, when present during the entire period of culture, or when injected into mice before culture initiation. Treatment with IFN-gamma, however, resulted in a slight increase in the expression of Ia antigen. These results indicate that the immunosuppressive activity of AM is neither related to a defect in IL-1 production or expression nor to a deficiency in Ia antigen expression and therefore can not be explained by the inefficient antigen-presenting function of alveolar macrophages.
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PMID:Relationship between ineffective antigen presentation by murine alveolar macrophages and their immunosuppressive function. 313 8

The growth of Mycobacterium avium in macrophages obtained from Mycobacterium bovis BCG-infected mice was compared with that in macrophages from uninfected mice. BCG vaccination resulted in substantial macrophage activation, measured as increased acid phosphatase and superoxide anion production, as well as enhanced leishmanicidal activity. However, the activated macrophages were only able to reduce the rate of intracellular growth by Listeria monocytogenes and M. avium in vivo and did not express detectable levels of mycobactericidal activity in vitro. Exposure of the macrophage monolayers to concanavalin A-stimulated spleen cell supernatant fluid and lipopolysaccharide did not further enhance the ability of the BCG-activated macrophages to control the intracellular replication of the M. avium. Macrophages from BCG-infected C57BL/6 (BCGs) mice were quantitatively better able to control the intracellular replication of the M. avium challenge than were similar phagocytes obtained from BCGr (A/J) mice. These findings have important implications with respect to the expression of acquired resistance to these atypical mycobacterial infections.
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PMID:Growth of Mycobacterium avium in activated macrophages harvested from inbred mice with differing innate susceptibilities to mycobacterial infection. 313 64

Serum amyloid P-component (SAP) is a major acute phase protein of mice which we have previously shown increases the bactericidal activity of elicited, inflammatory macrophages (M phi). The presence of specific receptors for mouse SAP on M phi was demonstrated and the receptor-ligand (SAP) interaction characterized. Purified 125I-labeled mouse SAP binds to elicited M phi with the characteristics of a receptor-mediated event, i.e., the binding was saturable, specific, and reversible. A single type of receptor population was detected with an affinity of 5 x 10(-8) M (KD) and the calculated number of receptor sites per cell was approximately 10(5). Binding of SAP to M phi required Ca2+ or Mg2+ and was inhibited at a pH less than or equal to 5.6. Activated M phi from mice given BCG bind less SAP than nonactivated M phi. Activation of M phi with mouse interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) also decreased their SAP binding capacity. SAP is a glycosylated protein with a high mannose content; therefore mannose and other sugars were tested for inhibition of binding. Specific binding of SAP was inhibited by less than 1 mM concentrations of mannose 6-P, mannose 1-P, and mannose; however, other monosaccharides did not inhibit the binding. Removal of the oligosaccharide from SAP with an endoglycosidase specific for N-linked carbohydrate reduced the binding of SAP to M phi. The pattern of inhibition by sugars, the divalent cation requirement, and the sensitivity to low pH indicate that the receptor binding SAP is the cation-dependent mannose 6-P receptor, or a closely related receptor. The results suggest that SAP may alter or trigger M phi functions associated with inflammation by binding to glycoprotein receptors.
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PMID:Receptor-mediated binding of the acute-phase reactant mouse serum amyloid P-component (SAP) to macrophages. 314 83

Mouse and rabbit sera from animals treated with Mycobacterium bovis BCG and lipopolysaccharide contained tumor necrosis factor (TNF) and induced malaria parasite crisis forms. However, neither purified mouse- nor recombinant DNA-produced human TNF induced crisis forms in cultured Plasmodium falciparum. Furthermore, rabbit polyclonal and mouse monoclonal antibodies against human TNF did not block the parasite inhibitory activity of human malaria crisis form factor serum from Sudan.
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PMID:Tumor necrosis factor does not induce Plasmodium falciparum crisis forms. 329 67

A monoclonal antibody (RM3/1), raised by immunizing mice with human monocytes, is described which detects a surface antigen on about 20% of freshly isolated peripheral blood monocytes and is increasingly expressed upon cultivation, reaching a maximum between day 2 and 3. By incubation of monocytes with interferon-gamma, 12-O-tetradecanoylphorbol-13-acetate and lipopolysaccharide, antigen expression is decreased but strongly enhanced after incubation with dexamethasone. In cryostat sections of normal tissue, the antibody detects histiocytes in the skin, Kupffer cells in the liver, few alveolar macrophages in the lung, macrophages in the red pulp of the spleen and in the cortex of the thymus, and many macrophages in the placenta. In acute inflammatory tissue, e.g. gingivitis, the antigen is preferentially expressed by macrophages appearing late in the inflammatory process. In chronic inflammation, e.g. BCG granulomas and rheumatoid arthritis, RM3/1-positive macrophages are seen to varying degrees. Double-staining experiments with the antigen 25F9, specific for resting mature macrophages, revealed that RM3/1 and 25F9 are expressed by distinct populations in normal and acute inflammatory tissues. From this it is concluded that the antibody RM3/1 specifically detects a macrophage phenotype which seems to be associated with the healing phase of the inflammatory process.
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PMID:A monoclonal antibody to a novel differentiation antigen on human macrophages associated with the down-regulatory phase of the inflammatory process. 345 May 46

Two-dimensional polyacrylamide gel electrophoresis (2D PAGE) analysis of biosynthetically labeled proteins of murine peritoneal macrophages elicited by inflammatory and activating stimuli indicated that the accumulation of a small number of cell-associated proteins was altered after in vitro treatment with bacterial lipopolysaccharide (LPS). Both increases and decreases in the accumulation of specific proteins were observed after LPS stimulation. Proteins of approximately 87, 43, 37, 30, and 28 Kd were similarly regulated by LPS in proteose peptone-, P. acnes-, and M. bovis BCG-elicited macrophages. Thioglycollate-elicited and resident peritoneal macrophages showed very few changes in the pattern of proteins synthesized after LPS treatment. Many of the proteins whose accumulation was increased by LPS in the elicited macrophages (proteins of approximately 87, 52, 43, 37, and 28 Kd) were already synthesized at high levels in resident macrophages. LPS stimulation also altered the accumulation of many of the same proteins in bone marrow-derived macrophages, indicating the lack of T lymphocyte influence on the LPS-induced changes in macrophages. LPS stimulation of highly purified B cells caused changes in the accumulation of several proteins of 70 and 78 Kd, which were different from those regulated by LPS in peritoneal macrophages.
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PMID:LPS regulation of specific protein synthesis in murine peritoneal macrophages. 348 2

Protein synthetic patterns of murine peritoneal macrophages were analyzed by two-dimensional polyacrylamide gel electrophoresis (2D PAGE) of 35S methionine-labeled proteins. While the protein synthetic patterns exhibited by resident, inflammatory, and activated macrophages had numerous common features that distinguished them from the other normal non-macrophage cell types examined, unique proteins also characterized each macrophage population from the others. The accumulation by resident macrophages of proteins 23, 25, and 37 distinguished them from elicited cells, as did the former's more abundant synthesis of proteins 54 and 52. The protein synthetic patterns of inflammatory thioglycollate- and proteose peptone-elicited macrophages were strikingly similar, save for the former's greater levels of accumulation of proteins 14 and 28, and the latter's more pronounced expression of p23.5. Peritoneal macrophages elicited by treatment with heat-killed Propionibacterium acnes, the live, attenuated Mycobacterium bovis strain BCG, Listeria monocytogenes, and the protozoan flagellate Trypanosoma rhodesiense, all exhibited tumoricidal activity in 16-h or 72-h functional assays. They shared a common protein synthetic profile that differentiated them from the synthetic patterns characteristic of the non-tumoricidal resident and inflammatory macrophages. These tumoricidal macrophages were unique in synthesizing a protein(s) of approximate molecular weight 26,000 daltons. A time-course study employing P. acnes-activated peritoneal macrophages indicated that p26 accumulation decayed with tumoricidal capacity as a function of time in culture, although no direct correlation between lytic activity and p26 expression could be definitively established. Peritoneal macrophages elicited with proteose peptone were not directly tumoricidal but were rendered so upon in vitro treatment with nanogram amounts of bacterial lipopolysaccharide. The accumulation of low levels of p26 by the newly explanted proteose peptone-elicited macrophages suggests the possibility that this protein characterizes macrophage populations primed as well as triggered for tumoricidal activity.
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PMID:Differential protein synthesis by murine peritoneal macrophages elicited by various stimuli. 349 10

Tumor necrosis factor (TNF) was detected in the sera of normal mice, unprimed by reticuloendothelial system (RES) stimulators, when such mice were injected with lipopolysaccharide (LPS). Amounts of TNF were approximately 200-fold less than those found in Corynebacterium parvum-primed mice. No TNF activity was detected in the sera of mice not administered LPS. TNF induction in unprimed mice was refractory to repeated administration of endotoxin, thus exhibiting a tolerance phenomenon. TNF produced in unprimed mice eluted similarly to Mycobacterium bovis, strain BCG-primed TNF on Sephacryl S-200 and DEAE Sephacel columns and was neutralized by rabbit antisera raised to partially purified BCG-primed TNF. When BALB/c mice having 7-day old subcutaneous Meth A tumor implants were administered TNF antiserum, endotoxin-induced hemorrhagic necrosis was largely prevented. These findings strongly suggest that endotoxin-induced hemorrhagic necrosis of tumors is mediated through TNF production and action.
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PMID:Production of tumor necrosis factor in unprimed mice: mechanism of endotoxin-mediated tumor necrosis. 352 51


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