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)

We examined the effect of purified human C-reactive protein (CRP) on induction of human peripheral blood monocyte (Mo)-mediated cytotoxicity (CTX) and oxidative metabolism. Exposure of Mo to acute phase serum levels of CRP in vitro resulted in dose-dependent expression of CTX against human tumor cell lines. Nonneoplastic human fibroblasts and glial cells were not affected by CRP-exposed Mo, and treatment of Mo monolayers with anti-Leu 11b (a natural killer marker) and complement did not abrogate or diminish CTX. Tumoricidal activity was observed after 20-44 h of Mo exposure to CRP, and after 48-72 h of coculture with radiolabeled target tumor cells. Mo exposed to CRP for 48 h also demonstrated elevated superoxide anion production when challenged with phorbol myristate acetate. Unlike CTX induced by lipopolysaccharide, CRP-induced CTX was completely inhibited by preincubation of CRP with phosphorylcholine, a CRP ligand, at a concentration of 5.5 molecules phosphorylcholine per molecule CRP. Further, when Mo medium (which contained 5% human AB serum) was preincubated with immobilized CRP, exposure of Mo to CRP in such medium did not result in CTX. In contrast, LPS-induced CTX was not affected. CRP-induced Mo CTX was observed, however, when Mo were exposed to CRP in medium preincubated with phosphorylcholine-treated immobilized CRP, suggesting that an active serum component which complexed with CRP was not removed. These findings indicate that one of the functions of the acute phase protein, CRP, may be to active Mo and that the process may require a CRP-binding serum component.
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PMID:Activation of human monocyte tumoricidal activity by C-reactive protein. 303 2

Acute-phase response of mRNAs for serum amyloid P component (SAP), C-reactive protein (CRP) and prealbumin was examined in C57BL/6 mouse liver by hybridization to specific cDNA probes. Although the level of SAP mRNAs in the unstimulated mouse was about one-tenth of that of CRP mRNAs, it increased up to 60-fold during the first 20 hr, and returned gradually to the original level at 69 hr after the administration of Escherichia coli lipopolysaccharide. On the other hand, the level of CRP mRNA rapidly increased up to 6-fold during the first 4 hr, and reverted to the original level as early as at 20 hr. In contrast, the level of mRNA for prealbumin decreased to about 0.5-fold during the first 20 hr, recovered and increased up to 1.6-fold of the original level during 32 to 69 hr.
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PMID:Acute-phase response of mRNAs for serum amyloid P component, C-reactive protein and prealbumin (transthyretin) in mouse liver. 304 57

In previous reports, we have shown that purified human C-reactive protein (CRP) enhances tumoricidal activity of murine macrophages and human blood monocytes. In the present study, we wished to determine whether CRP induced similar activity in human macrophages. We evaluated the effect of CRP on the generation of in vitro tumoricidal activity in alveolar macrophages from 24 normal volunteers, among whom 10 were smokers and 14 were nonsmokers. CRP, in concentrations comparable with those found in blood during acute inflammation, induced dose-dependent cytotoxicity in nonsmoker alveolar macrophages against tritiated thymidine-labeled human tumor cells. Tumoricidal responses of smoker and nonsmoker macrophages did not significantly differ after exposure to lipopolysaccharide although smoker responses tended to be lower. Responses to CRP, however, were significantly (p less than 0.01) depressed in smokers. These findings suggest that during acute inflammation, CRP may enhance the tumoricidal properties of human alveolar macrophages. Macrophage responsiveness to CRP, however, appears to be detrimentally affected by smoking.
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PMID:Modulation of human alveolar macrophage tumoricidal activity by C-reactive protein. 318 85

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

Purified C-reactive protein (CRP), the prototypical acute phase reactant of humans, activated inflammatory mouse macrophages to a tumoricidal state. The activation by CRP was not due to small amounts of contaminating lipopolysaccharide. CRP at 10 micrograms/ml induced significant tumoricidal capacity in resident macrophages; the mouse macrophage cell lines PU5 1.8, RAW 264.7, and J774; as well as elicited macrophages from two lipopolysaccharide nonresponder strains, C3H/HeJ and C57BL/10Sc. Macrophages obtained from bone marrow-derived monocytes grown in vitro and exudate macrophages depleted of T-cells were also readily activated by microgram/ml amounts of CRP. Removal of CRP from culture medium using anti-CRP antibodies or phosphorylcholine-agarose beads abrogated the induction of tumoricidal activity. CRP acted independently of both lymphokines and lipopolysaccharide. Therefore, CRP may serve as a physiologically relevant macrophage activator, contributing to the heightened nonspecific host resistance associated with the early stages of a systemic inflammatory response.
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PMID:Macrophage tumoricidal activity induced by human C-reactive protein. 348 21

A number of the activities currently ascribed to the mediator interleukin 1 (IL-1) are relevant to chronic inflammatory bowel disease. Using the mouse thymocyte stimulation assay, lymphocyte-activating factor (LAF) activity was measured in plasma samples and supernatants from cultures of peripheral blood mononuclear cells from 16 patients with Crohn's disease, six with ulcerative colitis, and 10 healthy subjects. Results were compared with disease activity, drug therapy, granulocyte count, and plasma levels of zinc and C-reactive protein (CRP). Very low levels of LAF were detected in a few plasma samples from each of the subject groups. Mononuclear cells from healthy subjects produced LAF only when cultured with lipopolysaccharide, but stimulated cells from patients produced greater amounts. Moreover, cells from six patients with Crohn's disease, not receiving steroids, produced LAF spontaneously. Crohn's disease patients also had low plasma zinc but elevated levels of CRP and granulocytes. This enhanced production of LAF in vitro may reflect a primary cellular defect in Crohn's disease, or a secondary consequence of monocyte activation.
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PMID:Interleukin 1 in Crohn's disease. 349 97

The toxicity by inhalation of various gram-negative bacteria, isolated from settings associated with inhalation disease, was studied by a variety of means. These microorganisms were not equally toxic. Citrobacter freundii aerosol challenges of rabbits provoked significant (up to fivefold) increases in plasma haptoglobin 24 to 48 h after inhalation. Other strains tested failed to provoke such statistically consistent increases. Measurements of C-reactive protein in these same animals did not lead to as reliable results, due to the variability of the responses. Mice responded differently to inhalation in that haptoglobin responses were either unaffected or depressed. When a strain of mice was used that exhibits more severe inflammatory responses to endotoxin (C3H/HeJ), C. freundii and Escherichia coli aerosols provoked significant haptoglobin increases. Free lung cell analyses demonstrated that the macrophage and neutrophil responses differed depending on the strain of bacteria used. Again, C. freundii induced the greatest responses. When murine B lymphocytes were stimulated with lipopolysaccharide preparations from different gram-negative bacteria, distinctly different dose-response curves were obtained. The types of responses obtained indicate that (i) brief inhalation of bacterial aerosols previously thought to be innocuous may lead to pulmonary inflammation, and (ii) that these bacteria differ in their toxicity, with C. freundii being the most toxic organism of the five studied.
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PMID:Differential toxicity of inhaled gram-negative bacteria. 633

The acute phase reactant of mice, serum amyloid P-component (SAP), was purified and separated from C-reactive protein (CRP). The purified SAP is composed of identical M, 31 Kd polypeptide subunits, determined by SDS-PAGE. SAP levels increased five-fold by 24 hr after challenge with lipopolysaccharide (LPS) or thioglycollate. This response closely correlated with blood monocytosis and required new macromolecule (protein + RNA) synthesis and secretion by the liver. The induction of the SAP response was adoptively transferred by a serum factor produced in optimal concentrations only 90 min after an inflammatory stimulus, which preceded a detectable increase in SAP. A potent SAP inducer was identified in culture supernatants of LPS-activated macrophages. The rapid induction of SAP synthesis in LPS-unresponsive C3H/HeJ mice was dependent on the amount of lymphocyte-activating factor, LAF(IL 1), present in the macrophage culture supernatants. Partially purified human IL 1 also induced a rapid increase in SAP. Thus the induction of SAP in mice appears to be mediated by a product of macrophages, a cell population that is also expanded as part of the systemic inflammatory response.
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PMID:Acute phase reactants of mice. I. Isolation of serum amyloid P-component (SAP) and its induction by a monokine. 680 78

1. Mean monthly serum levels of total protein, C-reactive protein (CRP) and serum amyloid P component (SAP) in plaice, showed no significant difference between the sexes. 2. Highest values for CRP and protein were found between June and September, with no significant seasonal variation in SAP. 3. There was no change in CRP concentration in plaice maintained for 7 days at a higher temperature of 18.5 degrees C. 4. Injection of lipopolysaccharide caused the highest value for CRP on day 1 and for the spleen index on day 5 after injection. 5. Phagocytic stimulation with carbon had no significant effect on the CRP response to endotoxin.
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PMID:Serum concentrations of C-reactive protein and serum amyloid P component in plaice (Pleuronectes platessa L.) in relation to season and injected lipopolysaccharide. 683 14

The acute-phase plasma protein response to disease activity in murine models of autoimmune lupus-like disease was investigated by measurement of the concentration of serum amyloid P component (SAP) in NZB X W and MRL/l mice. The levels of SAP, which is a major acute-phase protein in mice, did not rise at all in response to progression of disease in NZB X W mice between the ages of 1 and 9 mo. This resembles the behavior of acute-phase proteins such as C-reactive protein and serum amyloid A protein in human systemic lupus erythematosus, and just as in human lupus, where the occurrence of intercurrent microbial infection can stimulate an acute-phase response, so injection of bacterial lipopolysaccharide or casein into the NZB X W mice stimulated "normal" acute-phase SAP production. In marked contrast, MRL/l mice developed greatly increased levels of SAP, which correlated closely with progression of their pathology as they aged. The disease profile of the MRL/l strain includes rheumatoid factors and spontaneous polyarthritis and their SAP response resembles the behavior of acute phase proteins in human rheumatoid arthritis. Different patterns of acute-phase response in different autoimmune disorders may thus be a reflection of the genetic predisposition to particular diseases and/or contribute to their pathogenesis. The existence of animal counterparts for the various clinical patterns of human acute-phase protein production will assist in experimental investigation of the underlying mechanisms and of the biological role of the acute-phase response.
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PMID:The acute-phase response in (NZB X NZW)F1 and MRL/l MICE. 715 12


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