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Query: UNIPROT:P43026 (
lipopolysaccharide
)
62,215
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Studies were conducted to compare the interferon (IFN) production of four strains of mice when injected with Newcastle disease virus (NDV), polyinosinic-polycytidylic acid (poly I. C),
lipopolysaccharide
(
LPS
) or purified protein derivative (PPD). When injected with NDV, C57BL/6 and DDD mice generated higher levels of IFN than BALB/c and C3H/He mice. Upon injection with poly I. C or
LPS
, C57BL/6 and C3H/He mice produced higher levels of IFN than BALB/c and DDD mice. Differences in IFN production were also observed among
BCG
-sensitized mice of all four strains upon injection with PPD, C57BL/6 mice engendered the highest levels of IFN, while the C3H/He and DDD mice were intermediate in their response, with the BALB/c mice producing the least amount of IFN.
...
PMID:Strain differences in the production of mouse interferon. 620 87
Comparative studies on tumor and adjuvant-induced depression of in vitro mitogen responses were carried out using spleen cells obtained from syngeneic tumor bearing (TB) ACI rats or from rats which had been immunized with
BCG
cell walls attached to oil droplets (BCGcw). These in vitro studies demonstrated that: 1) the spleen cells from TB rats (TB-spleen cells) showed strongly depressed mitogen responses to concanavalin-A (Con-A), phytohemagglutinin-P (PHA-P) and
lipopolysaccharide
(
LPS
), 2) the mitogen response of lymph node cells from TB rats was slightly depressed, 3) the removal of plastic or nylon-wool adherent cells or phagocytic cells from TB-spleen cells resulted in a restoration of the mitogen response, 4) the Con-A response of normal spleen cells could be suppressed by the addition of TB-whole spleen cells, 5) the suppressor cell activity was not abrogated by the in vitro treatment with x-irradiation (2000 rads), 6) carbonyl-iron treated TB-spleen cells showed a normal level of mitogen response, and on addback to normal spleen cells no suppressive activity was detected in them. Similar results were observed when spleen cells were obtained from BCGcw immunized rats. These results suggest that in ACI rats tumor-induced nonspecific suppressor cells detected by in vitro assay are the same cell populations as BCGcw-induced nonspecific suppressor cells.
...
PMID:Comparative studies on tumor and adjuvant (BCGcw)-induced nonspecific suppressor cells in rats. 623 67
Sodium periodate (NaIO4) administered ip to mice was nontoxic and enhanced the in vitro tumoricidal activity of their peritoneal macrophages. The injection ip of 1 ml of 5 mM NaIO4 caused an influx of polymorphonuclear leukocytes (PMN) at 5-24 hours followed by an accumulation of macrophages and disappearance of the PMN at 48-72 hours. These peritoneal macrophages from mice given injections of NaIO4 were noncytotoxic and nontumoricidal in the absence of
lipopolysaccharide
(
LPS
), but in the presence of 5-25 ng/ml or more
LPS
in vitro, they became markedly cytotoxic and cytocidal for tumor cells. Peritoneal macrophages from mice given injections of phosphate-buffered saline became cytotoxic or cytocidal only with amounts of
LPS
exceeding 100-500 ng/ml in vitro. Like the peritoneal macrophages from
BCG
-infected mice that demonstrated selective tumor cytotoxicity, macrophages from mice given injections of NaIO4 had minimal lytic activity for nontransformed normal embryo fibroblasts. Thus when given ip to mice, the simple chemical NaIO4, much like complex and heterogeneous biologic preparations such as
BCG
, caused differentiation of peritoneal macrophages toward the tumoricidal state.
...
PMID:In vivo modulation of macrophage tumoricidal activity: enhanced tumor cell killing by peritoneal macrophages from mice given injections of sodium periodate. 625 99
Antitumour polysaccharide lentinan, capable of potentiating T-cell dependent reactions and some other antitumour polysaccharides such as pachymaran, carboxymethyl-pachymaran and zymosan were found to induce vascular dilatation and hemorrhage(VDH) in CD-1 normal mice starting the following day after a single injection. Polysaccharides which do not have the tumour-regressing activity, several immunopotentiators such as
BCG
,
lipopolysaccharide
, dextran sulfate and concanavalin A, and chemical mediators of inflammation such as histamine, serotonin and prostaglandin E1 did not induce VDH in mice. This response seems to be mediated by T-cells and macrophages, because VDH was not observed in CD-1 nu/nu mice treated with lentinan, and carrageenan, an antimacrophage drug, inhibited the appearance of VDH by lentinan. Furthermore, carrageenan inhibited the production of the VDH-inducing serum which was caused by lentinan, capable of passively transferring VDH to another mouse.
...
PMID:T-cell mediated vascular dilatation and hemorrhage induced by antitumour polysaccharides. 633 43
Sera (
BCG
-
lipopolysaccharide
[LPS] serum) were obtained from mice infected with Mycobacterium bovis
BCG
2 h after intravenous administration of bacterial endotoxin (LPS). Varying concentrations of sera were added to cultures of Plasmodium falciparum-infected human erythrocytes; parasite viability was assessed by hypoxanthine incorporation after 4 days in culture. At concentrations of 1 to 3%, cultures treated with
BCG
-LPS serum showed a two- to threefold increase in hypoxanthine incorporation; at higher concentrations (4 to 8%), hypoxanthine incorporation fell to 2 to 5% of that in control cultures. Concurrent assays with control sera (from untreated mice or mice treated with
BCG
or LPS alone) caused some stimulation but no inhibition at up to 8% concentration. Examination of cultures treated with
BCG
-LPS serum showed morphological, deterioration of parasites within erythrocytes. The presence of tumor necrosis factor in the
BCG
-LPS serum was confirmed by using a standard L-cell cytotoxicity assay. In addition, rabbit antiserum against partially purified tumor necrosis factor protected intraerythrocytic forms of P. falciparum from the toxic effects of
BCG
-LPS serum. These data suggest that the factor in
BCG
-LPS serum that is toxic to P. falciparum in human erythrocytes is antigenically similar or identical to tumor necrosis factor. This nonantibody mediator of killing may play a role in human malaria.
...
PMID:Serum containing tumor necrosis factor is cytotoxic for the human malaria parasite Plasmodium falciparum. 635 1
There is significant evidence that the macrophage plays a critical role in the host's defense against neoplasia. Tumor-necrosis factor was recognized by Carswell et al. during a study of the antitumor activity of serum from mice infected with
BCG
and subsequently injected with endotoxin. The same procedure was applied to rabbits in order to obtain serum containing tumor-necrosis factor (TNF). Sera from these mice and rabbits contained a factor that induced hemorrhagic necrosis of certain mouse sarcomas in vivo and had cytotoxic effects on mouse and human tumor cells in vitro. Sera from mice and rabbits singly treated with
BCG
or endotoxin did not have these properties. Other agents such as C. parvum, OK-432, lentinan or zymosan, that cause hyperplasia of reticuloendothelial system and increase sensitivity to endotoxin lethality, could substitute for
BCG
in priming for TNF release. However, the use of P. acnes as a priming agent was the most effective and
lipopolysaccharide
from gram-negative bacteria appeared to be unique in its ability to elicit TNF release. TNF is a protein with a molecular weight, ranging from 40,000 to 60,000 that has both tumor necrotizing activity in vitro and tumor killing activity in vitro. It is relatively stable to heating at up 70 degrees C. This result indicated that both in vitro and in vitro activities of mouse and rabbit TNF are a property of one and the same molecule. TNF is thought to be produced by macrophage and is distinguished from the other know macrophage products in serum containing TNF. TNF is cytotoxic to several but not all tumor cell lines. Its most interesting feature is that it reportedly dose not affect any non-transformed cell types, implying that it somehow recognizes transformed cells.
...
PMID:[Definition of tumor-necrosis factor and its production mechanism]. 637
The conditions and kinetics of tumor necrosis factor (TNF) production were examined. For TNF production, dual stimulation is necessary. Priming agents such as
BCG
, Corynebacterium parvum, and zymosan, which can stimulate the reticuloendothelial system (RES), are good substances for TNF production with the aid of
lipopolysaccharide
. Wide differences are observed in TNF producibility among different priming agents. The producibility of TNF depends on the degree of stimulation of the RES by the priming agents. Those priming agents, e.g., Propionibacterium acnes and Corynebacterium anaerobium, that are able to induce substantial RES hyperplasia are also able to induce high levels of TNF activity. Following administration of large doses of
BCG
or zymosan, mice were found to produce TNF activity. However, PPD, OK 432, PSK, and Choreito were unable to induce TNF activity.
...
PMID:Role of first stimulating agents in the production of tumor necrosis factor. 639 57
This study was designed to explore the effects of acute nutritional deprivation (starvation) on macrophage function in mice. In vivo macrophage activity was increased by starvation, as determined by multiplication of Listeria monocytogenes in both spleens and livers after intravenous injection. Similarly, in vitro studies revealed that the capacity of peritoneal macrophages to kill listeria was enhanced by starvation. This function was increased further by the addition of small concentrations of
lipopolysaccharide
(LPS; 10-100 ng/ml). The bactericidal activity of macrophages from starved mice, however, did not reach the levels observed with macrophages from
BCG
-infected mice. Furthermore, LPS did not appear to be an important second signal for macrophage activation in vivo, as LPS-unresponsive mice (C3H/HeJ and A/J) were protected by starvation. In contrast to these results we found that starved mice were not protected against Toxoplasma gondii infection and that macrophages from starved mice were unable to prevent multiplication of toxoplasma trophozoites in vitro. In toto, these experiments suggest that macrophage function is enhanced by starvation, but that this enhancement is not sufficient to fulfill all criteria for macrophage activation.
...
PMID:Effect of acute nutritional deprivation on immune function in mice. I. Macrophages. 640 45
Purified
lipopolysaccharide
(
LPS
), isolated from
BCG
and purified protein derivative of tuberculin (PPD) were used as antigens in an enzyme-linked immunosorbent assay (ELISA) of sera from patients with malignant melanoma undergoing immunotherapy with
BCG
. It was found that
LPS
and ELISA are useful tools in the monitoring of humoral immune response against
BCG
.
...
PMID:Immunological monitoring of melanoma patients on BCG immunotherapy. I. Enzyme-linked immunosorbent assay of human sera after BCG-treatment. 647 16
Vertebrate lectin purified from loach egg was tested for induction of tumor lysis mediated by macrophages. Loach egg lectin lysed tumor cells but not normal spleen cells in cooperation with
BCG
- or glucan (TAK)-elicited peritoneal macrophages of mice. Corynebacterium parvum-, OK432-, glycogen-,
lipopolysaccharide
-elicited or resident macrophages were not effective. Neither loach egg lectin nor
BCG
nor glucan macrophages alone had a cytolytic action on tumor cells. Thus, the vertebrate lectin from loach egg is a mediator in macrophage-mediated tumor lysis, inducing binding of macrophages to target cells. This lectin-dependent macrophage-mediated cytolysis (LDMC) was inhibited by galactose, N-acetylgalactosamine, fucose, or rhamnose. These results suggest that tumor cells can be recognized via glycoconjugates on cell membrane in addition to tumor-associated antigen and that some animal lectins participate in macrophage-mediated tumor lysis.
...
PMID:Macrophage-mediated tumor lysis induced by loach egg lectin. 658 20
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