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)

Natural killer (NK) cells are a subpopulation of lymphocytes capable of killing a variety of tumor targets. They can limit pulmonary metastases in vivo and thus might be important effectors of tumor defense in human lung. Lymphocytes were purified from whole lung specimens obtained from patients with lung cancer undergoing curative resection, and their NK activity was compared with that of lymphocytes purified from normal lung specimens obtained from cadavers undergoing medicolegal autopsy. The NK activity of pulmonary lymphocytes obtained from the patients with lung cancer was significantly lower (p less than 0.05) than the NK activity of normal lungs. This reduction occurred despite high levels of blood NK activity in the patients with cancer, suggesting that NK cells might be locally suppressed in the lungs of patients with bronchogenic carcinoma. Because human pulmonary macrophages (PM) are known to be potent inhibitors of NK function, we investigated the role that PM might play in the reduction of NK activity in these patients. The PM obtained from the patients with lung cancer released soluble inhibitors of NK activity when stimulated with lipopolysaccharide. Release of these inhibitors was blocked by indomethacin, strongly suggesting a role for arachidonic acid metabolites as an inhibitor of pulmonary NK function. Inhibition of NK function by PM may occur in vivo, as a significant inverse correlation (r = -0.71, p less than 0.001) existed between the NK activity of lymphocytes obtained from a lung and the number of PM present in the lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary natural killer cell activity is reduced in patients with bronchogenic carcinoma. 359 8

Fibrin deposition in the microenvironment of tumor cells may be critical to tumor growth and metastasis formation. Procoagulant activities of tumor cells themselves, or of infiltrating macrophages, activated by the host's immune system to the tumor, may both contribute to coagulopathies associated with metastases. Lymphokine (LK) supernatant activated procoagulant activity on normal peripheral blood monocytes but failed to induce activity on mononuclear cells from 18/22 patients with locally advanced or disseminated non-lymphoid tumors. Monocytes from the remaining patients had very low basal levels of MPCA and were less sensitive than normal cells to LK. Monocytes from 4 patients (3 with tumors with a high growth fraction) had extremely elevated levels of basal procoagulant activity, possibly due to maximal activation in vivo. Neither LK nor bacterial lipopolysaccharide (LPS) stimulated procoagulant production of these cells. By contrast, cells from 8/13 patients produced procoagulant in response to LPS. This study indicated that monocyte function of patients with disseminated cancer is suppressed with respect to LK stimulation, but that cells with normal basal levels of MPCA respond to LPS. Preactivation of mononuclear procoagulant in vivo precluded subsequent stimulation by either LPS or LK.
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PMID:Lymphokine-induced monocyte procoagulant activity is depressed in patients with advanced malignancies. 369 30

Pasteurellosis in the rabbit inoculated with a malignant variant of Shope fibroma virus (SFV-MV) is presented as a model for the study of immunosuppression and immunoprophylaxis in pasteurellosis. The rabbits, before the inoculation, were healthy carriers of Pasteurella multocida. They were intradermally inoculated with SFV-MV, and 3 to 6 days later, a primary tumor appeared at the site of inoculation. By postinoculation day (PID) 7 or 8, the rabbits had snuffles, conjunctivitis, and tumor metastases; death occurred on PID 10 to 14. Rabbits given the nonmalignant Patuxent strain of SFV developed local primary tumors, but not pasteurellosis nor metastases. In SFV-MV-inoculated rabbits, there was decreased responsiveness of spleen lymphocytes to B and T cell mitogens by day 6, and of spleen and peripheral blood lymphocytes by day 10. In addition, SFV-MV antigen was detected (by immunofluorescence) in mononuclear phagocytes in all major organs and in epithelial cells of the conjunctiva and nasal mucosa. Both nasal and conjunctival epithelia showed squamous metaplasia as well. These changes did not appear in SFV-infected rabbits. With SFV-MV-inoculated rabbits, we obtained partial protection against pasteurellosis by immunization with heat-killed P multocida or a cross-protective core lipopolysaccharide mutant of Escherichia coli (J5). Rabbits were immunized before the inoculation with SFV-MV which precipitated "spontaneous" pasteurellosis due to impaired defenses. Rabbits immunized with J5 or P multocida had less severe conjunctivitis and snuffles than nonimmunized controls, indicating that immunization with the J5 mutant may be useful as prophylaxis against pasteurellosis in compromised hosts.
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PMID:Immunity to pasteurellosis in compromised rabbits. 630 88

Murine Kupffer cells (RC) were isolated in sufficient number and purity to allow in vitro investigations of their tumoricidal capabilities. The identity of the adherent cells as KCs was established by morphologic, histochemical, and functional criteria. The yield of KCs varied from young (high) to old (low) mice but was not affected by the mouse strain. KCs activated in vitro by either endotoxins (lipopolysaccharide) or lymphokines were rendered highly cytotoxic against syngeneic melanoma or fibrosarcoma target cells. These studies indicate that KCs may indeed play a role in destruction of tumor cells in vivo and thus be important in host defense against developing hepatic cancer metastases.
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PMID:In vitro activation of murine Kupffer cells by lymphokines or endotoxins to lyse syngeneic tumor cells. 639 Nov 88

It has been reported that treatment with cimetidine, a histamine H2-receptor antagonist, increased survival and decreased the number of lung metastases in mice bearing the Lewis Lung carcinoma [29]. It was suggested that this effect was due to the ability of cimetidine to block histamine activation of suppressor lymphocytes and hence allow host defence mechanisms to inhibit tumour growth. In the present studies, C3H/He mice were implanted with a C3H mouse mammary adenocarcinoma on Day 0. This tumour metastasizes to the lungs in 30-50 days. Primary tumours were ablated with X-rays when they had grown to about 0.2 g and animals were given drinking water with or without cimetidine (10 mg ml-1) until the end of the experiment. Cimetidine reduced the number of mice dying from metastatic disease from 7/15 (controls) to 3/13. Cimetidine treatment also prolonged survival of mice that did succumb to metastatic disease by about 12 days. The response of spleen lymphocytes to the mitogens phytohaemagglutinin and lipopolysaccharide was assessed in vitro by uptake of 3H-thymidine 0, 16, 45 and 58 days after tumour implantation. Lymphocyte responsiveness was depressed by tumour burden. The influence of cimetidine treatment was equivocal being dependent upon time after tumour implantation and dose of mitogen. In this mouse-tumour system, the mechanism of the antimetastic effect of cimetidine is different from that previously suggested [29].
Clin Exp Metastasis
PMID:Antimetastatic effect of cimetidine on mice bearing a C3H mouse mammary adenocarcinoma: survival and lymphocyte function studies. 654 88

Four types of macrophage activities were studied in sarcoma 180-bearing ICR mice and EL4-bearing C57BL mice. Sarcoma 180 cells grow very slowly and do not metastasize, while EL4 cells grow very rapidly and metastasize rapidly to the liver. Chemotactic activity of macrophages was significantly reduced from an early stage in both sarcoma 180-bearing ICR mice and EL4-bearing C57BL mice as compared with that in normal mice. Digestive activity, which was determined by following O2- production by chemiluminescence measurements was also reduced from an early stage in tumor-bearing mice, whereas no reduction of engulfment activity of microorganisms was observed until an advanced stage in both sarcoma 180-bearing mice and EL4-bearing mice. In contrast enhancement activity of macrophages in the blastogenic response of spleen lymphocytes to bacterial lipopolysaccharide was retained at the normal level at the early stage of the tumor graft and was reduced in later stages. These results suggest that activities of Ia-negative macrophages were at first depressed generally in tumor-bearing hosts and later the activities of Ia-positive macrophages were depressed by factor(s) which might be produced by tumor cells.
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PMID:Macrophage activities in sarcoma 180-bearing mice and EL4-bearing mice. 674 90

Antitumour, antileukosis and antimetastatic effects of lipopolysaccharide (LPS) isolated from Pseudomonas solanacearum have been studied. It is established that LPS does not possess the antitumour effect on experimental animals with Lewis lung carcinoma, melanoma B-16 and sarcoma S-37 and vice versa, intensifies the tumour growth. The life time of animals with experimental leukoses lymphocytic leukemia P-388 and lymphoid leukemia L 1210 inconsiderably increases. At the same time LPS possesses the expressed antimetastatic effect that has manifested in the decrease of the volume (40 and 5 times) and of the amount (4-4.2 times) of metastases in mice with Lewis lung carcinoma and melanoma B-16, respectively. Study of the contribution of certain structural components of LPS molecule to the total biological activity has shown that O-specific polysaccharide and oligosaccharide of core take the expressed antimetastatic effect. Lipid A in the used dose weakly modified the development of Lewis lung carcinoma metastases.
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PMID:[The biological activity of Pseudomonas solanacearum polysaccharide]. 766 47

To establish an efficient cell-culture system for adoptive immunotherapy, we attempted to use lipopolysaccharide(LPS)-activated B cells (LPS blasts) as costimulatory-signal-providing cells in the in vitro induction of antitumor effector cells. Both normal and tumor-draining lymph node cells were efficiently activated by both anti-CD3 monoclonal antibody (mAb) and LPS blasts, and subsequently expanded by a low dose of interleukin-2 (IL-2; anti-CD3 mAb and LPS blasts/IL-2). The expanded cells were predominantly CD8+ T cells and showed a low level of tumor-specific cytotoxic T lymphocyte (CTL) activity. The adoptive transfer of B16-melanoma-draining lymph node cells expanded by anti-CD3 mAb and LPS blasts/IL-2 showed significant antitumor effect against the established metastases of B16 in combination with intraperitoneal injections of IL-2. This treatment cured all B16-bearing mice. In addition, these mice also showed tumor-specific protective immunity against B16 at the rechallenge. Considering that activated B cells express several kinds of costimulatory molecules, these findings thus indicate an efficacy of costimulation that is derived from activated B cells for the in vitro induction of tumor-specific CTL, in co-operation with anti-CD3 mAb. The culture system presented here may thus be therapeutically useful, providing potent effectors for adoptive immunotherapy against various types of cancer.
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PMID:The antitumor effect of tumor-draining lymph node cells activated by both anti-CD3 monoclonal antibody and activated B cells as costimulatory-signal-providing cells. 772 76

A syngeneic in vitro system was developed for investigation of the binding of purified murine interleukin-2 (IL-2) activated natural killer (A-NK) cells to murine microvascular endothelial cells. This system is potentially useful as a model to investigate biochemical and molecular events underlying the binding of A-NK cells to microvascular endothelial cells within metastases in vivo that we have previously noted using electron microscopy. A-NK/endothelial cell binding in the syngeneic system was compared with the binding of allogeneic A-NK cells to the endothelial cells. Among test agents used to pretreat the A-NK cells for modulation of binding, lipopolysaccharide (LPS) most consistently enhanced binding. Additionally, test agents were also used in concurrent assays of A-NK cytolytic activity versus YAC-1 and P815 tumor cell targets. Polyinosinic: polycytidylic acid (poly IC), and gamma interferon (gamma IFN) were among the test agents which enhanced A-NK cell cytolytic activity.
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PMID:Interleukin-2 (IL-2) activated natural killer (A-NK) cells: binding to microvascular endothelial cells and BRM enhancement of cytolytic activity. 805 14

This study examined the ability of the recombinant human interleukin 1 receptor antagonist (IL-1ra) to block interleukin 1 (IL-1)-mediated experimental metastases from the A375M human melanoma. In vivo, IL-1ra administrated at concentrations > or = 200 times IL-1 significantly inhibited the increase in lung colonies induced by IL-1 in nude mice. The response to IL-1 was significantly inhibited when IL-1ra was administered simultaneously with or 1 to 3 h before IL-1. In vitro, the incubation of IL-1-activated endothelial cells with IL-1ra prevented the increase in adhesion of A375M melanoma cells. At the same experimental conditions, IL-1ra inhibited the augmented expression of the intracellular and vascular cell adhesion molecules 1 and E-selectin induced by IL-1 on endothelial cells. Lipopolysaccharide, an IL-1 inducer, increased the number of lung colonies in nude mice. IL-1ra injected with or 1 h after lipopolysaccharide inhibited this augmentation, suggesting a role for host-produced IL-1 in metastasis formation.
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PMID:Interleukin 1 receptor antagonist inhibits the augmentation of metastasis induced by interleukin 1 or lipopolysaccharide in a human melanoma/nude mouse system. 826 95


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