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 accumulating that the illness and pathology observed in malaria are not caused directly by parasite products, but by normal components of the immune response, mainly monokines such as tumor necrosis factor (TNF), produced in excess. These mediators are released from the host's monocytes and macrophages, apparently in response to stimulation by parasite products. Recombinant TNF, if injected into a range of animal species or into tumour patients, is demonstrably toxic, giving rise to changes typical of acute malaria, and several groups have detected circulating TNF in serum from patients acutely ill with malaria. The short serum clearance time of TNF and TNF tolerance have to be considered when interpreting such data. Current studies indicate that some malarial antigens, in the absence of lipopolysaccharide, can trigger release of TNF. This and other monokines could contribute to cerebral malaria in at least 2 ways: by increasing thrombospondin secretion, and hence favouring local sequestration of knob-bearing parasitized red cells, and, as has been demonstrated in clinical trials in tumour patients, by causing neurological symptoms directly. In addition, it seems that TNF does not act alone, but as part of an interdependent synergizing network of polypeptide mediators. These evidently act together to induce secretion of other cell products, such as platelet-activating factor, prostaglandins, reactive oxygen species and procoagulant activity, that actually cause illness, biochemical change and tissue damage. Understanding these processes should lead to a range of new therapeutic interventions.
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PMID:Roles of tumour necrosis factor in the illness and pathology of malaria. 269 75

Gram-negative and gram-positive bacteria were found to display different sensitivities to pure singlet oxygen generated outside of cells. Killing curves for Salmonella typhimurium and Escherichia coli strains were indicative of multihit killing, whereas curves for Sarcina lutea, Staphylococcus aureus, Streptococcus lactis, and Streptococcus faecalis exhibited single-hit kinetics. The S. typhimurium deep rough strain TA1975, which lacks nearly all of the cell wall lipopolysaccharide coat and manifests concomitant enhancement of penetration by some exogenous substances, responded to singlet oxygen with initially faster inactivation than did the S. typhimurium wild-type strain, although the maximum rates of killing appeared to be quite similar. The structure of the cell wall thus plays an important role in susceptibility to singlet oxygen. The outer membrane-lipopolysaccharide portion of the gram-negative cell wall initially protects the bacteria from extracellular singlet oxygen, although it may also serve as a source for secondary reaction products which accentuate the rates of cell killing. S. typhimurium and E. coli strains lacking the cellular antioxidant, glutathione, showed no difference from strains containing glutathione in response to the toxic effects of singlet oxygen. Strains of Sarcina lutea and Staphylococcus aureus that contained carotenoids, however, were far more resistant to singlet oxygen lethality than were both carotenoidless mutants of the same species and other gram-positive species lacking high levels of protective carotenoids.
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PMID:Comparison of killing of gram-negative and gram-positive bacteria by pure singlet oxygen. 270 69

We tested the hypothesis that lipopolysaccharide (LPS) leads to an imbalance between mesenteric oxygen delivery (DO2) and gut metabolic demand for oxygen, even when cardiac index (CI) is within the normal range. Two groups of pentobarbital-anesthetized pigs (13 to 17 kg) were studied. The first group (LPS; n = 9) was infused over 20 min with Escherichia coli LPS (100 micrograms/kg) and resuscitated with normal saline (1.2 ml/kg.min). The second group (NS; n = 5) was not infused with LPS, but was resuscitated in the same way as the LPS group. Superior mesenteric arterial (SMA) blood flow and ileal intramucosal hydrogen ion concentration, [H+], were determined using a Doppler-shift probe and a tonometric catheter, respectively. Infusing LPS did not affect CI, although mean arterial pressure and systemic vascular resistance were significantly reduced. SMA flow and mesenteric DO2 decreased significantly in the LPS group. Although mesenteric oxygen utilization was well preserved in both groups, ileal intramucosal [H+] was significantly higher in endotoxic animals. These data support the idea that mesenteric oxygen consumption is flow-limited in this clinically relevant porcine model of septic shock.
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PMID:Effect of lipopolysaccharide on intestinal intramucosal hydrogen ion concentration in pigs: evidence of gut ischemia in a normodynamic model of septic shock. 273 25

We have studied a murine macrophage cell line, J774, and found these cells capable of a zymosan-triggered chemiluminescent oxidative burst. Such activity was enhanced by preincubation with Corynebacterium parvum (CP), bacillus Calmette-Guerin, and lipopolysaccharide (LPS). Under similar conditions, CP and LPS were shown to enhance J774-mediated tumor cell lysis. We have also demonstrated that murine interferon alpha + beta rendered J774 cells more sensitive to the actions of CP and LPS. These results indicate that J774 cells may be useful for the in vitro evaluation of biological response modifiers as well as the study of oxygen radical production by macrophages.
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PMID:Chemiluminescence in a macrophage cell line modulated by biological response modifiers. 274 37

Rhizobium leguminosarum bv. viciae 3841 was grown in liquid suspension culture to investigate how culture conditions could affect the expression of a developmentally regulated cell surface antigen associated with lipopolysaccharide. The antigen, which is recognized by monoclonal antibody AFRC MAC 203, was expressed when cultures were grown at neutral pH under low-oxygen conditions (less than 7.5% [vol/vol] O2 in the gas phase). Antigen was also expressed in aerobically grown cultures at pH values below 5.3. The nature of the nitrogen and the carbon sources had no effect on antigen expression except by indirect changes on the pH of the culture medium; similarly, growth in 0.3 M NaCl did not result in antigen expression. The induction of MAC 203 antigen by low-oxygen or low-pH culture conditions is discussed in the context of tissue-specific expression within the legume root nodule.
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PMID:Expression of a cell surface antigen from Rhizobium leguminosarum 3841 is regulated by oxygen and pH. 276 81

This study addresses macrophage activation in guinea-pigs vaccinated with radiation-attenuated cercariae of Schistosoma mansoni. Peritoneal exudate macrophages elicited in vaccinated animals by mineral oil injection were activated to kill larval schistosomes in vitro. Killing efficiency is dependent upon the cell: target ratio employed and is enhanced by, but is not strictly dependent on, the presence of specific antibodies. Macrophages co-cultured with parasites release superoxide radicals and hydrogen peroxide, but the use of inhibitors has shown that neither of these reactive oxygen intermediates are the causal agents of cellular cytotoxicity in this system. Oil-elicited macrophages from naive guinea-pigs do not show comparable activation; they can, however, be activated in vitro by incubation with culture supernatant fluids from schistosome antigen-stimulated spleen, or lymph node cells harvested from vaccinated guinea-pigs. Naive macrophages activated in this way kill schistosomula in vitro and release the activation markers IL-1 and superoxide anion. The macrophage-activating factor (MAF) present in spleen cell culture supernatant fluids has a MW of 35,000-55,000, but does not have the chemical characteristics of gamma-interferon. In this study MAF is shown to be released by a population of lymph node cells that does not adhere to nylon-wool columns, that responds well in proliferation assays to schistosome antigens and to the T-cell mitogen concanavalin A, but does not respond to the B-cell mitogen lipopolysaccharide. These cells have been identified as small lymphocytes.
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PMID:Immunity to Schistosoma mansoni in guinea-pigs vaccinated with radiation-attenuated cercariae. T-cell activation of macrophages for larval killing. 283 8

Neutrophils (polymorphonuclear leukocytes [PMNs]) are thought to contribute to the pathophysiology of adult respiratory distress syndrome (ARDS) by the release of toxic oxygen metabolites. This study investigated superoxide production by circulating and bronchoalveolar lavage (BAL) PMNs in a rat model of ARDS induced by chronic Escherichia coli (lipopolysaccharide) endotoxemia. Superoxide production was stimulated by fmet-leu-phe, opsonized zymosan, and phorbol myristate acetate. Circulating and BAL PMNs from lipopolysaccharide-infused rats compared with PMNs from control rats are primed for nonselective increased superoxide production. The BAL PMNs are not only partially primed to release superoxide on adherence, they concomitantly have a depressed superoxide response to a phagocytic (opsonized zymosan) stimulus. These PMN responses may partially explain both the pulmonary injury and the increased susceptibility to pulmonary infection seen in patients with ARDS.
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PMID:Superoxide production by neutrophils in a model of adult respiratory distress syndrome. 284 86

The physiological significance of the enzyme indoleamine 2,3,-dioxygenase (IDO) (EC 1.13.11.17), which consumes superoxide anion (O2-), is not known. Since this enzyme is found in high concentrations in lung tissue, we examined the possibility that IDO may protect against chemically induced oxidative stress in the lung. The induction of IDO by bacterial lipopolysaccharide (LPS) was found to be 20-fold in the mouse and 4-fold in the rat, but did not confer protection against paraquat-induced pulmonary toxicity. Moreover, paraquat, when dosed to rats or mice, did not induce pulmonary IDO activity. An elevation in the intracellular O2- concentration was sought by incubating lung slices with 5 mM diethyldithiocarbamate (DDTC) (to inhibit SOD), paraquat (10(-4) M), or methylene blue (10(-4) M) or under an atmosphere of 100% oxygen. These attempts did not enhance the IDO activity in lung slices prepared from control or LPS-treated rats and mice. There was also no evidence that the uptake of an IDO substrate, tryptophan, was limiting for IDO activity in rat and mouse lung slices. We have concluded in the case of rats and mice that the pulmonary IDO activity, even following induction, is too low for O2- to be the rate-limiting factor. For this reason IDO cannot act as a protective enzyme by scavenging O2- in the lung of these species. However, in the rabbit, a species comparatively resistant to paraquat- and oxygen-induced lung damage, pulmonary IDO activity is 170 times that of rats or mice. IDO activity in rabbit lung slices was increased 4-fold by incubation with 5 mM DDTC and 10-fold by incubation with methylene blue (10(-4) M). However, paraquat (10(-4) M and oxygen (100% atmosphere) were able to enhance IDO activity (5-fold) only when SOD had previously been inhibited. We have concluded that in the rabbit lung IDO is able to scavenge O2- and therefore has the potential to act as a protective enzyme in this species.
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PMID:Pulmonary indoleamine 2,3-dioxygenase activity and its significance in the response of rats, mice, and rabbits to oxidative stress. 284 33

Guinea pig Kupffer cells were obtained by partial digestion of the liver with pronase and collagenase and purified by centrifugal elutriation. Cells were kept in monolayer culture and their capacity to secrete superoxide anion in response to phagocytosis of zymosan was determined by the cytochrome c method. Compared to resident peritoneal macrophages, Kupffer cells produced somewhat less superoxide (60% +/- 30%). Both cell types were activated by 24 h preincubation with lipopolysaccharide from Salmonella minnesota or muramyl dipeptide to give twice as high a superoxide response to zymosan. The same effect was achieved when Kupffer cells in vitro were incubated for 3 days with supernatants from phytohaemagglutinin-activated peripheral T lymphocytes or recombinant gamma-interferon. These data demonstrate that the resident macrophages of the liver, the Kupffer cells, are able to increase their capacity to secrete reactive oxygen intermediates after proper activation; this fact is possibly important in the pathogenesis of hepatocyte damage upon inflammatory reactions in the liver.
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PMID:Guinea pig Kupffer cells can be activated in vitro to an enhanced superoxide response. I. Comparison with peritoneal macrophages. 285 90

We have tested the effects of hyperbaric oxygen on necrosis of rat liver induced by the administration of several toxins. The extent of liver necrosis was determined 24 h after the administration of the toxins by measurement of serum levels of alanine and aspartate amino-transferases and by histologic and ultrastructural analyses. Treatment with hyperbaric oxygen decreases carbon tetrachloride (CCl4)-induced necrosis in a manner dependent upon duration and pressure of oxygen exposure. Pretreatment of rats with phenobarbital diminishes this protective effect. Hyperbaric oxygen treatment before or immediately after CCl4 intoxication is protective. Loss of protection is rapid; hyperbaric oxygen treatment 6 h after CCl4 intoxication augments the liver necrosis. No delayed necrogenic effects of CCl4 are seen in the animals treated with hyperbaric oxygen immediately. Hyperbaric oxygen augments the liver necrosis induced by acetaminophen, bromobenzene, dimethylnitrosamine or thioacetamide. This augmented necrosis is averted by prolonged treatment with hyperbaric oxygen. Hyperbaric oxygen has no effect on liver injury induced by galactosamine or lipopolysaccharide. We conclude that hyperoxia decreases the hepatic necrosis induced by compounds which undergo reductive biotransformation by the cytochrome P-450 monooxygenase system; hyperoxia augments the necrosis induced by compounds which undergo oxidative biotransformation by this system. Biotransformation of toxins appears to be nonspecifically inhibited by hyperoxic exposure of long duration.
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PMID:Effect of hyperoxia on liver necrosis induced by hepatotoxins. 287 23


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