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PubMed1983

Lipopolysaccharide-mediated bovine endothelial cell injury in vitro.

Lipopolysaccharide (LPS) produced time- and dose-dependent bovine endothelial cell injury in vitro that was manifested initially by cell detachment from culture substrate with subsequent cell lysis. Bovine endothelial cell injury was observed with LPS derived from Salmonella minnesota R595, a LPS comprised only of lipid A and a trisaccharide core, as well as intact LPS preparations derived Escherichia coli and S. typhosa. LPS-mediated bovine endothelial cell detachment was prevented by incubation at 4 degrees C but was not prevented by indomethacin, lidocaine, chlorpromazine or trifluoperazine, methylprednisolone or p-bromophenacyl bromide, protease inhibitors, and catalase or superoxide dismutase. Of note, LPS-mediated injury was markedly enhanced by cycloheximide. Although augmented by serum, LPS-mediated bovine endothelial cell detachment was observed in C8-deficient serum and also in serum-free medium at higher LPS concentrations. Bovine aortic, pulmonary artery, mesenteric artery, and mesenteric vein endothelial cells were all sensitive to LPS at a concentration of 1 microgram/ml. In contrast, bovine aortic smooth muscle, human umbilical vein, goat aortic, and canine vena cava endothelial cells were unaffected by LPS at a concentration of 100 micrograms/ml. We conclude that the lipid A moiety of LPS mediates direct, complement-independent endothelial cell cytotoxicity and that this injury is not prevented by inhibitors of protein and prostaglandin synthesis, oxygen radical production, protease and phospholipase activity, and cytoskeletal function. Importantly, this direct LPS-mediated cytotoxic effect is dependent on the species from which the endothelial cells are derived.

Animals↗
PubMed1989

Prophylactic immunotherapy in newborn rat endotoxicosis.

The incidence and mortality of gram negative sepsis/septic shock remains high in newborns. In this paper, we postulated that prophylactic immunotherapy may be beneficial in newborn endotoxicosis. Lipopolysaccharide (LPS) tolerant rats were produced by serial Salmonella enteritidis LPS injections, and their sera were used for immunotherapy. Antiserum cotreatment blunted hypoglycemia and lactacidemia in S. enteritidis endotoxicosis and decreased the mortality. In 0-day-old rats, antiserum cotreatment groups had a decreased mortality when injected with S. enteritidis LPS (P less than .001), S. typhosa LPS (P less than .005), and Escherichia coli LPS (P less than .05). This global protection suggested that antibody to S. enteritidis LPS could be due to a common LPS antigen. Prophylactic antiserum administration to pregnant rats on the 18th day of gestation decreased the mortality of S. enteritidis endotoxicosis in 0-day-old rats (P less than .001). The prophylactic effects of antiserum was achieved by transplacental passage to the conceptus. We conclude that prophylactic as well simultaneous immunotherapy was beneficial in newborn rat endotoxicosis.

Animals↗
PubMed1970

Thrombosis prevention by acetylsalicylic acid in hyperlipemic rats.

In rats, administration of acetylsalicylic acid (ASA) by stomach tube two hours before blood removal, or addition of the drug to platelet-rich plasma in vitro, markedly inhibited platelet aggregation induced by thrombin, ADP and collagen. Addition of ASA in vitro to human platelet-rich plasma also inhibited platelet aggregation by thrombin, ADP and collagen. In hyperlipemic rats, ASA (100 to 200 mg./kg.), administered by stomach tube once or five times, markedly inhibited the production of thrombosis initiated by intravenous injection of S. typhosa endotoxin. In these experiments, thrombosis prevention by ASA was associated with both a decrease in platelet aggregation and an increase in the recalcification plasma clotting time.

Adenine Nucleotides↗
PubMed1961

Studies on infection and immunity in experimental typhoid fever. III. Effect of prophylactic immunization.

A study was made of the efficacy of various antityphoid immunizing agents in immunizing chimpanzees against typhoid fever produced by feeding viable S. typhosa. It was found that both acetone-killed and heat-killed, phenol-preserved typhoid vaccines were effective in protecting against infection induced with either homologous or heterologous strains of typhoid bacilli. Purified O antigen induced no discernible protection, but some immunity was afforded by the administration of purified Vi antigen.

Animals↗
PubMed1994

Anti-lipid A monoclonal antibodies and anti-LPS antiserum effects on limulus activity of LPS.

Anti-lipid A monoclonal antibodies (A78S1 and A523) and anti-LPS antiserum can decrease the mortality due to endotoxic shock in the newborn rat. However, in vitro LPS detoxification of anti-lipid A monoclonal antibodies is not known. Thus, we studied in vivo effects of A78S1 (IgG), A523 (IgM), and anti-LPS antiserum on Limulus activity. Anti-LPS antiserum decreased Limulus activity of S. enteritidis, E. coli and S. typhosa LPS. However, neither A78S1 nor A523 decreased the Limulus activity of E. coli and S. typhosa LPS. A78S1 or A523 incubation with S. enteritidis LPS at different doses (0.1 to 100 ng/ml) did not alter the Limulus activity. Perchloric acid treatment after LPS incubation with A78S1 or A523 significantly decreased Limulus activity. Therefore, antilipid A monoclonal antibodies (A78S1 and A523) can bind LPS, but do not decrease Limulus activity.

Animals↗
PubMed1975

Endotoxin binding by charged and uncharged resins.

Cholestyramine (Dowex 1-X2), a strongly basic anion-exchange resin, has previously been shown to bind bacterial endotoxin, preventing both its toxicity and intestinal absorption. Because hemoperfusion through charged and uncharged resins is practical, a study was undertaken to test the endotoxin-binding characteristics of a number of resins. The resin to be tested was washed and swelled overnight, and 1 mg/ml of 51Cr-labeled endotoxin was added and the mixture, agitated and incubated at 37 degrees for a specific time period. In the Dowex 1 series, the 1-X2 was superior to the 1-X4 and 1-X8 in its ability to bind E. coli endotoxin, removing about 90% from solution in 15 min. Increasing mesh size seemed to offer more binding sites for each Dowex 1 resin. Activated charcoal adsorbed about 90% of the endotoxin also, but Amberlite XAD-2 showed little binding capacity. Injection of filtrate from unlabeled E. coli and S. typhosa resin-treated solution into rats, demonstrated that both Dowex 1-X2 and activated charcoal prevented the transaminase rise noted in animals injected with solutions not so treated. It is concluded that Dowex 1-X2 resin and activated charcoal efficiently remove endotoxin in vitro, and may offer a unique method for removing circulating endotoxin in vivo.

Alanine Transaminase↗
PubMed1987

Activation of rat alveolar macrophages by gamma interferon to inhibit Toxoplasma gondii in vitro.

We have investigated the effects of murine interferons on the ability of rat alveolar macrophages (AM) to inhibit the proliferation of the intracellular protozoan Toxoplasma gondii. This activity was determined by measuring suppression of 3H-uracil uptake into the Toxoplasma and by microscopic enumeration of the intracellular organisms. Recombinant gamma interferon (rMulFN-gamma), but not alpha/beta interferon (IFN-alpha/beta) was able to activate AM for antimicrobial activity in vitro. Maximum activation was achieved by incubation with 50-200 units/ml rMulFN-gamma and the activity was lost at one unit/ml. The highest levels of activation were obtained when macrophages were incubated with interferon for 48-72 h prior to the challenge with Toxoplasma organisms. Activation could still be obtained, however, when the interferon was added to the cultures as late as 2 h after the phagocytosis of Toxoplasma. Neither MDP nor low concentrations (1-1-ng/ml) of S. typhosa lipopolysaccharide (LPS) were able to activate these cells to inhibit the growth of Toxoplasma. Phagocytosis of Toxoplasma by AM did not result in the release of O2-, in fact the spontaneous release of O2- by these cells was inhibited by Toxoplasma. This inhibition was reversed by preincubation of the cells with rMulFN-gamma.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMedDate not supplied

Fever produced by intrahypothalamic pyrogen: effect of protein synthesis inhibition by anisomycin.

In the unrestrained cat, the inhibition of protein synthesis by anisomycin, given either subcutaneously (5.0--25.0 mg/kg) or directly into the anterior hypothalamic, preoptic area (1.0--25.0 micrograms) impaired the development of a bacterial fever. S. typhosa infused intravenously (1:10 dilution in 1 ml) or into AH/POA (1.0 microliter) evoked an intense fever which was either significantly delayed or prevented by anisomycin. Conversely, anisomycin failed to affect the typical hyperthermia evoked by 100 ng PGE2 or 1.0--7.0 micrograms 5-HT similarly infused into AH/POA. These data demonstrate that an intermediary humoral factor of unknown nature is required in the hyperthermic effector pathway underlying the febrile response.

Animals↗
PubMed1987

[Distribution and typing in salmonellosis in children 1978-1983].

329 infants with salmonellosis were evaluated in Pediatric and Microbiology Department of Anadolu University Teaching and Training Hospital. It was established 127 (38.6%) S. typhimurium, 42 (12.8%) S. typhosa and 6 (1.8%) S. paratyphi A and B in our series. Besides these serotypes, 154 (46.8%) patients could not be typed. S. typhimurium was importantly noticed than other types (p less than 0.001) and this feature makes the distribution of typing of salmonellosis in children as characteristic. This infection was encountered especially between December (8.5%), it made peak in January (20.3%) and April (9.73%) period. Then, between April-December, this infections was established quite lower (p less than 0.001). This distribution is specific for Eskişehir district, and it was gradually decreased year by year (p less than 0.05).

Humans↗
PubMed1968

Endotoxin as adjuvator to the transplantation of a mouse mammary tumor.

The mouse mammary tumor MT 296 was used in a further series of experiments on the implantation of tumor, plated out in vivo, from suspensions of individual cells. Lipopolysaccharide from S. typhosa was shown to exert an adjuvator influence. But this adjuvator, an endotoxin, had no direct effect on the suspended tumor cells, unlike the liver preparations previously reported. Lipopolysaccharide from S. typhosa was shown to act on the host. It made the host's connective tissue expanses more susceptible to successful implantation by the tumor cells. It did this only if present at the time these connective tissue expanses were split. The increased susceptibility, caused by splitting the connective tissue expanses in the presence of lipopolysaccharide, declined quickly after 24 hr. The structural changes wrought upon the connective tissues by splitting them in the presence of lipopolysaccharide are described. They show kinship to a Schwartzman reaction of the local type. Their possible role in the adjuvator effect on the plating of single cell suspensions of this tumor is discussed.

Adjuvants, Immunologic↗
PubMedDate not supplied

Some characteristics of the hyperreactivity to bacterial lipopolysaccharide induced in mice by Trypanosoma cruzi infection.

Mice infected with T. cruzi, Y strain, acquire a high level of susceptibility to the effects of bacterial gram-negative LPS. The LD50 of adult female SW mice to LPS from S. typhosa, decreases from 450 to 2,5 mcg 10-12 days after T. cruzi infection. This hyperreactivity to LPS induced by T. cruzi presents all the characteristics of that found in infection caused by many other agents. During the acute phase of experimental infection with T. cruzi Y strain, mice generally die with a hypovolemic shock very similar to that induced in uninfected animals injected with an adequate dose of bacterial endotoxin. There is evidence for and against the hypothesis that LPS absorbed from the intestinal tract may be involved in the mechanism of death of mice during the acute phase of T. cruzi infection.

Animals↗
PubMed1977

[Experimental research on the artificially induced antibody immunity in the healthy man and in the patient with liver cirrhosis].

The ability to produce antibodies against strong (S. typhosa and S. paratyphi) and weak (tetanus toxide) antigens and the consequent changes in serum IgG's, IgA's, and IgM's were compared in patients with cirrhosis of the liver and healthy controls. A significantly higher response, especially to strong antigens, was noted in the cirrhotics, while their bone marrow contained an appreciably greater number of lymphocytes and plasma cells. Increased Ig production in cirrhosis is seen as the expression of general over-production of antibodies and hence devoid of any specific relation to its immune pathogenesis. The conclusion is drawn that the liver may be in some way responsible for the regulation of antibody synthesis and that this capability is "disinhibted" in cirrhosis.

Adult↗
PubMed2003

Lipopolysaccharides from different bacterial sources elicit disparate cytokine responses in whole blood assays.

The stimulatory effects of different purified lipopolysaccharide (LPS) preparations from E. coli, S. typhosa, P. aeruginosa, and K. pneumoniae on cytokine and chemokine production were measured in whole blood assays by ELISA. Incubation of 0.5 ml whole blood with 10 ng/ml E. coli and S. typhosa resulted in a time-dependent production of TNF-alpha, IL-1beta, IFN-gamma, IL-10 and MCP-1. K. pneumoniae, however, showed preferential effects on IL-1beta, IL-10 and MCP-1 production with less potent effects on TNF-alpha and IFN-gamma. LPS derived from P. aeruginosa showed a similar potency to other LPS preparations on MCP-1 production, yet completely failed to elicit the production of other cytokines. To further investigate potencies of the different LPS preparations, mediator production was determined following stimulation with agonist concentrations of 0.1 ng and 1000 ng per ml over a 24 h time period. Dose-response curves were obtained with LPS derived from E. coli, S. typhosa and K. pneumoniae on all mediators apart from IL-1beta and MCP-1. Most strikingly though, was the ability of LPS derived from P. aeruginosa to selectively elicit a significant dose-response effect on MCP-1 production, despite its very weak stimulatory effects on all other cytokines. These data imply that the bacterial origin of different LPS preparations can exhibit disparate effects on inflammatory mediator production. Furthermore, the potent, selective dose-response effect of P. aeruginosa LPS on MCP-1 production could help to explain the preponderance of a relentless inflammatory cellular infiltrate in diseases such as cystic fibrosis (CF).

Chemokines↗