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 have analyzed gastrointestinal immune function in both DBA/2 and spontaneously autoimmune New Zealand Black (NZB) mice. We have studied both in vitro proliferation and differentiation of Peyer's patch cells and have measured immunoglobulin (Ig) secretion by cultured jejunal segments. Peyer's patch B cells and T cells from both DBA/2 and NZB mice showed similar proliferative responses to Con A and lipopolysaccharide (LPS), respectively. Unlike NZB splenic B cells, isolated Peyer's patch B cells from NZB mice did not spontaneously secrete Ig of any isotype. Seven-day cultures of equal numbers of Peyer's patch T cells and B cells resulted in similar patterns of secretion of IgA, IgG, and IgM in both strains. The addition of Con A to cultures of DBA/2 Peyer's patch cells consistently resulted in a onefold to threefold increase in IgA secretion after 7 days. Con A stimulation of NZB Peyer's patch cells did not produce any increment in IgA secretion. LPS stimulation of Peyer's patch cells from either strain resulted in a similar increase in IgG secretion with little effect on IgA secretion. The in vivo correlate of this finding was seen in the IgA to IgG ratio of Ig secreted by cultured jejunal fragments. In DBA/2 mice the rates of IgA/IgG varied from 2.36 to 4.85, whereas in NZB mice the ratio never exceeded 0.5. These experiments show that defects on the T cell compartment of NZB mice encompass gut-associated lymphoid tissue. The possible relationship of these findings and previously observed defects in oral tolerance is discussed.
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PMID:Analysis of T cell and B cell function in Peyer's patch and lamina propria of New Zealand Black and DBA/2 mice. 348 25

Fifteen patients hospitalized with acute, watery diarrhea and with enterotoxigenic Escherichia coli (ETEC) detected from stool samples were studied to evaluate the extent to which natural ETEC diarrhea induces local and systemic antibody responses to E. coli heat-labile toxin (LT), homologous lipopolysaccharide (LPS), and colonization factors (CFA/I and CFA/II). Specific IgA and IgG antibodies to LT, CFA I and II, and each patient's homologous LPS were determined by ELISA in serum, saliva, breastmilk, and intestinal lavage fluid. The majority of patients had greater than a twofold rise in local levels of IgA antibodies in the intestine: 80% of LT+ patients responded to LT, 63% of CFA+ patients responded to CFA, and 78% of all toxin-positive patients responded to the LPS of their infecting strain. Local antibody responses in the intestine were associated with responses in breastmilk and saliva, but relationships were not clear-cut, and the usefulness of these secretions as proxy measures of local intestinal antibody production remains unclear. Antibody responses in serum also occurred in most patients and were significantly more frequent in cases than in controls. This study demonstrates that natural ETEC disease results in local IgA responses to LT, CFA, and LPS in the gut and also in immune responses in breastmilk, saliva, and serum.
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PMID:Local and systemic antibody responses to naturally acquired enterotoxigenic Escherichia coli diarrhea in an endemic area. 351 29

Enterotoxigenic Escherichia coli (ETEC) may have profound effects on the capacity of gut-associated lymphoid tissue to mount a secretory immune response because of the potential ability of heat-stable toxin or heat-labile toxin to modulate the immune response. To examine the effects of ETEC or its purified enterotoxins upon the humoral immune response of murine small intestinal Peyer's patch lymphocytes, BDF1 (lipopolysaccharide-responder) and C3H/HeJ (lipopolysaccharide-nonresponder) mice were orally primed with sheep erythrocytes (SRBC) four times during a 2-week period to initiate differentiation of Peyer's patch B lymphocytes to cells committed to anti-SRBC immunoglobulin A (IgA) production. Halfway through the oral priming regimen the mice were gastrically intubated with 10(8) ETEC, 10(8) non-ETEC, or saline. ETEC persisted in the small intestine for at least 7 days at a level of 10(3) to 10(4) bacteria per mouse. Seven days after the last oral dosing with SRBC, Peyer's patch lymphocytes were removed from infected or saline-treated mice and incubated in vitro with SRBC. The ETEC infection had a small effect on the anti-SRBC IgM plaque-forming cell response of SRBC-primed mice but inhibited significantly the anti-SRBC IgA plaque-forming cell response in both BDF1 and C3H/HeJ mice as compared with uninfected controls. The non-ETEC, an isolate from normal mouse small intestine, had no significant effect on either IgM or IgA anti-SRBC plaque-forming cell response. Purified heat-labile toxin, not heat-stable toxin, alone in a dose-dependent manner significantly inhibited both the IgA and IgM plaque-forming cell response of Peyer's patch lymphocytes from primed mice. These data suggest that ETEC can inhibit the development of the gut-associated lymphoid tissue IgA immune response through the immunopharmacological effect of an enterotoxin, the heat-labile toxin.
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PMID:Modulation of murine Peyer's patch immunoglobulin A response by enterotoxigenic Escherichia coli. 355 86

Specific antibodies to V. cholerae lipopolysaccharide (LPS), cell-bound haemagglutinin (CHA) and toxin (CT) in the intestinal lavages of healthy Thais and Thai cholera patients during the convalescence period were determined by enzyme-linked immunosorbent assay. Only IgM and IgA specific antibodies were detectable in the specimens. All of the persons who were just recovered from cholera had IgA anti-CT and IgA anti-LPS and 82.4% had IgA anti-CHA. The IgA anti-CT, anti-LPS and anti-CHA were detected also in the gut fluids of 70.6%, 94.1% and 88.2%, respectively, of the healthy controls. The mean levels of the IgA antibodies of all specificities between the two groups of individuals were not different. However, the IgM anti-CT and IgM anti-LPS of the cholera patients increased during the convalescence period. The levels, therefore, were significantly higher than those of the controls. The ratios of IgA anti-CT: IgM anti-CT and IgA anti-LPS: IgM anti-LPS among the patients were 2.93:1 and 2.02:1, respectively while those of the controls were 10:1 and 34:1, respectively. IgA antibodies predominated in the lavages of both groups of the individuals.
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PMID:Antibodies against Vibrio cholerae lipopolysaccharide, cell-bound haemagglutinin and toxin in the intestinal fluid during convalescence. 366 66

Four anaesthetised monkeys were given oral kanamycin (15 mg 1 kg 12 hourly) over five consecutive days before being heat stressed. Four other anaesthetised monkeys served as controls. The plasma lipopolysaccharide concentration in control primates increased initially from 0.044 (SEM 0.004) ng/ml to 0.062 (0.006) ng/ml as the rectal temperature increased from 37.5 to 39.5 degrees C. A second increase in lipopolysaccharides started at 42 degrees C and reached 0.308 (0.038) ng/ml (p less than 0.01) at 44.5 degrees C. Before heat stress the plasma lipopolysaccharide concentration in the primates who had been pretreated with kanamycin was 0.007 (0.006) ng/ml, and despite heating these animals to 44.5 degrees C no increase in plasma lipopolysaccharide concentrations were seen in this group. The cardiovascular variable during heat stress were more unstable in the control group and began to deteriorate at a lower temperature than in the group receiving antibiotic. These data suggest that the increased plasma lipopolysaccharide concentration during heat stress originates mainly from the gut.
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PMID:Prevention of endotoxaemia by non-absorbable antibiotics in heat stress. 369 72

Ischemia of the intestines damages the permeability of the intestinal wall, allowing lipopolysaccharide (LPS) (endotoxin) to leak from the gut lumen into the blood circulation, causing shock and death. We measured LPS levels associated with corticosteroid treatment vs. no treatment in cats whose superior mesenteric artery had been occluded for 60 min. In untreated cats, the preocclusion mean plasma LPS concentration remained stable at 0.069 +/- 0.015 ng/ml. Toward the end of the occlusion period, mean plasma LPS rose to 0.239 +/- 0.032 ng/ml (p less than .01). Release of the clamp and reperfusion with oxygenated blood was followed within 20 min by a large rise in plasma LPS concentration to 0.825 +/- 0.11 ng/ml (p less than .01), which had returned to preocclusion levels about 80 min later. Methylprednisolone (30 mg/kg) was infused into a second group of cats 1.5 h before SMA occlusion. In these cats there was a complete inhibition of the LPS rise both during and after occlusion. These data suggest that the reported beneficial effect of corticosteroids in the treatment of septic shock may be mediated, in part, by reducing LPS leakage from the gut.
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PMID:Effect of corticosteroid prophylaxis on lipopolysaccharide levels associated with intestinal ischemia in cats. 375 30

Acute hypoxia is known to cause a marked reduction in intestinal and peripheral blood flow, in favor of blood flow to the brain and heart. Complete occlusion of the intestinal circulation is known to damage the gut wall, allowing potentially lethal endotoxins present within the intestines to escape into the circulation. We examined here whether the breathing of a hypoxic gas mixture could lead to sufficient damage of the intestinal wall to cause endotoxemia. Six anesthetized monkeys breathed air for 1 hr, then an hypoxic mixture (FIO2 = 0.13) containing N2O for 1 h and, finally, 100% O2. Plasma endotoxin concentrations were determined by two methods. After approximately 40 min of hypoxia, the plasma endotoxin level rose significantly from 0.39 to 1.60 ng X ml-1 (p less than 0.001) and then subsided to near control levels. Control monkeys breathing air only or 70% N2O in oxygen (FIO2 = 0.3) for 3 h showed no such elevation in plasma endotoxin concentration. We conclude that hypoxia leads to a temporary endotoxemia in primates. Reticuloendothelial system depression by whole body X-irradiation (200 rads) increased both the magnitude and duration of the hypoxia-induced endotoxemia. Prior administration of equine anti-lipopolysaccharide (anti-LPS) hyperimmune plasma greatly reduced the magnitude of the induced endotoxemia. Since endotoxemia may be lethal, the use of anti-LPS as possible prophylaxis should be considered in persons breathing artificial atmospheres or where acute hypoxia may be a danger.
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PMID:Hypoxia-induced endotoxemia in primates: role of reticuloendothelial system function and anti-lipopolysaccharide plasma. 379 22

We have previously shown that Salmonella minnesota R345 (Rb) spontaneously binds to 50 to 55% of human peripheral blood mononuclear cells (PBMC). In the present study, we have compared Rb cytoadherence to lymphoid cells from various tissues of lipopolysaccharide (LPS) hyporesponsive (Lpsd) and LPS responsive (Lpsn) mouse strains. A higher number of spleen cells from Lpsd mice (C3H/HeJ and C57BL/10ScN) bound Rb bacteria (22 to 30%) than cells from Lpsn mice (4 to 9%). Rb bound mainly to T cells, and cytoadherence occurred in both Lyt-1+ and Lyt-2+ T cell subsets. By contrast, purified splenic B cells from Lpsd and Lpsn mice gave less than 4% Rb cytoadherence. In both mouse strains, cytoadherence was mediated by the homologous LPS structure, because purified Rb-LPS blocked Rb Salmonella binding to T cells. On the other hand, smooth Salmonella typhimurium LT-2 LPS (S-LPS) and Salmonella R595 (Re) LPS (Re-LPS), which contain mainly lipid A, were without effect on Rb binding. Increased Rb binding was seen with T cells from Peyer's patches (PP), mesenteric lymph nodes (MLN), and peripheral blood than from spleen of C3H/HeN (Lpsn) mice; however, greater cytoadherence was always seen with T cells of these tissues from C3H/HeJ mice. Interestingly, treatment of whole spleen or purified T cells from C3H/HeN mice with neuraminidase enhanced cytoadherence to levels seen with C3H/HeJ cells. The observed Rb binding to PP, MLN, and PBMC cells in both mouse strains suggests that gut microbial environment may play an important role in Rb cytoadherence. This is also supported by the evidence that when spleen cells of germfree and conventional mice were tested for Rb binding, higher cytoadherence was observed in conventional mice only. Taken together, these results indicate that T cells of Lpsd mice express binding site(s) for Salmonella, whereas Lpsn mice have T cells with these structure(s) in a cryptic configuration.
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PMID:Relationship between immune system and gram-negative bacteria. IV. T lymphocytes from Lpsd mice possess binding site(s) for Rb Salmonella. 387 86

This laboratory has proposed that endogenous gut-derived bacterial endotoxin primes the pancreatic secretion of insulin in normal rats. Endogenous lipopolysaccharide (LPS) is continually absorbed from the gut into intestinal capillaries, and low-grade portal venous endotoxemia is the status quo. Under physiologic conditions, Kupffer cells of the liver totally phagocytize and degrade endotoxin from the portal circulation. Evidence from this and other laboratories indicates that administration of exogenous LPS to humans and rats enhances pancreatic secretion of both insulin and glucagon. Conversely, findings of the present study demonstrate that restriction of endogenous LPS in fasted rats depresses the basal and arginine-stimulated concentrations of plasma insulin. Techniques used to restrict gut-derived LPS availability included chronic daily gavage with neomycin and cefazolin for gut sterilization and with cholestyramine or lactulose to reduce endotoxin within the gut. In addition, induction of endotoxin tolerance was produced by progressively higher doses of LPS intraperitoneally (i.p.), and polymyxin B was administered subcutaneously (s.c.) daily to neutralize the lipid A portion of circulating LPS. Finally, isolator-reared, defined flora rats, which were gram-negative-bacteria-deficient, and, therefore, LPS-deficient, were compared with conventional counterparts. Basal plasma insulin but not glucagon levels were consistently and significantly reduced in endogenous LPS-restricted animals. Glucose-stimulated plasma insulin was decreased only after parenteral treatment by tolerance induction and polymyxin B administration. Both plasma insulin and glucagon were depressed in response to arginine challenge in most LPS-restricted rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous gut-derived bacterial endotoxin tonically primes pancreatic secretion of insulin in normal rats. 390 58

Death in humans from ionising radiation overexposure in the 3-8 Gy (300-800 rad) range is in part due to the toxaemia caused by the entry of gram-negative bacteria and/or their lipopolysaccharide toxin (LPS) into the blood circulation through the walls of partially denuded gut. Anti-LPS hyperimmune equine plasma was evaluated for its ability to lower irradiation-induced lethality. Mice were irradiated with 6.3 Gy (630 rad) and six days later received equine Anti-LPS hyperimmune plasma, control plasma or saline. Mortalities in the three groups were 58%, 92% and 79% (p less than 0.01) respectively. Thus Anti-LPS may prove useful as an adjunct to conventional therapy in treating radiation sickness.
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PMID:Anti-lipopolysaccharide toxin therapy for whole body X-irradiation overdose. 391 66


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