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)

Three mouse monoclonal antibodies (mAbs) (ICL3, ICL4, and ICL5) were produced that specifically recognized the lipopolysaccharide antigen of the newly recognized Shigella dysenteriae serotype-13 strain. All three mAbs reacted with all nine reference isolates of S. dysenteriae 13 in different tests. The mAbs also detected colonies of S. dysenteriae-13 isolates by direct slide agglutination test. The mAbs also reacted with the reference Escherichia coli 0150 strain and showed its close antigenic relationship with S. dysenteriae 13. Use of these mAbs in our clinical laboratory during an 8-month period detected three S. dysenteriae-13 isolates that were also detected by a polyclonal rabbit antiserum. It should now be possible to define the epidemiologic importance of S. dysenteriae serotype 13 in diarrhea by using these mAbs.
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PMID:Monoclonal antibodies specific for Shigella dysenteriae serotype 13. Production, characterization, and diagnostic application. 792 5

In view of the potential roles of intestinal immunodeficiency and hypersensitivity in the infection/diarrhea/malnutrition cycle, we need a safe and ethical method to study intestinal immunity of children in the developing world. Work in adults has shown that the fluid obtained by whole-gut lavage (WGLF), essentially a gut perfusate, can be used to assess intestinal immunity, inflammation, and gut losses of protein and blood. Gut lavage was successfully performed in 24 of 25 "normal" children aged 6-9 years, from Freetown, Sierra Leone, with parental informed consent. WGLF was treated with protease inhibitors, stored at -20 degrees C, and transferred to Edinburgh for laboratory studies. These showed that no child had occult blood loss but four had evidence of protein-losing enteropathy. Compared with values for Scottish adults, WGLF from the Sierra Leonean children had significantly higher concentrations of IgA and IgM and of IgA and IgM antibodies to dietary antigens and to Salmonella typhi lipopolysaccharide. In three children, very low levels of IgA and IgA antibody were present: Two of these were the only cases with detectable sIL2R in lavage fluid, indirect evidence of intestinal T cell activation; tumor necrosis factor was not detectable. Substantial information on childrens' intestinal immunity can be obtained by the method described.
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PMID:Use of whole-gut lavage to measure intestinal immunity in healthy Sierra Leonean children. 796 57

Microsporidia cause opportunistic infections in AIDS patients and commonly infect laboratory animals, as well. Euthymic C57B1/6 mice experimentally infected with intraperitoneal injections of 1 x 10(6) Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923, Encephalitozoon hellem Didier et al., 1991, or Nosema corneum Shadduck et al., 1990 displayed no clinical signs of disease. Athymic mice, however, developed ascites and died 8-16 days after inoculation with N. corneum, 21-25 days after inoculation with E. cuniculi, and 34-37 days after inoculation with E. hellem. All athymic mice displayed hepatomegaly, dilated intestine and accumulation of ascites fluid. Granulomatous lesions are primarily located in the liver, lung, pancreas, spleen, and on serosal surfaces of abdominal organs. The murine microsporidiosis model also was used to examine immune response that inhibit microsporidia growth in vitro. Recombinant murine interferon-gamma (mIFN-gamma, 100 mu/ml) alone or in combination with lipopolysaccharide (LPS; 10 ng/ml) could activate thioglycollate-induced peritoneal murine macrophages to destroy E. cuniculi. The production of the nitrogen intermediate, NO2-, correlated with parasite destruction. Inhibition of NO2- generation by addition of the L-arginine analogue, NG-monomethyl L-arginine (NMMA), inhibited microsporidia killing, as well. Since microsporidiosis is becoming an important opportunistic infection in AIDS patients, a microsporidiosis model is being developed using SIV/DeltaB670-infected rhesus macaque monkeys (Macaca mulatta). SIV-infected immunocompetent monkeys given E. cuniculi or E. hellem per os developed specific antibodies, and microsporidia could be detected sporadically by calcofluor or antibody fluorescence staining of stool and urine sediment smears. As immunodeficiency progressed, monkeys developed diarrhoea, cachexia, and anorexia, and organisms were detected in urine and stool with greater frequency. Immunodeficient SIV-infected monkeys died approximately 27 days after receiving E. hellem by intravenous inoculation, and approximately 110 days after receiving E. hellem per os. Lesions typical for SIV-infection were observed in both groups of monkeys and microsporidia were detected in kidney and liver of the intravenously-injected monkeys. The murine microsporidiosis model provides an efficient means for studying protective immune responses to microsporidiosis, and may prove useful for screening immunological and chemotherapeutic agents. The pathogenesis of Encephalitozoon microsporidiosis in SIV-infected monkeys appears to parallel encephalitozoonosis in AIDS patients, suggesting that simian microsporidiosis may provide a useful model for evaluating diagnostic methods and therapeutic strategies during various stages of progressing immunodeficiency.
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PMID:Experimental microsporidiosis in immunocompetent and immunodeficient mice and monkeys. 805 Jul 48

Shiga-like-toxin (SLT)-producing Escherichia coli strains, especially serotype O157:H7, are important causes of bloody diarrhea and are associated with the development of hemolytic-uremic syndrome (HUS). Enzyme-linked immunosorbent assays (ELISAs) were developed for the serologic detection of immunoglobulin M (IgM), IgG, and IgA to Shiga toxin (ST) and SLT-I, IgG to SLT-II, and IgM and IgG reactive against E. coli O157 lipopolysaccharide (LPS). Serum samples were collected from 27 HUS patients (25 pediatric and 2 adult) and tested in the ELISAs. Of 27 patients, 10 (37%) were positive for at least one class of antibody to ST/SLT-I. None of the patients were positive for IgG antibody to SLT-II. Twenty-one of the 27 patients (78%) were positive for antibody to E. coli O157 LPS; 19 of 27 (70%) were positive for IgM, and 20 of 27 (74%) were positive for IgG. None of 48 control serum samples were positive in any of the toxin assays, and only 1 of 48 (2%) and 2 of 48 (4%) were positive for IgM and IgG, respectively, to E. coli O157 LPS. Twelve of the 24 patients (50%) from whom stool specimens were collected were positive by culture for E. coli O157. Overall, serology and culture produced confirmation of infection by SLT-producing organisms in 23 of 27 (85%) HUS patients. A combination of ELISA for antibodies to E. coli O157 LPS and culture provided evidence for 22 of 27 (82%) of these patients. The results indicate that while ELISAs for ST/SLT-I and SLT-II antibodies were of limited diagnostic value, the ELISAs for IgM and IgG to E. coli O157 LPS provided valuable and sensitive adjuncts to culture.
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PMID:Humoral immune responses to Shiga-like toxins and Escherichia coli O157 lipopolysaccharide in hemolytic-uremic syndrome patients and healthy subjects. 805 Dec 41

Thirty-nine Escherichia coli strains of the enteropathogenic (EPEC) serogroup O126 isolated from sporadic and outbreak cases of infantile diarrhoea between 1982 and 1988 were studied. These strains consisted of four serotypes showing close genetic relationships between their virulence markers, outer-membrane protein and lipopolysaccharide profiles, and electrophoretic types by multilocus enzyme electrophoresis. None of these strains exhibited localised adherence to HEp-2 cells or the attaching-effacing properties of classical type I EPEC. Of the 39 strains, 31 were of serotype O126:H12 and enterotoxigenic; one strain was serotype O126:H10 and enteroaggregative. The remaining six strains of serotype O126:H21 and one strain of serotype O126:H8 harboured no known virulence factors for diarrhoeagenic E. coli.
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PMID:Genetic relationships and virulence factors among classical enteropathogenic Escherichia coli serogroup O126 strains. 815 71

The live, auxotrophic Shigella flexneri vaccine strain SFL124 was given in a single dose of 10(7), 10(8) or 10(9) colony forming units (cfu), respectively, to each of three groups of 10 Vietnamese children aged 9-14 years. The vaccine was well tolerated by all the children without any severe side effects such as diarrhoea or fever being observed. Mild symptoms were reported by five children. Only five children were found by culture to excrete SFL124 but, by PCR, 28 of 30 children were found to excrete the vaccine strain for up to 5 days (mean 2.8 days) with insignificant differences among the groups. Local mucosal immune responses and antibody secreting cell (ASC) responses to S. flexneri lipopolysaccharide (LPS) and invasion plasmid-coded antigens (Ipa) were elicited in the children in a dose-dependent manner. Doses of 10(9) cfu induced most prominent responses, followed by those of 10(8) and 10(7) cfu. The sIgA responses were the highest whereas the ASC were modest. High titres of serum antibodies to Shigella LPS and Ipa were found in all the children before ingestion of the vaccine which elicited increases in serum antibody titres in only a few of them. The immune response patterns seen indicate a booster rather than a primary response and may be a consequence of the endemic nature of shigellosis in Vietnam.
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PMID:Immune responses in Vietnamese children after a single dose of the auxotrophic, live Shigella flexneri Y vaccine strain SFL124. 816 28

Interleukin-1 (IL-1) may be involved in gut permeability to macromolecules and gut glutamine metabolism during endotoxemia. We developed a sensitive radioimmunoassay specific for mouse IL-1 alpha (detection limit of 100 pg/ml, or 5 pM) and measured intestinal levels of IL-1 alpha in response to endotoxin. CD-1 mice (N = 190) were randomized to intraperitoneal (ip) or intravenous (i.v.) lipopolysaccharide (LPS) infusion (15 micrograms/g or 1.5 micrograms/g Escherichia coli 0111:B4 LPS) or saline. Mice were sacrificed at Time 0, 30 min, 1 hr, 2.5 hr, 4 hr, 6 hr, 12 hr, and 24 hr (3 mice/group/time point). Small bowel (SB) and large bowel (LB) were harvested and compared to liver. Duodenum, upper jejunum, midjejunum, terminal ileum, cecum, ascending colon, and sigmoid were analyzed in separate experiments. Tissues were frozen, weighed, and homogenized, the homogenates were centrifuged, and the supernates were assayed for immunoreactive IL-1 alpha. IL-1 alpha was expressed as pg/g wt +/- SEM (lowest detectable amount = 1000 pg/g wet tissue (WT)). SB but not LB from normal controls had constitutively elevated levels of IL-1 alpha (6177 +/- 1640 pg/g WT). LPS ip or i.v. produced lethargy, diarrhea, and a dramatic elevation of IL-1 alpha levels in both SB and LB. In SB, IL-1 alpha was elevated compared to baseline at 1 hr (19201 +/- 626 pg/g WT) and reached a fivefold maximal increase at 2.5 hr (31775 +/- 503 pg/g WT) following 15 micrograms/g ip.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal production of interleukin-1 alpha during endotoxemia in the mouse. 841 68

The live, auxotrophic dependent Shigella flexneri Y vaccine strain SFL124 with a deleted aroD gene was tested in 30 healthy adult male Vietnamese volunteers. A single dose of 2 x 10(9) live bacteria was given orally to 15 volunteers, whereas 15 received three doses every other day. None of the volunteers reacted with fever or diarrhoea and SFL124 was excreted by all for a mean of 2.8 (single dose) and 2.6 (three doses) days. A total of 27 of 30 (90%) and 26 of 30 (87%) responded with significantly (0.001 < p < 0.01) increased antibody-secreting cell (ASC) numbers against Shigella flexneri Y lipopolysaccharide (LPS) and invasion plasmid-coded antigens (Ipa). A faecal IgA antibody response to LPS and Ipa was seen in 20 of the 30 (67%) volunteers against both antigens. Serum antibody responses were seen in 23 of 30 (77%) against the LPS and in 17 of the 30 against Ipa. The three-dose schedule elicited only somewhat stronger immune responses than the single-dose schedule. A booster dose of 2 x 10(9) live bacteria was given to half of the volunteers in each group after 6 months, the other half received the same dose after 12 months. Following the booster at 6 or 12 months (i) the excretion of SFL124 was significantly shorter (p < 0.05) than after primary vaccination; (ii) the anti-S. flexneri LPS and anti-Ipa faecal sIgA titres were significantly higher (p < 0.05 to p < 0.01) than after primary vaccination; (iii) the anti-LPS and anti-Ipa ASC responses were significantly lower (p < 0.05) and of shorter duration than after primary vaccination, and (iv) the serum anti-LPS and anti-Ipa responses were significantly elevated (p < 0.05) and similar to those seen after primary vaccination. The results indicate that SFL124 is a safe, live vaccine strain with a negligible reactogenicity in adults living in a Shigella endemic area. SFL124 induces specific immune responses against LPS and Ipa with a mucosal memory lasting for at least 1 year.
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PMID:Safety and immunogenicity of the live oral auxotrophic Shigella flexneri SFL124 in adult Vietnamese volunteers. 843 16

An enzyme immunoassay (EIA) for detection of serum antibodies in patients with typhoid fever was developed using Salmonella typhi outer membrane protein (OMP) preparations as antigen. Acute phase (first week) sera from adult typhoid fever patients were tested as well as sera from the following control groups: adult travellers with diarrhea caused by enterotoxigenic Escherichia coli, children infected with Campylobacter jejuni, healthy Mexican adult blood donors, and adults with septicemia caused by other organisms. At a 1:3,125 serum dilution, the mean absorbance values were 1.41 in the typhoid fever patients, and 0.57, 0.55, 0.51 and 0.52 in the respective control groups. Inhibition EIA studies using OMP preparations or lipopolysaccharide (LPS) as free antigen indicated that proteins can play an important role in the detection of antibodies in early typhoid fever. This EIA may be useful for the diagnosis of typhoid fever since results were obtained within about five hours and in an endemic area antibodies against Salmonella typhi OMP preparations appear early in the course of the disease.
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PMID:Early diagnosis of typhoid fever by an enzyme immunoassay using Salmonella typhi outer membrane protein preparations. 851 12

Endotoxemia occurs when intestinal ischemia allows bacterial lipopolysaccharide to translocate from colonic flora into the bloodstream, which triggers release of cytokines that can cause hypotension, rigors, fever, shock, and even death. Recently, blood endotoxin levels were shown to be higher in athletes needing medical attention (330 pg.ml-1) than in their competitors with similar performances (81 pg.ml-1). Though there were no data showing that these athletes had elevated core temperatures or severe illness, speculation followed that endotoxin may play a causal role in heat stroke. We examined the relationship between endotoxemia and mild post-exertional illness in 39 cyclists after a 100-mile ride. Thirteen cyclists had at least one of the following: orthostatic hypotension, rigors, nausea, vomiting, diarrhea, or syncope. Only 2/26 case-controls had any of these symptoms. Data were collected on vital signs, hemoglobin, sodium, creatine kinase, creatinine, and uric acid. Endotoxin titer was determined by chromogenic assay; tumor necrosis factor alpha (TNF-alpha) titer was determined by ELISA. One ill cyclist had an endotoxin level of 330 pg.ml-1, one control had an endotoxin level of 150 pg.ml-1, but endotoxin level was < or = 64 pg.ml-1 in all others. Comparison of pre- and post-ride data showed that controls increased creatine kinase activity (154 +/- 34 vs 561 +/- 191 IU.dl, P < 0.05), creatinine concentration (1.5 +/- 0.0 vs 1.6 +/- 0.0 mg.dl-1, P < 0.05), and uric acid concentration (5.4 +/- 0.3 vs 6.3 +/- 0.3 mg.dl-1, P < 0.05). Ill cyclists had lower serum sodium than post-ride controls (138 +/- 2 vs 142 +/- 0.6 mEq.l-1, P < 0.05), but there were no differences between groups in CK, creatinine, or uric acid. These findings suggest that endotoxemia may complicate, but does not cause mild post-exertional illness in cyclists.
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PMID:Exercise-associated collapse in cyclists is unrelated to endotoxemia. 853 21


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