Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The humoral antibody response to Bacteroides fragilis infections in humans, with particular reference to ss. fragilis, was studied using an enzyme immunosorbent assay (EIA). Phenol-water extracted polysaccharide fractions (PS) from B. fragilis ss. fragilis, ss. ovatus, ss. distasonis and ss. vulgatus were used as antigens. Antibody titer determinations were done on sera collected from 57 patients where B. fragilis had been cultured and from 50 controls. In patients with septicemia caused by B. fragilis ss. fragilis a significant titer increase (greater than or equal to doubling) against PS from strain 9343 was seen during the course of the illness. In sera from patients with appendicitis, and where B. fragilis was isolated from the appendix, a titer increase against B. fragilis ss. fragilis 9343 was observed for 6 of 17 patients. However, in sera from 9 of the 17 patients a titer increase against B. fragilis ss. ovatus was also seen. No titer increase was observed in sera from most of the patients with salpingitis where B. fragilis had been isolated. In sera from 10 patients with Crohn's disease the median antibody titer against all four B. fragilis antigens was slightly higher than in sera from the controls. The median antibody titer against B. fragilis ss. ovatus was, however, significantly higher. Our experience is that a humoral antibody response against B. fragilis ss. fragilis can be expected in patients where the organism is isolated from blood. In diseases like appendicitis and salpingitis titer increases are less common. When they occur they are not necessarily directed against ss. fragilis only but are as frequent against ss. ovatus. Titer increases against ss. vulgatus and ss. distasonis are also seen. This raises the question if the observed titer increases are a consequence of a specific pathogenic role of B. fragilis in these infections, or if they merely represent the result of an antigenic stimulus as a result of an increased permeability of the mucosal barriers caused by inflammation and/or surgical manipulation.
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PMID:The humoral antibody response to Bacteroides fragilis infections in humans. 28 65

Non-O1 Vibrio cholerae produced two distinct colony types, designated as opaque and translucent. NRT36S, a clinical isolate shown to be virulent in volunteers, produced predominantly opaque colonies, but translucent colonies appeared on subculture. Opaque variants were recovered exclusively following exposure to normal human serum or animal passage. A nonreverting translucent mutant of NRT36S, JVB52, was isolated following mutagenesis with the transposon Tn5 IS50L::phoA (TnphoA). Only translucent colonies were produced by a nonpathogenic environmental isolate, A5. Electron microscopic examination of the opaque form of NRT36S revealed thick, electron-dense, fibrous capsules surrounding polycationic ferritin-stained cells. The ferritin-stained material around translucent NRT36S or A5 was patchy or absent. JVB52 had a thin but contiguous capsular layer. The amount of ferritin-stained capsular material correlated with the amount of surface polysaccharide determined by phenol-sulfuric acid assay: opaque NRT36S had approximately three times as much polysaccharide as translucent NRT36S or A5 and four times as much as JVB52. The encapsulated, opaque variant of NRT36S was protected from serum bactericidal activity, while translucent non-O1 V. cholerae was readily killed. The encapsulated form also had increased virulence in mice. Our data provide the first indication that non-O1 V. cholerae strains can have a polysaccharide capsule. This capsule may be important in protecting the organism from host defenses and may contribute to the ability of some non-O1 V. cholerae strains to cause septicemia in susceptible hosts.
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PMID:Non-O1 Vibrio cholerae NRT36S produces a polysaccharide capsule that determines colony morphology, serum resistance, and virulence in mice. 131 6

After ligation of the mesenteric arteries an intestinal ischaemia was obtained. Endotoxin was measured from the peritoneal cavity, the portal und the peripheral blood. The limulus test for Endotoxin was used after phenol-water-extraction of the plasma. Microbiological investigations were done simultaneously. The endotoxin concentrations correlated to the clinical state of gram negative sepsis.
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PMID:[Endotoxin in experimental mesenteric infarction]. 271 17

A review of the prelegal abortion scene in the US precedes discussion of the effect of injected soap, phenol, cresol, and their compounds. The latter is based on a review of 4 toxicology books. There is little difference in the symptoms after the instillation of phenols, cresols, or soaps. Any one of those agents can cause vaginal bleeding, abdominal pain and distension, nausea, vomiting, and cramps. The damage produced by the use of Lysol thus is due to both the phenol and soap components of the compound. Following instillation into the uterus, there is coagulation necrosis of the decidua and placental site. The toxin will invariable cause thrombosis of the intrauterine and parametrial veins. The thrombosis may spread to the entire pelvic vein plexus and paravaginal, paracervical, and ovarian veins. The liver and kidney are affected by the toxin. Icterus and bile pigments in the urine and clinical evidence of liver damage are seen often. Pulmonary edema has been described as have microscopic to massive pulmonary oil emboli and thrombosis. Depression of all bone marrow elements due to toxin has been reported. The red blood cells are further depressed in number because of hemolysis. Cerebral changes include oil emboli, cerebral coagulation, necrosis, and petechial hemorrhages. Until Studdiford and Douglas described gram-negative sepsis causing shock, patients admitted with hypotension accompanying septic abortion were thought to have concealed blood loss. Studdiford and Douglas showed that gram-negative septicemia could produce hypotension. With the advent of massive antibiotic therapy for septic abortion and septic shock, most of these patients could be saved. The kidneys, after exposure to phenolic-soap comounds, show mainly lower nephron changes. As long as the toxin is in the system those changes continue until irreversible renal damage occurs. It is essential to remove the source of the poison (the affected uterus) and then remove the circulating toxins. the main problem is removal of the circulating toxin. In addition to the problems produced by fixed and circulating toxin, it has been shown that most phenol-soap induced abortions are infected. Thus it is necessary to employ the optimal antibiotic therapy for septic incomplete abortion. The initial management phase moves along classic lines. First is monitoring the vital state and supporting the systems. This includes maintaining an intravenous solution with a large-bore needle, monitoring central venous pressure, measuring urinary output, monitoring the vital signs, maintaining adequate oxygenation, and supporting the blood pressure with blood vasopressors or other agents, as needed. Second is diagnosing the extent of the illness. Third is the initial treatment, which includes reestablishment of the blood volume with blood transfusions; aggressive coverage with double or triple antibiotic therapy; correction of hypofibrinogenemia with cryoprecipitate, fresh whole blood or fresh frozen plasma, as indicated; and avoidance of overhydration in the presence of actual or suspected renal failure. After antibiotic coverage has been established, removal of retained products of conception is indicated.
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PMID:Treatment of women who have undergone chemically induced abortions. 404 35

Lipopolysaccharides (LPS) were extracted from 13 of the 16 Heddleston serotypes of Pasteurella multocida by phenol-chloroform-petroleum ether (PCP). Serotypes 3, 9, and 13 were extracted only by phenol-water (PW). After extraction of LPS of serotype 9 by PW, an additional LPS was isolated by PCP. All LPS contained glucose, 2-keto-3-deoxyoctonate, and heptose. Two isomers of heptose, D-glycero-D-mannoheptose and L-glycero-D-mannoheptose, were found in serotypes 2 and 5. Antisera made against purified LPS of serotypes 2 and 5 reacted with both heat-stable antigens and LPS from serotypes 2 and 5 in the gel-diffusion precipitin test. Antisera against serotype 2 LPS protected turkeys against challenge with capsulated serotype 5, indicating that a structural relationship exists between LPS of strains that cause hemorrhagic septicemia and fowl cholera. Rhamnose was a component of serotype 9 LPS, and galactose was found in all LPS, except for serotype 11. The LPS of serotype 13 contained an isomer of heptose that has not been identified. The LPS had buoyant densities in CsCl of 1.40 +/- 0.0148 g/ml, and all hemagglutinated chicken and turkey, but not sheep or horse, RBC.
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PMID:Lipopolysaccharides of the Heddleston serotypes of Pasteurella multocida. 673 91

Strain Y3343 isolated from a goat with septicemia and polyarthritis was studied. The strain was virulent and induced septicemia, polyarthritis and coagulopathy in two goats. Limulus amebocyte lysate active material was present in plasma, but not in higher titre in inoculated goats. Sonicated mycoplasma material induced a dramatic somatic cell response in the mammary gland of cows and goats and marked clotting of the cows' milk, but it did not clot limulus amebocyte lysate or kill chick embryos. Phenol-water extract clotted limulus amebocyte lysate and induced somatic cell response in cows but not in goats. The phenol-water extract did not kill chick embryos, was not pyrogenic in rabbits or goats, and did not induce generalized Shwartzman reaction or change the leukocyte kinetics in rabbits. It therfore appears that the virulence mechanisms of strain Y3343 can not be explained on the basis of factors with strong endotoxin activity.
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PMID:Biological effects of sonicated suspension and phenol-water extract of Mycoplasma mycoides subspecies mycoides in goats. 704 90

Staphylococcus epidermidis releases factors that activate the HIV-1 long terminal repeat, induce cytokine release, and activate nuclear factor B in cells of macrophage lineage. The active material had a mass of 34,500 daltons, was inactivated by proteases and partitioned into the phenol layer on hot aqueous phenol extraction, and thus was termed phenol-soluble modulin (PSM). High performance liquid chromatography (HPLC) of crude PSM yielded two peaks of activity designated PSM peak 1 and peak 2. MALDI-TOF (matrix-assisted laser desorption ionization-time of flight) mass spectroscopy indicated the presence of two components in peak 1, which were designated PSM and PSM. Peak 2 contained a single component, designated PSM. Separation of PSM and PSM in peak 1 could be achieved by a second HPLC procedure. The structure of each component was determined by amino acid sequence analysis and identification and sequencing of their genes. PSM, PSM, and PSM were 22-, 44-, and 25-amino acid, respectively, strongly hydrophobic polypeptides. PSM was identified as Staphylococcus epidermidis delta toxin, whereas PSM and PSM exhibited more distant homology to previously described staphylococcal toxins. They appeared to exist as a complex or aggregate with activity greater than the component parts. The properties of the S. epidermidis PSMs suggest that they may contribute to the systemic manifestations of Gram-positive sepsis.
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PMID:An inflammatory polypeptide complex from Staphylococcus epidermidis: isolation and characterization. 1007 74

In general there is a poor correlation between serum lipopolysaccharide (LPS; the biologically active constituent of endotoxin) levels and mortality in septic patients. The objective of this study was to determine if chemical, structural, or biological differences among LPS from different clinical isolates of gram-negative bacteria might explain this discrepancy. LPS preparations were made using the hot phenol-water extraction method from eight clinical isolates of gram-negative bacteria. As a percentage of the total weight of the LPS, the phosphate content ranged from 3.0 to 13.8% (average, 6.7 +/- 3.6%), and the 2-keto-3-deoxyoctonate content ranged from 1.9 to 27.4% (average, 8.9 +/- 8.5%). These values were not dissimilar to those obtained for a reference endotoxin. In a standard measure of LPS activity, the Limulus amoebocyte lysate assay, there was approximately a twofold difference between the least and most active preparations. The two preparations with the greatest difference in their ability to elicit the secretion of tumor necrosis factor alpha from a mouse peritoneal macrophage cell line were similar in lethality when administered to mice sensitized to the effects of LPS by D(+)-galactosamine. These relatively minor differences in LPS activity seem unlikely to explain the generally observed discrepancy between serum endotoxin levels and mortality in patients with gram-negative sepsis.
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PMID:Comparable endotoxic properties of lipopolysaccharides are manifest in diverse clinical isolates of gram-negative bacteria. 1072 80

Modulins represent microbial products that stimulate cytokine production in host cells. The modulins responsible for gram-positive sepsis remain poorly understood. Staphylococci release a factor (or factors) that activates nuclear factor-kappa B and stimulates cytokine production in cells of macrophage lineage. This factor, termed phenol-soluble modulin (PSM), has been recently isolated from culture supernatant of Staphylococcus epidermidis. We examined the effects of PSM on proinflammatory properties of human neutrophils and monocytes in vitro. PSM activated the respiratory (oxidative) burst in neutrophils and primed neutrophils for enhanced respiratory burst activity in response to formyl-methionyl-leucyl-phenylalanine. PSM also stimulated neutrophil degranulation as reflected by increased surface expression of CD11b and CD18, which was accompanied by rapid shedding of L-selectin. Spontaneous apoptosis of both neutrophils and monocytes was inhibited by PSM. Furthermore, PSM also functioned as a chemoattractant factor for both neutrophils and monocytes. Thus, the proinflammatory properties of PSM resemble those of both lipopolysaccharide and bacterial chemotactic peptides. These findings suggest that PSM may play a role in the pathogenesis and systemic manifestations of sepsis caused by staphylococci.
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PMID:Stimulation of human neutrophils and monocytes by staphylococcal phenol-soluble modulin. 1143 91

The alpha 4/beta 1 integrin very late antigen-4 (CD49d/CD29) is up-regulated on circulating neutrophils of septic patients. Although no individual agent mimics this effect of sepsis, we now report that following priming of human neutrophils with lipopolysaccharide or tumor necrosis factor alpha (TNF-alpha), addition of formyl-Met-Leu-Phe (fMLP) results in a "stimulated", sepsis-like, four- to fivefold rise in CD49d expression. TNF/fMLP stimulation also produced a similar increase in CD49d-mediated adhesion of neutrophils to a vascular cell adhesion molecule-1 (VCAM-1)-coated surface. Adenosine is a naturally occurring, anti-inflammatory mediator released from injured or inflamed tissues. We observed that stimulated neutrophil CD49d expression was decreased by activation of A(2A) adenosine receptors (A(2A)AR) with the selective agonist 4-[3-[6-amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl]-cyclohexanecarboxylicacid methyl ester (ATL146e; EC(50)=6.4 nM). ATL146e (100 nM) also reduced the fraction of stimulated neutrophils that adhered to VCAM-1 from 38 +/- 6% to 27 +/- 5%. Inhibition of CD49d expression was equally inhibited by ATL146e, added before or after TNF priming, and was reversed by incubation with the A(2A)AR-selective antagonist 4-[2-[7-amino-2-(2-furyl) (1, 2, 4)triazolo(2,3-a) (1, 3, 5)triazin-5-yl-amino]ethyl]-phenol (ZM241385; 100 nM). A suboptimal ATL146e concentration (1 nM) combined with the type IV phosphodiesterase inhibitor rolipram (100 nM) synergistically decreased stimulated CD49d expression by >50%. The cyclic adenosine monophosphate (cAMP)-dependent kinase [protein kinase A (PKA)] inhibitor H-89 (10 microM) reversed the effect of ATL146e on stimulated CD49d expression. Other means of increasing cAMP in neutrophils also decreased stimulated CD49d expression. We conclude that adenosine binding to A(2A)AR counteracts stimulation of neutrophil CD49d integrin expression and neutrophil binding to VCAM-1 via a cAMP/PKA-mediated pathway.
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PMID:Activation of A2A adenosine receptors inhibits expression of alpha 4/beta 1 integrin (very late antigen-4) on stimulated human neutrophils. 1452 68


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