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At least 1,243 records · Page 69Linked to original sources
PubMed1981

International conference on byssinosis. Mechanisms of disease induction.

From this work and other published data there are at least three distinct compounds that have been shown to be capable of inducing symptoms of byssinosis. There is an aminopolysaccharide-protein complex in cotton plant bracts that acts by causing histamine release in the human lung and also causes necrosis of bronchiolar epithelium. There is endotoxin or endotoxin-like material present in cotton plant bracts that acts by a mechanism other than by causing histamine release. This can induce histologic features of chronic bronchitis over a period of time. There is a polyphenol compound whose action is unlikely to be via complement activation, even though higher titers of antibody to it are present in byssinotic compared with nonbyssinotic subjects. It is postulated that such a compound is held in the lungs by antibody and exerts its effect on the pulmonary vasculature, altering capillary resistance. It also produces pathologic change as might be expected from its ability to precipitate proteins and activate complement.

Alcohols↗
PubMed1983

Role of endotoxin in the expression of human monocyte cytotoxicity.

The role of bacterial endotoxin in the expression of human monocyte cytotoxicity was studied. Endotoxin contamination of all reagents and steps of the experimental procedure were assessed by the limulus amebocyte lysate (LAL) assay. Peripheral blood monocytes were separated by adherence, and cytotoxicity was measured as [3H]-thymidine release from prelabeled mKSA-TU5 murine target cells in a 48-hr assay. Human monocytes expressed appreciable levels of spontaneous cytotoxicity under LAL- conditions irrespective of the serum source employed (LAL- or LAL+ fetal bovine serum, FBS, or LAL- human cord serum, HCS). HCS gave the highest cytotoxicity levels and LAL- FBS the lowest. Polymyxin B (10 micrograms/ml), which inhibited endotoxin-induced gelation of LAL and activation of mononuclear cells for procoagulant activity, did not affect the expression of spontaneous monocyte cytotoxicity with all three sera used. Three preparations of endotoxin used in the present study (Escherichia coli, S. typhosa, S. minnesota) caused small increases in monocyte killing in micrograms per milliliter concentrations only in 5 of 19 experiments performed. Human lymphoblastoid interferon (LAL-) and phytohemagglutinin-elicited lymphokine supernatants (LAL-) enhanced the tumoricidal activity of human monocytes under LAL- conditions and were not affected by Polymyxin B. It is concluded that exposure to endotoxin is not a prerequisite for the expression of spontaneous cytotoxicity by human blood monocytes.

Animals↗
PubMed1978

Mitogenicity of cell wall fractions of Micropolyspora faeni.

Cell wall fractions of Micropolyspora faeni, a causative agent of hypersensitivity pneumonitis, have been shown to possess non-specific mitogenic activity for guinea pig, rabbit and human lymphocytes. This activity was unrelated to endotoxin and may not be associated with peptidoglycan. This lymphocyte proliferation stimulus may play a role in the adjuvant properties of this organism and in the etiology of hypersensitivity lung disease.

Animals↗
PubMed1983

[Pathogenesis of endogenous endotoxemia in chronic liver disease--with special reference to the experimental fatty liver in germfree animals].

The effect of intestinal bacterial flora and endotoxin on fatty liver with germfree (GF) and conventional (CV) rat in the 12th and 24th week was investigated after giving fatty diet which was added 1% cholesterol-0.5% cholic acid to the basic diet. Results are as follows. Serum biochemistry Serum GOT, GPT, ALP and cholesterol values increased after giving the fatty diet in both groups. Limulus Gelation Test In CV group, endotoxin was detected in 2 of 10 cases in portal blood and was completely absent in arterial blood. After the fatty diet, endotoxin increased gradually both in portal and arterial blood. Cyclic AMP values on glucagon challenge (P/B ratio) In both groups, the levels of the P/B ratio maintained low values compared with control. In CV group, the values were lower in endotoxin positive cases than negative ones. Hepatic carbohydrate metabolism Abnormal hepatic F6P , glucose, FDP and PEP values were observed in CV group and reduction of the levels of hepatic F6P , G6P and glucose values were remarkable in GF group. Hepatic G6P in CV group and FDP in GF group remained unchanged. Impairment of F6P and G6P in CV group, was significant in endotoxin positive cases than in negative ones.

Animals↗
PubMed1984

The fate of E. coli lipopolysaccharide after the uptake of E. coli by murine macrophages in vitro.

The fate of bacterial lipopolysaccharide (LPS) after the uptake of Escherichia coli by macrophages in vitro was studied. The LPS of the galactose epimerase-deficient E. coli J5 mutant was specifically radiolabeled with [3H]galactose by growing the organism in a basic salts medium containing galactose. Control bacteria were uniformly radiolabeled by growth in [14C]glucose and unlabeled galactose-containing medium. Surface constituents of E. coli were also labeled with 125I. After in vitro phagocytosis of labeled E. coli by murine peritoneal exudate macrophages, the rate of exocytosis of LPS, as assessed by release of 3H over a 72-hr period, was considerably reduced in comparison with other bacterial constituents (14C and 125I release). The [3H]galactose-labeled material exocytosed from macrophages and that remaining intracellularly (obtained from macrophage lysates) were isolated by cesium chloride (CsCl) density gradients and were shown to have altered density profiles as compared with purified E. coli LPS. The macrophage-"processed" [3H] galactose-containing fractions from CsCl density gradients of culture supernatants or macrophage lysates were capable of clotting Limulus amebocyte lysate. The [3H]galactose material obtained from 48-hr macrophage lysates and culture supernatants could also induce a lethal response in actinomycin D-treated mice. These data suggest that bacterial LPS may be selectively retained by the macrophage and that the post-phagocytic events that result in bacterial degradation are not accompanied by the degradation of LPS. Furthermore, although the LPS may be modified by the macrophage, it retains its biologic activity.

Animals↗
PubMed1984

Unusual lipopolysaccharide antigens of a Salmonella typhi oral vaccine strain expressing the Shigella sonnei form I antigen.

Salmonella typhi 5076-1C, a potential live, oral vaccine for protection against typhoid fever and Shigella sonnei shigellosis, expresses the S. sonnei form I antigen and normal S. typhi somatic antigens. Polysaccharide antigens of this galactose epimeraseless genetic derivative strain were hot phenol-water extracted from cells grown with (+gal) and without (-gal) galactose. Ultracentrifugation of the aqueous layer from (+gal) cells resulted in a lipopolysaccharide (LPS) pellet having core-linked S. typhi O-antigen but no core-linked form I antigen; the LPS from (-gal) cells lacked O-antigen. The form I antigen, obtained from the supernatant, was purified by alcohol precipitation and ion exchange chromatography. Unlinked form I and S. typhi O-polysaccharide antigens, both present in the (+gal) supernatant, were further separated by gel filtration. Chemical analyses revealed the 5076-1C form I antigen to be a polymer (Mr = 14,000-20,000) having O-disaccharide repeating units comprised of 2-acetamido-4-amino-2, 4,6-trideoxy-D-galactose and 2-acetamido-2-deoxy-L-altruronic acid. Unlike parental S. sonnei form I LPS, the 5076-1C form I antigen lacked core lipid A, had low phosphorus content, and migrated in polyacrylamide gels with lower relative mobility. In contrast to current concepts of LPS assembly, these data indicate that 5076-1C form I antigen is transported to the cell surface without covalent linkage to core lipid A, and exists as a polymerized, antigenic surface entity.

Administration, Oral↗
PubMed1984

Purification and characterization of two Serratia marcescens proteases.

The exocellular proteases of two Serratia marcescens strains (strains SF 178 and SH 186; both of serotype 06/014:H12 and bacteriocin type 18) were separated from the culture supernatants through precipitation with ammonium sulfate, followed by hydroxylapatite adsorption chromatography, Sephadex G-100 gel filtration, and DEAE-Sephadex A-25 ion exchange chromatography. The molecular weights amounted to 54,400 Daltons (SDS-PAGE electrophoresis). Both enzymes contained 1 g-atom of zinc and 7 g-atoms of calcium per mol. The amino acid sequences were essentially identical. Serologically, both enzymes cross-reacted strongly, suggesting similar antigenic determinants. The two enzymes were microheterogeneous; isoelectric focusing revealed two protein bands at pH 5.4 and 5.5, respectively. The optimal temperature for hydrolysis of azocasein was 30 degrees C. Both proteases revealed 2 optimal pH values (SF 178 = pH 6-7 and pH 8-10; SH 186 = pH 7 and pH 9).

Amino Acids↗
PubMed1984

Protective effects and role of endotoxin in experimental septicemia.

An experimental model was used in mice in which septicemia develops following invasion of the animals' own intestinal flora after cecal ligation and puncture. Pretreatment with 1 microgram of endotoxin administered 24 hours before surgery significantly reduced the rate of lethality. Bacteria were counted and differentiated in cardiac blood at various times throughout a 48-hour period after induction of septicemia in mice, with and without pretreatment. Endotoxin levels and plasma-related interference of the Limulus-amebocyte-lysate (LAL)-endotoxin reaction also were determined as were hematologic and metabolic parameters. A shift from mixed gram-positive and gram-negative to predominantly gram-negative bacteria occurred in both groups. In pretreated mice, a reduction in aerobic bacterial counts and reduced hyperglycemia were seen in the initial phase; and a decrease in anaerobic and aerobic bacteria and in endotoxin levels were observed at the end of the experiment. This appears to be related to endotoxin-induced increased resistance against the consequences of intraabdominal sepsis. These studies also indicate that the measured amount of circulating endotoxin does not necessarily correlate to the severeness of infection. Individual differences in plasma-related interference with the LAL-endotoxin reaction also emphasize the requirement for sample-internal standardization in order to reliably quantify endotoxin in plasma.

Animals↗
PubMed1984

The virulence in mice of Neisseria meningitidis variants differing in free endotoxin activities and cell envelope properties.

The virulence of two serogroup B meningococcal strains (270E+ and 840E+) having a high endotoxin release during in vitro growth, was compared with the virulence of corresponding variants (270E- and 840E-) liberating less endotoxin. The E-variants were isolated during subcultivations from the E+ strains. 270E+ and 840E+ were both serotype 15:P1.16, while 270E- was serotype 15:P1.2 and 840E- was non-typable. The SDS-PAGE patterns of the E+ and E- variants were also dissimilar. The E+ and E- variants differed in several other properties. Groups of mice were inoculated intravenously (i.v.) or intraperitoneally (i.p.) with E+ and E- meningococci. The endotoxin activities of inoculates and mouse blood were assayed by a Limulus lysate test. The mice received a similar infective dose of E+ and E- variants. A higher level of CFU and endotoxin was found in heart blood of E+ than of E-infected mice during the first hours after infection. Both 30h and 72h after inoculation, E+ variants were significantly more lethal to mice than E- variants (p less than 0.01).

Animals↗