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PubMed2001

Cell lysis is responsible for the appearance of extracellular urease in Helicobacter pylori.

BACKGROUND: Helicobacter pylori is a neutralophilic bacterium that colonizes the acidic human gastric surface using the neutralizing capacity of a constitutively produced urease. Urease is present both in the cytoplasm and bound to the outside surface of the bacteria. The origin of the surface urease continues to be controversial. This study provides additional evidence that the origin of surface urease is cell lysis, not secretion. METHODS: H. Pylori was transformed with a plasmid encoding green fluorescent protein (GFP), a non-native cytoplasmic protein. Cultures supplemented with beta-cyclodextrin or horse serum were collected over various time periods and spun through a ficoll cushion to gently separate whole bacteria from released protein. The pellet and supernatant fractions were analyzed by fluorimetry, SDS-PAGE and Coomassie blue or Western analysis. RESULTS: GFP fluorescence and antigenic reactivity in the supernatant increased at each time point. GFP, the non-native cytoplasmic protein, and UreB, a native cytoplasmic protein, increased over time in the supernatant and both proteins were always present in the pellet fraction. UreI, an inner membrane protein, was only present in the pellet fraction. beta-galactosidase, a protein not found in H. pylori, was used as a negative control. CONCLUSIONS: Since it is unlikely that there is an intrinsic secretion system for GFP, a non-native protein, its increasing presence over time in the supernate fraction along with UreB, and retention of UreI in the pellet fraction implies that cell lysis accounts for the presence of urease on the surface of H. pylori.

Bacteriolysis↗
PubMed2002

Antibacterial activities of beta-lactamase inhibitors associated with morphological changes of cell wall in Helicobacter pylori.

BACKGROUND: Recent study has demonstrated that beta-lactamase inhibitors including clavulanate, sulbactam and tazobactam have an vitro antibacterial effect on Helicobacter pylori. Here we describe the relationship between viability and cell profiles of H. pylori exposed to beta-lactamase inhibitors and some antibiotics in a short-time course. MATERIALS AND METHODS: The antibacterial effects of beta-lactamase inhibitors including clavulanate, sulbactam and tazobactam on the bacterial viability of and morphological changes in H. pylori ATCC43504 were examined. RESULTS: The beta-lactamase inhibitors such as clavulanate and sulbactam alone decreased the viable counts of H. pylori, depending on the antibiotic concentrations. Exposure to these beta-lactamase inhibitors resulted in morphological changes of cell shape, cell-wall disintegration and cell lysis. Among these beta-lactamase inhibitors, clavulanate was the most active, causing a decrease in viable counts and morphological changes such as short filamentous to sphaeroplast formation and lysis. One x minimum inhibitory concentration (MIC) of amoxicillin plus 1 x MIC of clavulanate decreased viable counts effectively compared with 1 x MIC of amoxicillin or 1 x MIC of clavulanate alone, and induced morphological changes of cell shape and cell wall. CONCLUSION: Our results suggest that the beta-lactamase inhibitors alone have concentration-dependent antibacterial activities against H. pylori and affect the morphology of the cell shape and the cell wall in vitro.

Anti-Bacterial Agents↗
PubMed1975

Activation of the properdin pathway of complement in patients with gram-negative bacteremia.

To determine the pathway used for activation of complement component C3, serum levels of components C1, C4, C2, C3, C5, C6, and C9 and two properdin factors, properdin and factor B, were measured in 42 patients with gram-negative bacteremia, in 19 of whom shock subsequently developed. Mean levels of the classical components C1, C4, and C2 in bacteremic patients in whom shock subsequently developed did not differ significantly (p greater than 0.05) from those of patients with uncomplicated bacteremia. Levels of properdin, factor B and C3, C5, C6, and C9 were significantly (p less than 0.05) decreased in patients with shock in comparison with those with uncomplicated bacteremia. Taken together, these findings are consistent with activation of C3 and the terminal complement sequence, C5-C9, occurring primarily by the properdin pathway, in patients with gram-negative bacteremia eventuating in shock. Biologically active products released during activation of C3-C9 may contribute to the development of shock.

Bacteria↗
PubMed2004

Bacteriolytic therapy can generate a potent immune response against experimental tumors.

When spores of the anaerobic bacterium Clostridium novyi-NT are systemically injected into animals, they germinate exclusively within the hypoxic regions of cancers. The germinated bacteria destroy adjacent tumor cells but spare a rim of well oxygenated tumor cells that subsequently expand. Surprisingly, we found that approximately 30% of mice treated with such spores were cured of their cancers despite the viable tumor rim initially remaining after spore germination. The mechanism underlying this effect was shown to be immune-mediated, because cured animals rejected a subsequent challenge of the same tumor. Similar effects were observed in rabbits with intrahepatic tumors. It was particularly notable that the induced immune response, when combined with the bacteriolytic effects of C. novyi-NT, could eradicate large established tumors.

Adoptive Transfer↗
PubMed2005

Competence-programmed predation of noncompetent cells in the human pathogen Streptococcus pneumoniae: genetic requirements.

Natural competence for genetic transformation is the best-characterized feature of the major human pathogen Streptococcus pneumoniae. Recent studies have shown the virulence of competence-deficient mutants to be attenuated, but the nature of the connection between competence and virulence remained unknown. Here we document the release, triggered by competent cells, of virulence factors (e.g., the cytolytic toxin pneumolysin) from noncompetent cells. This phenomenon, which we name allolysis, involves a previously undescribed bacteriocin system consisting of a two-peptide bacteriocin, CibAB, and its immunity factor, CibC; the major autolysin, LytA, and lysozyme, LytC; and a proposed new amidase, CbpD. We show that CibAB are absolutely required for allolysis, whereas LytA and LytC can be supplied either by the competent cells or by the targeted cells. We propose that allolysis constitutes a competence-programmed mechanism of predation of noncompetent cells, which benefits to the competent cells and contributes to virulence by coordinating the release of virulence factors.

Amidohydrolases↗
PubMed2006

Topological dynamics of holins in programmed bacterial lysis.

The fate of phage-infected bacteria is determined by the holin, a small membrane protein that triggers to disrupt the membrane at a programmed time, allowing a lysozyme to attack the cell wall. S(21)68, the holin of phage 21, has two transmembrane domains (TMDs) with a predicted N-in, C-in topology. Surprisingly, TMD1 of S(21)68 was found to be dispensable for function, to behave as a SAR ("signal-anchor-release") domain in exiting the membrane to the periplasm, and to engage in homotypic interactions in the soluble phase. The departure of TMD1 from the bilayer coincides with the lethal triggering of the holin and is accelerated by membrane depolarization. Basic residues added at the N terminus of S(21)68 prevent the escape of TMD1 to the periplasm and block hole formation by TMD2. Lysis thus depends on dynamic topology, in that removal of the inhibitory TMD1 from the bilayer frees TMD2 for programmed formation of lethal membrane lesions.

Amino Acid Sequence↗
PubMed1971

DNA uptake during genetic transformation and the growing zone of the cell envelope.

Continuous cellular incorporation of choline molecules is essential for DNA binding to competent pneumococci. The choline molecules are incorporated into the cell surface at the equatorial region of the cocci. As a working hypothesis, it is proposed that DNA molecules enter these bacteria at the growing zone(s) of the cell envelope.

Amino Alcohols↗
PubMed1971

Control of lambda repressor synthesis.

Direct measurements of the intracellular level of lambda repressor have been made by a DNA-filter assay and a radioimmune assay. Transcription of cI, the structural gene for repressor, appears to initiate at two different promoters, prm and pre. Promoter pre is activated during the establishment of lysogeny by the action of cII and cIII proteins at the DNA site cY. Phage mutated in cII, cIII, or cY do not make a normal burst of repressor after infection and do not efficiently lysogenize the cell. Cro product stops repressor synthesis midway in the infective cycle. Promoter prm maintains the repressor level in established lysogens. Delection mapping places it very near the right operator (Or). Prm is activated by repressor bound to the right operator. In the absence of cII or cIII protein, repressor synthesis requires active repressor and only proceeds on genomes able to bind repressor at Or.

Autoradiography↗
PubMed1971

Establishment and maintenance of repression by bacteriophage lambda: the role of the cI, cII, and c3 proteins.

To define the events necessary for the establishment and maintenance of repression in a lambda-infected cell, we have studied the requirements for efficient synthesis of the cI protein ("lambda-repressor"). Three classes of lambda mutants defective in the establishment of repression are also defective in the appearance of cI protein activity at the normal time. Two of these mutational classes (cII(-) and cIII(-)) probably result from inactivation of lambda-specified proteins, but the third class (cy(-)) may involve a structural defect. We conclude that at least three regulatory elements are likely to be required for the normal turn-on of cI protein synthesis in an infected nonlysogenic cell: cII and cIII proteins and an "active" y-region of lambda DNA. From these and other results, the complete role of cII and cIII proteins in the establishment of repression may involve a bifunctional regulatory activity: positive regulation of the cI gene and negative regulation of late genes. A possible molecular model for cII and cIII action is discussed. Since the cII and cIII genes are repressed by the cI protein under conditions of stable lysogeny, a separate mechanism is required for the maintenance of cI protein synthesis. After infection of a lysogen by cII(-) phage, the rate of increase of cI protein activity is substantially greater than after infection of a nonlysogen. From these and other results, the cI protein may also have a bifunctional regulatory activity: positive regulation of the cI gene and negative regulation of early lytic genes.

Autoradiography↗
PubMed1971

Adenosine 3':5'-cyclic monophosphate concentration in the bacterial host regulates the viral decision between lysogeny and lysis.

Mutants of Salmonella typhimurium defective in adenylate cyclase (cya gene) or in cAMP receptor protein (crp gene) are lysogenized at reduced frequency by phage P22. One class of the bacterial mutants with an altered RNA polymerase (rif gene) is also lysogenized at reduced frequency. In the three types of mutant bacteria, the phage's decision between lysogeny and lysis is shifted to lysis and the phage form clear plaques. We propose that in wild-type bacteria the cAMP-receptor protein, in combination with cAMP, activates bacterial RNA polymerase to transcribe certain phage genes that are required for efficient lysogenization. Under conditions of strong catabolite repression, when the supply of energy and biosynthetic components is abundant and the concentration of cAMP is low, the phage would multiply and lyse the cell. When the supply of energy is deficient and the concentration of cAMP is high, the phage would lysogenize the cell. Phage mutants have been isolated that form turbid plaques on the three classes of bacterial mutants due to a higher frequency of lysogeny. These phage mutants have been shown by complementation to be defective in the same gene, which we have called the cly gene. These cly mutants lysogenize the wild-type bacteria with a 99% frequency and, thus, do not form plaques on them. Other kinds of bacterial mutants are also lysogenized at reduced frequency by phage P22. They may be altered in other physiological control systems that influence the frequency of lysogenization.

Adenylyl Cyclases↗
PubMed1972

Kinetics of integration of transforming DNA in pneumococcus.

Integration of donor genes, as measured by recovery of their transforming activity from eclipse in lysates of newly transformed cells of pneumococcus, has been followed at temperatures from 0 to 40 degrees . There is a lag in the recovery curve that is marker-dependent and increases as temperature falls. An Arrhenius plot of the rates shows a sharp break between 15 and 20 degrees . Brief exposure of the system to 37 degrees before incubation at 10 or 15 degrees removes the lag and raises the subsequent rate of recovery. This activation is unstable, however, and disappears when the cells are held at 0 degrees after the exposure at 37 degrees and before incubation at 15 degrees . The results are interpreted in terms of a reaction sequence A right harpoon over left harpoon B --> C, with activation energies for the first forward rate-constant of the order of 50 Cal/mol, for the second, 20-21 Cal/mol, and for the reverse reaction, less than 20 Cal/mol. The properties of the first step, including its marker dependence, are the same as those observed earlier for stabilization of donor markers against intracellular inactivation, and it is suggested they may reflect an activation of the recipient chromosome prerequisite to synapsis.

Bacteriolysis↗