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S Merino

Publications and source records attributed to S Merino.

84 records · Page 5Linked to original sources

The role of lipopolysaccharide in complement-killing of Aeromonas hydrophila strains of serotype O:34.

The role of lipopolysaccharide (LPS) in the susceptibility of Aeromonas hydrophila strains of serotype O:34 to non-immune human serum was investigated using isogenic mutants (serum-sensitive), previously obtained on the basis of phage resistance, and characterized for their surface components. The classical complement pathway was found to be principally involved in the serum-killing of these sensitive strains. LPS preparations from serum-resistant or serum-sensitive strains, or purified core oligosaccharides (low-molecular-mass LPS) inactivated both bactericidal and complement activity of whole serum, while the O-antigen molecules (high-molecular-mass LPS) did not. The results indicate that LPS core oligosaccharide composition contributes to complement resistance of A. hydrophila strains from serotype O:34 with moderate virulence.

Aeromonas hydrophila↗

Surface exposure of O1 serotype lipopolysaccharide in Klebsiella pneumoniae strains expressing different K antigens.

Surface exposure of the O1 serotype lipopolysaccharide in encapsulated Klebsiella pneumoniae strains belonging to different serotypes was examined by using the O1 antigen-specific bacteriophages FC3-1 and FC3-2 in conjunction with immunogold electron microscopy and enzyme immunoassays with specific antisera. Despite the presence of the capsular polysaccharide, the O1 antigen was exposed at the cell surface in strains producing K2, K7, K8, K12, K19, K21, K22, K34, K35, K42, K45, K55, K57, K62, K66, K69, and K70 capsular polysaccharides. However, in strains producing K1, K10, and K16 capsular polysaccharides, the O1 antigen was masked by the K antigen. These results suggest that, since the O1 antigen is surface exposed in many different strains of K. pneumoniae with different capsular serotypes and is also able to immunoprotect, its potential as a useful vaccine component should not be overlooked.

Animals↗

Isolation and characterization of bacteriophage PM3 from Aeromonas hydrophila the bacterial receptor for which is the monopolar flagellum.

PM3 is an Aeromonas-specific bacteriophage which was isolated and characterized on A. hydrophila strain TF7. Spontaneous mutants resistant to PM3 were non-motile having lost their characteristic monopolar flagellum. In addition, purified flagella inactivated PM3. PM3 is the first filamentous bacteriophage isolated on Aeromonas, the adsorption site for which is the monopolar flagellum.

Aeromonas↗

Isolation and characterization of bacteriophage PM2 from Aeromonas hydrophila.

PM2 is an Aeromonas-specific bacteriophage isolated on A. hydrophila strain AH-3. The bacteriophage receptor for this phage was found to be the lipopolysaccharide (LPS), specifically a low-molecular weight LPS fraction (LPS-core oligosaccharides). Mutants resistant to this phage were isolated and found to be devoid of LPS O-antigen and altered in the LPS-core. No other outer-membrane (OM) molecules appeared to be involved in phage binding.

Aeromonas↗

Identification of the cell surface receptor for bacteriophage 18 from Aeromonas hydrophila.

Bacteriophage 18 was previously isolated by multiplication in Aeromonas hydrophila. The bacteriophage receptor was shown to be the lipopolysaccharide (LPS), specifically the low MW polysaccharide fraction (LPS core oligosaccharide) A. hydrophila mutants, resistant to this phage were isolated and found to be devoid of LPS O antigen by several criteria and had alterations in the lipopolysaccharide core.

Aeromonas↗

Aeromonas hydrophila strains with moderate virulence.

A group of Aeromonas hydrophila strains was obtained from very different origins which showed very similar characteristics (lipopolysaccharide, outer-membrane protein profile, toxin production, bacteriophage sensitivity and moderate virulence), besides the heterogenicity observed among the A. hydrophila strains. This group of A. hydrophila strains with moderate virulence can be easily recognized by their bacteriophage sensitivity pattern.

Aeromonas↗

Salicylate-enhanced exposure of Klebsiella pneumoniae subcapsular components.

The capsular polysaccharide (CPS) of Klebsiella pneumoniae is an important virulence factor. Salicylate, which inhibits CPS production, was used to expose subcapsular antigens and components that may play an important role in host defense. Salicylate treatment greatly increased phagocytosis of five O1 serotypes by human polymorphonuclear leukocytes with normal rabbit serum and rabbit antisera against purified O1 lipopolysaccharide (O1LPS) as opsonins (p < 0.01 or < 0.05). Similar results were obtained with rabbit antiserum against a non-encapsulated isogenic strain. To further determine how salicylate increases susceptibility to phagocytosis, the binding of monoclonal antibodies against O1LPS or the LPS core and the binding of complement component C3b were measured by ELISA. The data indicate that salicylate reduced the barrier of CPS in serotypes O1:K1, O1:K10, and O1:K16 and unmasked subcapsular antigenic components in serotypes O1:K2 and O1:K66 so that bound opsonins could react with receptors on phagocytes. Serum bactericidal assays supported this conclusion. Therefore, decapsulating agents such as salicylate accentuate phagocytosis of K. pneumoniae by making subcapsular antigens and components accessible to immune and nonimmune host defences and vaccination with subcapsular antigens may exhibit optimal protection against lethal infection when combined with salicylate therapy.

Animals↗

The role of the capsular polysaccharide of Aeromonas hydrophila serogroup O:34 in the adherence to and invasion of fish cell lines.

The ability of Aeromonas hydrophila serogroup O:34 strains grown under different conditions (capsulated and non-capsulated) to adhere to and invade two fish cell lines was compared. The level of adherence was slightly higher when the strains were grown under conditions promoting capsule formation than when the same strains were grown under conditions which did not promote capsule formation. However, the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade the fish cell lines, which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation. Isogenic unencapsulated mutants grown under conditions promoting capsule formation showed a lower ability to invade the fish cell lines than the parental capsulated strains. From these results, we concluded that the capsular polysaccharide is an important factor in intracellular invasion.

Aeromonas hydrophila↗

Two genes from the capsule of Aeromonas hydrophila (serogroup O:34) confer serum resistance to Escherichia coli K12 strains.

The Escherichia coli DH5alpha strain as well as other K12-derived strains are unable to produce O-specific lipopolysaccharide and are thus rough and serum-sensitive. One representative recombinant clone (COS-SR1) containing Aeromonas hydrophila (serogroup O:34) chromosomal DNA conferred serum resistance to E. coli K12 strains. Genetic, biochemical, and immunological studies suggested that the two genes (orf1 and wcaJ) identified in a subclone (pAC-SR9) of COS-SR1 are necessary for the production of the colanic acid capsule at 37 degrees C on E. coli DH5alpha, rendering the strain serum-resistant. A. hydrophila strains from serogroup O:34 are able to produce capsule when they grow both in synthetic medium and in an autolysate of fish viscera. However, defined wcaJ insertion mutants of A. hydrophila 1051-88 (serogroup O:34) are unable to produce capsule on these media. This strongly suggests that both genes belong to the gene cluster responsible for capsule production (wca) of A. hydrophila 1051-88 (serogroup O:34).

Aeromonas hydrophila↗