Passive immunization with monoclonal antibodies specific for lipopolysaccharide (LPS) O‐side chain protects mice against intravenous <i>Yersinia enterocolitica</i> serotype O:3 infection

Skurnik, Mikael; Mikkola, Pasi; Toivanen, Paavo; Tertti, Risto

doi:10.1111/j.1699-0463.1996.tb04917.x

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…Because the biological basis of benefit in the previous studies relied on the neutralization of potent immunomodulators that act in concert within a complex series of pathways, the variability of the clinical responses was considerable. In addition, the tremendous heterogeneity in the patient population receiving the early antibody-based products, such as HA-1A MAb (anti-lipid A on lipopolysaccharide) (21,45) or tumor necrosis factor alpha MAb (1,8), contributed significantly to the well-documented failures.…”

Section: Discussionmentioning

confidence: 99%

Characterization of a Protective Monoclonal AntibodyRecognizing Staphylococcus aureus MSCRAMM ProteinClumping FactorA

et al. 2003

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The Staphylococcus aureus MSCRAMM (microbial surface components recognizing adhesive matrix molecules) protein clumping factor A (ClfA) has been shown to be a critical virulence factor in several experimental models of infection. This report describes the generation, characterization, and in vivo evaluation of a murine monoclonal antibody (MAb) against ClfA. Flow cytometric analysis revealed that MAb 12-9 recognized ClfA protein expressed by all of the clinical S. aureus strains obtained from a variety of sources. In assays measuring whole-cell S. aureus binding to human fibrinogen, MAb 12-9 inhibited S. aureus binding by over 90% and displaced up to 35% of the previously adherent S. aureus bacteria. Furthermore, a single infusion of MAb 12-9 was protective against an intravenous challenge with a methicillin-resistant strain of S. aureus in a murine sepsis model (P < 0.0001). These data suggest that anti-ClfA MAb 12-9 should be further investigated as a novel immunotherapy for the treatment and prevention of life-threatening S. aureus infections.

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Section: Discussionmentioning

confidence: 99%

Characterization of a Protective Monoclonal AntibodyRecognizing Staphylococcus aureus MSCRAMM ProteinClumping FactorA

et al. 2003

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“…Two observations support this last conclusion: (i) better protection was elicited by the WT bacteria than by the OC mutants, and the latter had ≈fourfold lower antibody titres by EIA with no clear specificity differences by immunoblot; and (ii) YeO3‐R2 generated a very poor protection (Table 3). It is likely that the absence in YeO3‐R2‐immunized mice of the O‐antigen‐specific antibodies, previously shown to be protective in passive immunizations (Skurnik et al ., 1996), causes the difference. It is known that antibodies against polysaccharide antigens are T‐cell independent.…”

Section: Discussionmentioning

confidence: 99%

The lipopolysaccharide outer core of Yersinia enterocolitica serotype O:3 is required for virulence and plays a role in outer membrane integrity

Skurnik

Venho

Bengoechea

et al. 1999

Molecular Microbiology

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Lipopolysaccharide (LPS) of Yersinia enterocolitica O:3 has an inner core linked to both the O‐antigen and to an outer core hexasaccharide that forms a branch. The biological role of the outer core was studied using polar and non‐polar mutants of the outer core biosynthetic operon. Analysis of O‐antigen‐ and outer core‐deficient strains suggested a critical role for the outer core in outer membrane properties relevant in resistance to antimicrobial peptides and permeability to hydrophobic agents, and indirectly relevant in resistance to killing by normal serum. Wild‐type bacteria but not outer core mutants killed intragastrically infected mice, and the intravenous lethal dose was ≈104‐fold higher for outer core mutants. After intragastric infection, outer core mutants colonized Peyer's patches and invaded mesenteric lymph nodes, spleen and liver, and induced protective immunity against wild‐type bacteria. In mice co‐infected intragastrically with an outer core mutant–wild type mixture, both strains colonized Peyer's patches similarly during the first 2 days, but the mutant was much less efficient in colonizing deeper organs and was cleared faster from Peyer's patches. The results demonstrate that outer core is required for Y. enterocolitica O:3 full virulence, and strongly suggest that it provides resistance against defence mechanisms (most probably those involving bactericidal peptides).

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“…In many bacterial species the O-antigen has been shown to be an essential virulence factor [6] and is thought to be involved in protecting the bacteria against the activity of complement [7], by causing the membrane-attack complex to form at a distance from the bacterial surface. The LPS of Y. pseudotuberculosis and Y. enterocolitica have been shown to possess an O-antigen which is an essential virulence determinant [8]. However, the composition of the O-antigen can vary between strains; in Y. pseudotuberculosis seven di¡erent O-antigen polysaccharides have been identi¢ed and these di¡erences can be exploited to serotype di¡erent strains of the bacteria [9].…”

Section: Introductionmentioning

confidence: 99%

The failure of different strains of Yersinia pestis to produce lipopolysaccharide O-antigen under different growth conditions is due to mutations in the O-antigen gene cluster

Prior¹

2001

FEMS Microbiology Letters

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The lipopolysaccharide (LPS) from eight strains of Yersinia pestis which had been cultured at 28³C appeared to be devoid of an O-antigen when analysed by sodium dodecyl sulfate^polyacrylamide gel electrophoresis. LPS isolated from three of these strains which had been cultured at 37³C also appeared to be devoid of an O-antigen. When the LPS from Y. pestis strain CO92 was purified and analysed by matrix-assisted laser desorption-ionisation time-of-flight mass spectrometry, the observed signals were in the mass range predicted for molecules containing lipid A plus the core oligosaccharide but lacking an O-antigen. The nucleotide sequence of Y. pestis strain CO92 revealed the presence of a putative O-antigen gene cluster. However, frame-shift mutations in the ddhB, gmd, fcl and ushA genes are likely to prevent expression of the O-antigen thus explaining the loss of phenotype. ß 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Microbiological Societies.

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Passive immunization with monoclonal antibodies specific for lipopolysaccharide (LPS) O‐side chain protects mice against intravenous Yersinia enterocolitica serotype O:3 infection

Cited by 9 publications

References 17 publications

Characterization of a Protective Monoclonal AntibodyRecognizing Staphylococcus aureus MSCRAMM ProteinClumping FactorA

Characterization of a Protective Monoclonal AntibodyRecognizing Staphylococcus aureus MSCRAMM ProteinClumping FactorA

The lipopolysaccharide outer core of Yersinia enterocolitica serotype O:3 is required for virulence and plays a role in outer membrane integrity

The failure of different strains of Yersinia pestis to produce lipopolysaccharide O-antigen under different growth conditions is due to mutations in the O-antigen gene cluster

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