Comparative Opsonic and Protective Activities of
            <i>Staphylococcus aureus</i>
            Conjugate Vaccines Containing Native or Deacetylated Staphylococcal Poly-
            <i>N</i>
            -Acetyl-β-(1-6)-Glucosamine

Maira-Litrán, Tomas; Kropec, Andrea; Da, Goldmann; Gb, Pier

doi:10.1128/iai.73.11.7789.2005

Cited by 46 publications

(84 citation statements)

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“…Most normal (i.e., nonimmunized) human or animal sera have little to no natural antibodies that mediate opsonic killing of S. aureus (17)(18)(19), a process that also requires a significant contribution from complement (20,21), which was determined to be present at ∼5% of serum levels in the abscesses of infected mice. We thus hypothesized that control of this microbe within abscesses possibly could be due to a secreted antimicrobial factor.…”

Section: Resultsmentioning

confidence: 99%

Antibody-mediated enhancement of community-acquired methicillin-resistant Staphylococcus aureus infection

Yoong

Pier

2010

Proc. Natl. Acad. Sci. U.S.A.

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Community-acquired infections caused by methicillin-resistant Staphylococcus aureus (MRSA) expressing the Panton-Valentine leukocidin (PVL) are rampant, but the contribution of PVL to bacterial virulence remains controversial. While PVL is usually viewed as a cytotoxin, at sublytic amounts it activates protective innate immune responses. A leukotoxic effect might predominate in high inoculum studies, whereas protective proinflammatory properties might predominate in settings with lower bacterial inocula that more closely mimic what initially occurs in humans. However, these protective effects might possibly be neutralized by antibodies to PVL, which are found in normal human sera and at increased levels following PVL + S. aureus infections. In a low-inoculum murine skin abscess model including a foreign body at the infection site, strains deleted for the pvl genes replicated more efficiently within abscesses than isogenic PVL + strains. Coinfection of mice at separate sites with isogenic PVL + and PVL -MRSA abrogated the differences in bacterial burdens, indicating a systemic effect on host innate immunity from production of PVL. Mice given antibody to PVL and then infected with seven different PVL + strains also had significantly higher bacterial counts in abscesses compared with mice given nonimmune serum. Antibody to PVL had no effect on MRSA strains that did not produce PVL. In vitro, antibody to PVL incapacitated PVL-mediated activation of PMNs, indicating that virulence of PVL + MRSA is enhanced by the interference of PVL-activated innate immune responses. Given the high rates of primary and recurring MRSA infections in humans, it appears that antibodies to PVL might contribute to host susceptibility to infection.bacterial pathogenesis | immunity | Panton-Valentine leukocidin | MRSA

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Section: Resultsmentioning

confidence: 99%

Antibody-mediated enhancement of community-acquired methicillin-resistant Staphylococcus aureus infection

Yoong

Pier

2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Opsonophagocytic Killing Assay-An opsonophagocytic killing assay was performed with modifications as described previously (35,36). S. aureus strains were grown to the logarithmic phase (A 578 ϭ 0.5) in LB medium and diluted in RPMI medium containing 0.05% human serum albumin.…”

Section: Methodsmentioning

confidence: 99%

Glycoepitopes of Staphylococcal Wall Teichoic Acid Govern Complement-mediated Opsonophagocytosis via Human Serum Antibody and Mannose-binding Lectin

Kurokawa

Jung

et al. 2013

Journal of Biological Chemistry

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Background:The exact staphylococcal antigenic determinants of anti-staphylococcal IgG and mannose-binding lectin (MBL) have not been determined. Results:The antigenic epitopes of the staphylococcal wall teichoic acid (WTA) for serum IgG and MBL are O-N-acetyl-Dglucosamine residues. Conclusion: The sugar moiety of WTA is an important molecular determinant in host responses to S. aureus. Significance: The results provide new insights into the host-pathogen interaction.

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“…Immunisation with either highly acetylated (>95%) or poorly acetylated ( 15%) PIA conjugated to diphtheria toxoid showed in-vitro opsonic killing of both S. aureus and S. epidermidis (Maira-Litrán et al 2005). Protection was due to antibodies directed against the non-acetylated PIA antigen (Maira-Litrán et al 2005). A monoclonal antibody against staphylococcal lipotechoic acids has been developed by Biosynexus Inc.…”

Section: Novel Prophylactic Approachesmentioning

confidence: 99%

Staphylococcus epidermidis device-related infections: pathogenesis and clinical management

McCann

Gilmore

Gorman

2008

Journal of Pharmacy and Pharmacology

158

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Staphylococcus epidermidis, the most frequently isolated coagulase‐negative staphylococcus, is the leading cause of infection related to implanted medical devices (IMDs). This is directly related to its capability to establish multilayered, highly structured biofilms on artificial surfaces. At present, conventional systemic therapies using standard antimicrobial agents represent the main strategy to treat and prevent medical device‐associated infections. However, device‐related infections are notoriously difficult to treat and bacteria within biofilm communities on the surface of IMDs frequently outlive treatment, and removal of the medical device is often required for successful therapy. Importantly, major advances in this research area have been made, leading to a greater understanding of the complexities of biofilm formation of S. epidermidis and resulting in significant developments in the treatment and prevention of infections related to this member of the coagulase‐negative group of staphylococci. This review will examine the pathogenesis of the clinically significant S. epidermidis and provide an overview of the conventional and emerging antibiofilm approaches in the management of medical device‐associated infections related to this important nosocomial pathogen.

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Comparative Opsonic and Protective Activities of Staphylococcus aureus Conjugate Vaccines Containing Native or Deacetylated Staphylococcal Poly- N -Acetyl-β-(1-6)-Glucosamine

Cited by 46 publications

References 0 publications

Antibody-mediated enhancement of community-acquired methicillin-resistant Staphylococcus aureus infection

Antibody-mediated enhancement of community-acquired methicillin-resistant Staphylococcus aureus infection

Glycoepitopes of Staphylococcal Wall Teichoic Acid Govern Complement-mediated Opsonophagocytosis via Human Serum Antibody and Mannose-binding Lectin

Staphylococcus epidermidis device-related infections: pathogenesis and clinical management

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