Shigella dysenteriae LPS Specific Neutra™ Antibody Products

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Are you challenged by the complexity of neutralizing Shigella endotoxins or hindered by inconsistent assay outcomes in dysentery research? Creative Biolabs' S. dysenteriae LPS specific Neutra™ antibody products leverage advanced hybridoma engineering and epitope-specific validation to deliver high-affinity antibodies, enabling precise neutralization of lipopolysaccharide-mediated virulence and accelerating therapeutic discovery.

Introduction to S. dysenteriae LPS

Shigella dysenteriae lipopolysaccharide (S. dysenteriae LPS) is a glycolipid critical to the virulence and immune evasion strategies of S. dysenteriae, the causative agent of severe bacillary dysentery. As a primary component of the bacterial outer membrane, LPS directly mediates host-pathogen interactions and drives inflammatory responses. Its endotoxic properties are central to the pathogenesis of Shigella infections, making it a high-priority therapeutic and diagnostic target.

  • Structural Complexity

S. dysenteriae LPS comprises three domains: lipid A, core oligosaccharide, and O-antigen. Lipid A, the hydrophobic anchor, triggers innate immune responses via Toll-like receptor 4 (TLR4) binding. The core region provides structural stability, while the O-antigen's hypervariable polysaccharide chain determines serotype specificity and immune evasion. Notably, S. dysenteriae serotype 1 expresses a unique O-antigen linked to severe clinical outcomes, including hemolytic-uremic syndrome. Structural heterogeneity in the O-antigen poses challenges for antibody development, necessitating antibodies that cross-react with conserved epitopes.

Schematic representation of LPS structure. (OA Literature) Fig.1 Representative structure of LPS.1

  • Signaling Pathways

LPS binding to TLR4 activates downstream NF-κB and MAPK pathways, driving pro-inflammatory cytokine release (e.g., IL-1β, TNF-α). Overactivation of these pathways contributes to endotoxic shock and tissue damage during Shigella infection. Additionally, S. dysenteriae LPS synergizes with Shiga toxin to exacerbate endothelial injury and renal dysfunction by amplifying oxidative stress and apoptosis pathways.

  • Associated Pathologies

S. dysenteriae causes acute inflammatory diarrhea, dysentery, and systemic complications such as hemolytic-uremic syndrome (HUS). High morbidity rates in resource-limited regions underscore the urgency for improved diagnostics and therapeutics. Antibiotic resistance further complicates treatment, highlighting the need for LPS-targeted strategies to mitigate bacterial virulence without inducing antibiotic-associated dysbiosis.

Applications of S. dysenteriae LPS Neutralizing Antibodies

  • Therapeutic Interventions for Severe Dysentery

Neutralizing antibodies against S. dysenteriae LPS are explored as passive immunotherapies to reduce mortality in acute infections. Preclinical studies demonstrate that antibody administration within 24 hours of infection significantly lowers systemic inflammation and prevents progression to HUS.

  • Rapid Diagnostic Assay Development

High-affinity anti-LPS antibodies enable the design of lateral flow assays for point-of-care detection of S. dysenteriae in stool samples. These assays reduce diagnostic turnaround times from days to minutes, critical for outbreak containment in low-resource settings.

  • Vaccine Efficacy Evaluation

Anti-LPS antibodies quantify immune responses in vaccine trials, correlating O-antigen-specific IgG titers with protection against Shigella challenge in animal models. This supports rational vaccine design targeting conserved LPS epitopes for broad coverage.

  • Mechanistic Studies of Endotoxin Neutralization

Researchers employ neutralizing antibodies to map LPS-TLR4 binding interfaces and identify host proteins that modulate endotoxin clearance. These insights inform the development of small-molecule inhibitors targeting LPS signaling.

Our Anti-S. dysenteriae LPS Antibodies

Neutralizing antibodies targeting S. dysenteriae LPS block endotoxin-receptor interactions, suppress cytokine storms, and enhance bacterial clearance. Key attributes of therapeutic-grade antibodies include:

- Cross-serotype reactivity: Targeting conserved lipid A or core epitopes to overcome O-antigen variability.

- High neutralization potency: Reducing endotoxin activity by >90% in vitro.

- Synergy with antibiotics: Resensitizing multidrug-resistant strains to conventional therapies.

Creative Biolabs' antibodies are validated for specificity in ELISA, flow cytometry, and in vivo neutralization models, offering researchers robust tools to dissect LPS-mediated pathogenesis and advance therapeutic candidates.

Creative Biolabs' S. dysenteriae LPS specific Neutra™ antibody products offer unmatched precision for researchers tackling Shigella-related therapeutic and diagnostic challenges. Our antibodies are engineered to neutralize endotoxin activity, resolve assay variability, and accelerate translational outcomes. Contact our scientific team today to explore custom solutions for your project.

REFERENCE

  1. Hatlem, Daniel, et al. "A trimeric coiled-coil motif binds bacterial lipopolysaccharides with picomolar affinity." Frontiers in Cellular and Infection Microbiology 13 (2023): 1125482. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3389/fcimb.2023.1125482
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Recombinant Anti-S. dysenteriae LPS Antibody (V3S-1022-YC4657) (CAT#: V3S-1022-YC4657)

Target: S. dysenteriae LPS

Host Species: Rat

Target Species: S. dysenteriae serotype 1 114Sd,

Application: Inhib,

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Anti-S. dysenteriae LPS Neutralizing Antibody (V3S-1022-YC4781) (CAT#: V3S-1022-YC4781)

Target: S. dysenteriae LPS

Host Species: Mouse

Target Species: Shigella dysenteriae,

Application: Block,ELISA,

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Anti-S. dysenteriae LPS Neutralizing Antibody (V3S-1022-YC4783) (CAT#: V3S-1022-YC4783)

Target: S. dysenteriae LPS

Host Species: Mouse

Target Species: Shigella dysenteriae,

Application: Block,ELISA,

For research use only, not directly for clinical use.


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