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Related Experiment Video

Updated: Jun 3, 2026

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Published on: September 20, 2019

Toll-like receptor 4 signalling attenuates experimental allergic conjunctivitis.

S-H Chung¹, S H Choi, K J Cho

¹Department of Ophthalmology and Visual Science, Seoul St. Mary's Hospital, Korea.

Clinical and Experimental Immunology

|March 12, 2011

Summary

Bacterial lipopolysaccharide (LPS) suppresses allergic conjunctivitis by reducing T helper type 2 (Th2) responses via Toll-like receptor 4 (TLR-4) signaling. This finding offers a potential therapeutic pathway for allergic eye diseases.

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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

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Published on: July 26, 2017

Area of Science:

Immunology
Ophthalmology

Background:

Allergic conjunctivitis involves T helper type 2 (Th2) responses and eosinophil infiltration.
Toll-like receptor 4 (TLR-4) signaling is linked to adaptive immunity in allergic airway disease.

Purpose of the Study:

To investigate the effect of bacterial lipopolysaccharide (LPS) on allergic conjunctivitis development.
To determine if LPS modulates immune responses to ovalbumin (OVA) allergen in an experimental allergic conjunctivitis (EAC) model via TLR-4.

Main Methods:

Mice were sensitized with OVA and challenged to induce allergic conjunctivitis.
LPS was administered with OVA during sensitization in wild-type and TLR-4(-/-) mice.
Allergic indicators, including immunoglobulin E (IgE) and cytokine levels, were evaluated.

Main Results:

LPS administration significantly suppressed IgE-mediated and eosinophil-dependent conjunctival inflammation.
Mice treated with OVA plus LPS showed reduced levels of interleukin-4 (IL-4), IL-5, and eotaxin.
LPS-induced suppression of allergic responses was dependent on TLR-4 signaling and associated with a Th1 shift.

Conclusions:

LPS suppresses Th2-driven allergic conjunctivitis through a TLR-4-dependent mechanism.
This study demonstrates the potential of LPS in modulating allergic inflammation via TLR-4 in an EAC model.