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Seong Hyun Choi, So-Hyang Chung, Kyong Jin Cho, Choun-Ki Joo; Toll-like Receptor 4 Signaling Attenuates Experimental Allergic Conjunctivitis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1932.
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Allergic conjunctivitis from an allergen-driven Th2 response is characterized by conjunctival eosinophilic infiltration. Association between signaling through Toll-like receptor 4 (TLR4) and adaptive immune responses has been observed in allergic airway disease. We examined whether administration of bacterial LPS, a prototypic bacterial product that activates immune cells via the TLR4 could affect the development of allergic conjunctivitis and modify the immune response to ovalbumin (OVA) allergen in an experimental allergic conjunctivitis (EAC) model.
Mice were challenged with two doses of OVA via conjunctival sac after systemic challenge with OVA in alum. Several indicators for allergy were evaluated in wild-type and TLR4-/- mice with or without adding of different doses of LPS into OVA in alum.
Mice challenged with OVA via conjunctival sac following systemic challenge with OVA in alum had severe allergic conjunctivitis. Of interest, LPS administration markedly suppressed IgE-mediated and eosinophil-dependent conjunctival inflammation. In addition, mice challenged with OVA had more IL-4, IL-5 and eotaxin secretion than mice in the non-inoculated group. The suppression of allergic response by LPS administration was due to Th1 shift. In contrast, inoculation of TLR4-/- mice with had no effect on severity of allergic conjunctivitis.
Our findings demonstrate, for the first time, that LPS suppresses Th2 responses via the TLR4-dependent pathway in EAC model.
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