|  Help  |  About  |  Contact Us

Publication : Toll-like receptor 4 signalling attenuates experimental allergic conjunctivitis.

First Author  Chung SH Year  2011
Journal  Clin Exp Immunol Volume  164
Issue  2 Pages  275-81
PubMed ID  21391988 Mgi Jnum  J:172082
Mgi Id  MGI:5003403 Doi  10.1111/j.1365-2249.2011.04368.x
Citation  Chung SH, et al. (2011) Toll-like receptor 4 signalling attenuates experimental allergic conjunctivitis. Clin Exp Immunol 164(2):275-81
abstractText  Allergic conjunctivitis from an allergen-driven T helper type 2 (Th2) response is characterized by conjunctival eosinophilic infiltration. Association between signalling through Toll-like receptor 4 (TLR-4) and adaptive immune responses has been observed in allergic airway disease. We examined whether administration of bacterial lipopolysaccharide (LPS), a prototypic bacterial product that activates immune cells via TLR-4, 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 TLR-4(-/-) 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 immunoglobulin (Ig)E-mediated and eosinophil-dependent conjunctival inflammation. In addition, mice sensitized with OVA plus LPS had less interleukin (IL)-4, IL-5 and eotaxin secretion than mice sensitized with OVA only. The suppression of allergic response by LPS administration was due to Th1 shift. In contrast, the presence of LPS during sensitization with OVA had no effect on severity of allergic conjunctivitis and Th2 responses in TLR4-4(-/-) mice. Our findings demonstrate, for the first time, that LPS suppresses Th2 responses via the TLR-4-dependent pathway in the EAC model.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

4 Authors

3 Bio Entities

Trail: Publication

0 Expression