downregulation of allergic rhinitis with a modification of mast cells In relation with toll-like receptors

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Mast cells which is the key player at the eliciting phase of allergic rhinitis, have been reported to produce Th2 cytokines in vitro with LPS stimulation via TLR4, but in vivo study remains to be performed. Therefore, we investigated the LPS effect on the eliciting phase of murine allergic rhinitis model. As a result, LPS aggravated the eliciting phase of type-I allergic reaction, in a murine allergic rhinitis model. Furthermore, the significant difference in sneezing rates between C3H/HeN mice challenged with OVA alone and OVA with LPS was found, but this difference was not detected in C3H/HeJ mice, which are TLR4-deficient natural mutants . Eosinophil infiltration was more prominent in C3H/HeN mice challenged with OVA and LPS, in comparison with those in mice challenged with OVA alone. In western blot analysis, IL-5,IL-10,IL-13 expression was seen in both groups, but IL-5 expession was upregulated in mice challenged with OVA and LPS. However, there was no significant difference in eosinophil infiltration and Th2 cytokine expression between C3H/HeJ mice challenged with OVA alone and OVA with LPS. These data taken together suggests that LPS aggravates nasal symptom, upregulating Th2 cytokine production of mast cells via TLR4. In a future study, soluble form of TLR4 should be examined to be one of promising treatment options in a murine model of allergic rhinitis and patients with allergic rhinitis as well.