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Background & Aims: Allergic diseases have increased in the last decade worldwide and researchers have been trying to introduce new strategies and drugs to treat these types of diseases. Nicotine shows anti-inflammatory properties and the studies have revealed that it can reduce the inflammation and the allergic responses. The mammalian target of rapamycin (mTOR) is a multifunctional protein kinase that forms two complexes in the signaling pathway. It has been shown that mTOR Complex 2 (mTORC2) tends to promote the immune response toward Th2. Also, the studies have indicated that the signal transducer and activator of transcription 3 (STAT3) is an essential transcription factor in anti-inflammatory responses and nicotine exert its anti-inflammatory effects using the STAT3 signaling pathway
Materials & Methods: In this experimental Study, we investigated the effects of nicotine on the expression RICTOR-mTORC2 and STAT3 genes in a mouse model of allergic asthma. The mice were sensitized using ovalbumin and alum and 2 weeks later treated tree times with nicotine in the concentration of 10 mg/kg every other day. The mice were challenged with ovalbumin aerosols on days 35, 38 and 41 and sacrificed the next day
Results: Our results showed that nicotine treatment resulted in down-regulation of RICTOR-mTORC2 expression. Also, the results indicated that nicotine could up-regulate the expression of STAT3
Conclusion: Such data proposed that nicotine administration may decrease allergic responses and the inflammation in the airways of the allergic mice by down-regulating the expression of RICTOR-mTORC2 and up-regulating the expression of STAT3 genes.

Keywords: Allergy, Nicotine, mTORC2, STAT3

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