Evaluation of the Effects of Nicotine on Mammalian Target of Rapamycin Complex 2 and Signal Transducer and Activator of Transcription 3 Genes Expression in a Mouse Model of Allergic Asthma: An experimental study

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.