2023 Volume 54 Issue 3 Pages 147-158
Nasal inflammation may trigger neuropsychiatric disorders such as cognitive impairment and mental diseases, however, the underlying mechanism is not elucidated. To address this question, we have made mouse models of nasal inflammation by administering lipopolysaccharide (LPS) intranasally and have analyzed their brain and gut microbiota. In acute time after the intranasal LPS administration, variety of peripheral immune cells infiltrated the olfactory bulb and produced pro-inflammatory cytokines, but these cells disappeared within 72 hours. Repeated LPS intranasal administration induced prominent atrophy of the olfactory bulb, which can recover after nasal inflammation subsided. In addition, we recently found that male mice with chronic nasal inflammation had dysbiosis of gut microbiota, suggesting that nasal inflammation perturbs the balance of the gut-brain axis. On the basis of these data, we aim to reveal the cellular and molecular mechanisms underlying nasal inflammation-induced neuropsychiatric disorders, focusing on the potential pathological changes in the other brain regions than the olfactory bulb, the infiltration and ejection systems of peripheral immune cells that enter the olfactory bulb, and the mechanisms of the perturbation of the balance of gut microbiota by nasal inflammation.
