Affiliations: [a] Department of Pediatrics, Shanghai East Hospital, the Affiliated East Hospital of TongJi University, Shanghai, China
| [b] Department of Pediatrics, Changzheng Hospital Affiliated to the SMMU, Shanghai, China
| [c] Department of Respiration, Shanghai Children’s Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Correspondence:
[*]
Correspondence to: Fang Liu, Department of Pediatrics, Shanghai East Hospital, the Affiliated East Hospital of TongJi University, 1800 Yuntai Road, Shanghai 200123, China. Tel.: +8613386057192; E-mail: [email protected] and Hao Zhang, Department of Respiration, Shanghai Children’s Medical Center, Shanghai Jiao Tong University School of Medicine, 1678 Dongfang Road, Shanghai 200127, China. Tel.: +8618930830639; E-mail: [email protected].
Abstract: Recent studies suggest that severity of asthma can be modulated by neuropsychiatric conditions, while the underlying mechanisms are not clear. Here, we used ovalbumin (OVA) to induce asthma in APP/PS1 mice, a mouse model of Alzheimer’s disease (AD), or in their wildtype control C57BL/6J mice. We found that all hallmarks of asthma by OVA were significantly attenuated in APP/PS1 mice, compared to age- and gender-matched C57BL/6J mice. Interestingly, significantly higher number of regulatory T cells (Treg) was detected in the APP/PS1 mouse lung, compared to those in the C57BL/6J mouse lung. Since Foxp3 is crucial for differentiation of naive T cells into Treg and is the most important marker for Treg, we examined the Foxp3 levels in the T cells from the lung of these mice. We found that the Foxp3 levels in the APP/PS1 mouse lung were significantly higher than those in the C57BL/6J mouse lung, likely resulting from reduced Foxp3 promoter methylation. Thus, our study suggests that AD may affect severity of asthma through methylation control of Foxp3 promoter in T cells.
Keywords: Alzheimer’s disease, asthma, Foxp3, regulatory T cells (Treg cells)
