Published online Feb 26, 2021. doi: 10.4252/wjSC.v13.i2.177
Peer-review started: July 31, 2020
First decision: October 21, 2020
Revised: October 31, 2020
Accepted: November 11, 2020
Article in press: November 11, 2020
Published online: February 26, 2021
Processing time: 208 Days and 0.6 Hours
Motion sickness (MS) is a disease that occurs during an unbalanced movement, and approximately 90% of people experience MS at least once in their lives. MS can present with gastrointestinal symptoms and activation of the autonomic nervous system. Additionally, it is accompanied by an increase in the levels of pro-inflammatory factors in the inner ear. However, the commonly used anti-inflammatory hormonal drugs have many side effects. Mesenchymal stem cells (MSCs) exert strong immunosuppressive effects and thus may serve as a therapeutic option for MS.
We can use the immunoregulatory properties of MSCs to suppress MS. Additionally, clarification of the molecular mechanisms underlying these properties may yield novel targets for the preventive treatment of MS.
In this study, we aimed to explore whether umbilical cord-derived MSCs (UC-MSCs) can suppress MS in a mouse model.
UC-MSCs were cultured and phenotypically characterized. A total of 144 (equal numbers of males and females) 5wkold BALB/c mice were randomly divided into five groups, and UC-MSCs were infused into the tail veins of the MSCs group and MS + MSCs group. AS101-treated UC-MSCs were infused into the MS + AS101/MSCs group for prophylaxis. The mice were subjected to the Morris water maze test to experience MS and monitored for any sign of dizziness. Enzyme-linked immunosorbent assay (ELISA) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to assess the expression levels of inflammatory cytokines in the peripheral blood and petrous temporal bones of the mice. The petrous temporal bone samples were also histologically evaluated via hematoxylin-eosin (HE) staining. Additionally, Western blot analysis was performed to assess the cochlear levels of proteins involved in the JAK2/STAT3 signaling pathway.
Results of the Morris water maze test demonstrated that transplantation of UC-MSCs suppressed the symptoms of MS in mice. The UC-MSC-transplanted mice found the water maze platform faster than the MS group. The levels of interleukin-10 (IL-10) in the cochlear tissues were increased after transplantation with UC-MSCs, based on the ELISA and RT-qPCR results. Moreover, Western blot analysis showed that transplantation of UC-MSCs activated the JAK2/STAT3 signaling pathway in the cochlear tissues. These effects were abolished when the transplanted mice were treated with the IL-10 inhibitor AS101. Histologically, no obvious difference was observed among the petrous temporal bones of the mice in the five groups.
Prophylactic transplantation of UC-MSCs can suppress MS in mice, particularly at 3-5 d after transplantation. This reduced sensitivity of the vestibular cortex to imbalance presumably results from improvement of the immune microenvironment by IL-10 secreted by UC-MSCs.
In the future, we will explore additional MSC culture methods and cell-free administration of the MSC-derived active factors into mice. For example, we will culture MSCs in three dimensions (3D) to mimic their in vivo microenvironment, and administer MSC-derived exosomes to the oral or nasal mucosa. In this way, we hope to translate the anti-MS effect of MSCs to the clinic.