5-5OAS Immunomodulatory Effect of Tonsil Derived Mesenchymal Stem Cells in a Mouse Model of Allergic Rhinitis

Thursday, 15 October 2015: 14:30 - 14:45
Room R2 ABC (Floor 3) (Coex Convention Center)

Ji-Hye Kim , Beckman Laser Institute Korea, Dankook University, Cheonan, South Korea

Ramachandran Samivel, PhD , Beckman Laser Institute Korea, Dankook University, Cheonan, South Korea

Eun-Hee Kim , Beckman Laser Institute Korea, Dankook University, Cheonan, South Korea

Young-Jun Chung, MD, PhD , Otorhinolaryngology, Dankook University, Cheonan, South Korea

Ji-Hun Mo, MD, PhD , Otorhinolaryngology, Dankook University, Cheonan, South Korea

Background: Although several studies have claimed that mesenchymal stem cells (MSCs) derived from human tissues can ameliorate allergic airway inflammation, the immunomodulatory mechanism of MSCs remains unclear.

Objective: We aimed to determine the effects and underlying mechanism of tonsil derived MSCs (T-MSC) on allergic inflammation as compared to adipose tissue derived stem cells (ASCs) in mouse model of allergic rhinitis (AR).

Methods: MSCs were isolated from human palatine tonsil (T-MSC) and adipose tissues (ASC), and the surface markers were analyzed. The effect of T-MSCs was evaluated in 24 BALB/c mice that were randomly divided into 4 groups (negative control group; positive control group; T-MSC group and ASC group). MSCs were administered intravenously to OVA-sensitized mice (T-MSC and ASC groups) on days 18 to 23 and subsequent OVA challenge was conducted daily from days 24 to 28. Several parameters of allergic inflammation were assessed.

Results: T-MSC and ASC had similar characteristics in surface markers. Intravenous injection of T-MSC significantly reduced allergic symptoms, eosinophil infiltration, serum total and OVA specific-IgE and the nasal and systemic Th2 cytokine profile. Further analysis revealed that nasal innate cytokines such as IL-25 and IL-33, and chemokines such as CCL11, CCL24 induction were suppressed in T-MSCs injected groups, explaining their underlying mechanism. Additionally, the T-MSC group had more inhibition of allergic inflammation than the ASC group, which might be attributed to the more proliferative activity of T-MSC.

Conclusion:  Administration of T-MSC effectively reduced allergic symptoms and inflammatory parameters in the mouse model of AR. T-MSC treatment reduced Th2 cytokines and OVA specific IgE secretion from B cells. In addition, innate cytokine (interleukin-25 and inteleukin-33) expression and eotaxin mRNA expression was inhibited in the nasal mucosa, suggestive of the mechanism of reduced allergic inflammation. Therefore, T-MSC treatment is potentially an alternative therapeutic modality in AR.