Effects of Lactobacillus rhamnosus on allergic march model by suppressing Th2, Th17, and TSLP responses via CD4+CD25+Foxp3+ Tregs

- A novel mouse model of AM was developed by epicutaneous sensitizations.
- Th2, Th17, and TSLP were associated with the developing mechanism of AM.
- Lcr35 could prevent the development of AM by immune modulation.
- Lcr35 could be a potential therapeutic alternative in allergic diseases.

Allergic march (AM) is characterized by the progression of clinical signs of atopic dermatitis (AD) to allergic asthma or rhinitis, but its pathogenesis is not completely understood.We developed mouse model of AM with three 1-week exposures (separated by 2-week interval) to an OVA or saline (control) followed by OVA challenge. The development of AM was confirmed by phenotypes of AD and allergic asthma. Increases in IL-4, IL-17, and thymic stromal lymphopoietin (TSLP) responses were associated with the progression of AM, and these responses were suppressed by treatment with Lcr35. Moreover, Lcr35 treatment led to an increase in the number of CD4+CD25+ Foxp3+ regulatory T (Treg) cells in the mesenteric lymph nodes (MLNs) of AM mice.In conclusion, the oral application of Lcr35 prevented the development of AM in this model by suppressing Th2, Th17, and TSLP responses via a mechanism that may involve CD4+CD25+Foxp3+ Tregs in MLNs.