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Pneumococcal Δpep27 Immunization Attenuates TLRs and NLRP3 Expression and Relieves Murine Ovalbumin-Induced Allergic Rhinitis

  • Yu, Jae Ik (School of Pharmacy, Sungkyunkwan University) ;
  • Kim, Ji-Hoon (School of Pharmacy, Sungkyunkwan University) ;
  • Nam, Ki-El (School of Pharmacy, Sungkyunkwan University) ;
  • Lee, Wonsik (School of Pharmacy, Sungkyunkwan University) ;
  • Rhee, Dong-Kwon (School of Pharmacy, Sungkyunkwan University)
  • Received : 2022.03.03
  • Accepted : 2022.04.15
  • Published : 2022.06.28

Abstract

Allergic rhinitis (AR), one of the most common inflammatory diseases, is caused by immunoglobulin E (IgE)-mediated reactions against inhaled allergens. AR involves mucosal inflammation driven by type 2 helper T (Th2) cells. Previously, it was shown that the Streptococcus pneumoniae pep27 mutant (Δpep27) could prevent and treat allergic asthma by reducing Th2 responses. However, the underlying mechanism of Δpep27 immunization in AR remains undetermined. Here, we investigated the role of Δpep27 immunization in the development and progression of AR and elucidated potential mechanisms. In an ovalbumin (OVA)-induced AR mice model, Δpep27 alleviated allergic symptoms (frequency of sneezing and rubbing) and reduced TLR2 and TLR4 expression, Th2 cytokines, and eosinophil infiltration in the nasal mucosa. Mechanistically, Δpep27 reduced the activation of the NLRP3 inflammasome in the nasal mucosa by down-regulating the Toll-like receptor signaling pathway. In conclusion, Δpep27 seems to alleviate TLR signaling and NLRP3 inflammasome activation to subsequently prevent AR.

Keywords

Acknowledgement

This work was supported by the National Research Foundation grant (NRF-2018R1A2A1A05078102) and the Technology development Program of MSS (S3201794). The funding body played no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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