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자료유형
학술저널
저자정보
Yu Jae ik (School of Pharmacy Sungkyunkwan University Suwon 16419 Republic of Korea) Kim Ji-Hoon (School of Pharmacy Sungkyunkwan University Suwon 16419 Republic of Korea) Nam Ki-El (School of Pharmacy Sungkyunkwan University Suwon 16419 Republic of Korea) Lee Wonsik (School of Pharmacy Sungkyunkwan University Suwon 16419 Republic of Korea) Rhee Dong-kwon (School of Pharmacy Sungkyunkwan University Suwon 16419 Republic of KoreaDNBIO Research Center Sungk)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제32권 제6호
발행연도
2022.6
수록면
709 - 717 (9page)
DOI
10.4014/jmb.2203.03006

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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.

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