Individualized Treatment for Allergic Rhinitis

Cho, Sung Woo; Kim, Dong Young

doi:10.4168/aair.2017.9.5.383

Cited by 2 publications

(1 citation statement)

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“…In line with the effect observed, previous IgE-independent AR models, such as lipopolysaccharides-or double stranded DNA or RNA -induced rhinitis mice models, have showed IL-17 dominancy, which can explain the possible correlation between NLRP3 and Th17 rather than that with Th1 25,26 . The role of IL-17 in allergic rhinitis had recently been elucidated by recruiting neutrophils 27 , and IL-17 is known to be associated with the severity of allergic rhinitis 28 . In the future, additional studies are required to assess the correlation between NLRP3 and IgE-independent, Th17-related allergic reaction, with optimized methods.…”

Section: Discussionmentioning

confidence: 99%

NLRP3 inhibition attenuates the allergic rhinitis symptoms in an mice model

Lee,

Ko,

Gil

et al. 2023

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This study aimed to identify the mechanism underlying the activation of Nod-like receptor family, pyrin domain‐containing 3 (NLRP3) inflammasome signaling pathway in an ovalbumin (OVA)-induced allergic rhinitis (AR) mice model and to validate the effect of a specific inhibitor of the NLRP3, MCC950. Mice were divided into three groups and each group consisted of ten mice (saline group, the negative control group; OVA group, the OVA-induced AR model group; and OVA + MCC group, treated with 10 mg/kg MCC950). MCC950 was administered intraperitoneally every second day. Multiple parameters of AR, including NLRP3, caspase-1, interleukin (IL)-1β, and IL-18 were evaluated by using ELISA, RT-qPCR, histopathology, and immunohistochemistry. The mRNA and protein levels of NLRP3, caspase-1, IL-1β and IL-18 were upregulated in the OVA group compared with those of the saline group. MCC950 significantly inhibited the mRNA and protein levels of NLRP3, caspase-1, IL-1β and IL-18 in nasal tissue. Further, AR symptoms and eosinophil count were normalized after MCC950 treatment. However, OVA-specific IgE was not restored in the OVA + MCC group. In conclusion, NLRP3 inflammasome signaling pathway may be an alternative pathway to induce AR symptoms in OVA-induced AR model. MCC950 is a specific inhibitor of NLRP3 cascade, which attenuates AR symptoms regardless of IgE.

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Section: Discussionmentioning

confidence: 99%