International archives of allergy and immunology · 2026
Role of a Calcitonin Gene-related Peptide-Neutralizing Antibody in theTreatment of Allergic Rhinitis in a Murine Model.
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Sun Yongling, Zeng Yiyun, Guo Ying, Liu Yubiao, Li Fu, Zhang Yue, Ye Jun, Mao Guangyao, Kong Xuhui
Аннотация
INTRODUCTION: This study aimed to characterize the expression of calcitonin gene-related peptide (CGRP) in patients with allergic rhinitis (AR) and to investigate the effects of CGRP intervention on AR symptoms, nasal mucosal inflammation, and the number of group 2 innate lymphoid cells (ILC2s) in a murine model.
METHODS: Peripheral blood and inferior turbinate mucosal samples were collected from 20 patients with AR and 20 control subjects. CGRP levels in serum and nasal mucosa were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC), respectively. Thirty-two C57BL/6J mice were randomly assigned to four groups: Control, AR, AR + isotype IgG, and AR + anti-CGRP. Mice in the AR group were sensitized and intranasally challenged with ovalbumin (OVA). During the challenge phase, mice in the AR + isotype IgG group and the AR + anti-CGRP group received isotype IgG and AR + anti-CGRP treatment, respectively, whereas mice in the Control group received phosphate-buffered saline (PBS) only. AR-related nasal symptoms were evaluated based on the frequency of nose rubbing and sneezing, as well as the severity of rhinorrhea. Hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining were used to assess histopathological changes in the nasal mucosa and the increased number of goblet cells. IHC was used to detect the expression levels of IL-1β, IL-6, TNF-α, and CGRP. Double immunofluorescence staining was performed to quantify ILC2s in the nasal mucosa. Western blotting (WB) was used to determine the phosphorylation levels of the key proteins in the MAPK pathway, including JNK, ERK1/2, and p38.
RESULTS: CGRP expression levels in the nasal mucosa and serum of patients with AR were significantly higher than those in the control group. Serum CGRP levels were positively correlated with visual analog scale (VAS) scores, and nasal mucosal CGRP expression was positively correlated with the number of inflammatory cells. Compared with the AR group and the AR + isotype IgG group, mice in the Anti-CGRP group showed significantly alleviated nasal symptoms and markedly reduced inflammatory cell infiltration in the nasal mucosa. In addition, the expression levels of IL-1β, IL-6, TNF-α, and CGRP in the nasal mucosa were decreased, the number of ILC2s was reduced, and the phosphorylation levels of p-JNK, p-ERK1/2, and p-p38 were significantly lowered.
CONCLUSION: CGRP may serve as a potential therapeutic target for AR. CGRP-neutralizing antibody can alleviate AR symptoms, suppress inflammatory responses, and regulate the number of ILC2s.
METHODS: Peripheral blood and inferior turbinate mucosal samples were collected from 20 patients with AR and 20 control subjects. CGRP levels in serum and nasal mucosa were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC), respectively. Thirty-two C57BL/6J mice were randomly assigned to four groups: Control, AR, AR + isotype IgG, and AR + anti-CGRP. Mice in the AR group were sensitized and intranasally challenged with ovalbumin (OVA). During the challenge phase, mice in the AR + isotype IgG group and the AR + anti-CGRP group received isotype IgG and AR + anti-CGRP treatment, respectively, whereas mice in the Control group received phosphate-buffered saline (PBS) only. AR-related nasal symptoms were evaluated based on the frequency of nose rubbing and sneezing, as well as the severity of rhinorrhea. Hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining were used to assess histopathological changes in the nasal mucosa and the increased number of goblet cells. IHC was used to detect the expression levels of IL-1β, IL-6, TNF-α, and CGRP. Double immunofluorescence staining was performed to quantify ILC2s in the nasal mucosa. Western blotting (WB) was used to determine the phosphorylation levels of the key proteins in the MAPK pathway, including JNK, ERK1/2, and p38.
RESULTS: CGRP expression levels in the nasal mucosa and serum of patients with AR were significantly higher than those in the control group. Serum CGRP levels were positively correlated with visual analog scale (VAS) scores, and nasal mucosal CGRP expression was positively correlated with the number of inflammatory cells. Compared with the AR group and the AR + isotype IgG group, mice in the Anti-CGRP group showed significantly alleviated nasal symptoms and markedly reduced inflammatory cell infiltration in the nasal mucosa. In addition, the expression levels of IL-1β, IL-6, TNF-α, and CGRP in the nasal mucosa were decreased, the number of ILC2s was reduced, and the phosphorylation levels of p-JNK, p-ERK1/2, and p-p38 were significantly lowered.
CONCLUSION: CGRP may serve as a potential therapeutic target for AR. CGRP-neutralizing antibody can alleviate AR symptoms, suppress inflammatory responses, and regulate the number of ILC2s.