Application of macrophage G3bp1 gene in targeted intervention treatment of allergic rhinitis

Abstract

The invention belongs to the field of biotechnology and medicine, and particularly relates to application of a macrophage G3bp1 gene in targeted intervention treatment of allergic rhinitis. The invention provides a pharmaceutical composition for treating allergic rhinitis, which comprises an active ingredient capable of inhibiting the assembly of stress particles in macrophages, and a pharmaceutically acceptable carrier, the active component inhibits the assembly of stress particles by inhibiting the activity of proteins or molecules associated with the assembly of the stress particles. Through mouse model experimental analysis, the treatment effect of the G3BP1 inhibitor G3Ia on an AR mouse model and the related action mechanism of the G3BP1 inhibitor G3Ia in AR patient nasal mucosa macrophages are comprehensively verified, and a solid experimental foundation is provided for further development of an AR treatment method based on SG regulation.

Description

Technical Field

[0001] The present application belongs to the fields of biotechnology and medicine, and specifically relates to the application of macrophage G3bp1 gene in targeted intervention treatment of allergic rhinitis. Background Art

[0002] Allergic rhinitis (AR), a very common respiratory allergic disease, is prevalent worldwide, severely impacting patients' quality of life. Authoritative statistics show that its incidence rate is as high as 20% to 30% and is increasing annually.

[0003] Among existing treatment options, medication is a common approach. While nasal glucocorticoids can alleviate nasal mucosal inflammation to a certain extent, long-term use can cause adverse reactions such as nasal dryness and epistaxis, and some patients may also develop medicamentous rhinitis. Antihistamines can relieve symptoms such as nasal itching and sneezing, but their effectiveness in improving nasal congestion is often suboptimal, and some patients experience side effects such as drowsiness and dry mouth, which can impact their daily lives. Oral leukotriene modifiers, while effective for some patients, carry a risk of hepatotoxicity and require regular liver function monitoring. Furthermore, while immunotherapy is considered a potential cure for AR, it has numerous drawbacks. For example, its lengthy treatment cycle, typically lasting two to three years or even longer, places a significant strain on patient compliance. The complex treatment process requires multiple visits to the hospital for allergen testing and dosage adjustments, significantly inconvenient for patients. Furthermore, in actual clinical practice, long-term efficacy is inconsistent, with some patients experiencing relapses even after completing treatment.

[0004] In recent years, the role of cellular stress granules (SGs) in the development and progression of various diseases has gradually become a research hotspot. SGs are membrane-less cytoplasmic organelles formed when cells are exposed to various stress stimuli. They aggregate RNA-binding proteins and untranslated mRNAs, affecting the protein translation process, thereby playing a key role in the cell's stress response and fate regulation. SGs have demonstrated important regulatory functions in physiological and pathological processes such as antiviral immune responses, neurodegenerative diseases, and tumor progression. However, in the field of allergic rhinitis, research on the role of SGs is still in its infancy, and their potential mechanisms and application value need to be further explored.

[0005] Therefore, given the limitations of current treatments for allergic rhinitis and new advances in SG in disease research, there is an urgent need to explore new treatment methods based on SG regulation to provide patients with allergic rhinitis with more effective, safer and more convenient treatment options. Summary of the Invention

[0006] In order to overcome the above technical problems, the present application accurately identifies the key regulatory factors closely related to allergic rhinitis (AR) from the complex cellular stress response mechanism - macrophage stress granule (SG) assembly-related proteins and molecules, especially G3BP1 protein and its related regulatory molecules, thereby providing a new strategy and new use for effectively treating AR by regulating stress granule (SG) assembly.

[0007] On the one hand, the present application provides a pharmaceutical composition for treating allergic rhinitis, which comprises an active ingredient capable of inhibiting the assembly of stress granules in macrophages, and a pharmaceutically acceptable carrier. The active ingredient inhibits the assembly of stress granules by inhibiting the activity of proteins or molecules related to stress granule assembly.

[0008] Furthermore, the protein associated with stress granule assembly in the macrophages is G3BP1, and the active ingredient can specifically inhibit the function or expression of G3BP1, thereby reducing stress granule assembly in the macrophages.

[0009] Furthermore, the active ingredient is G3Ia FAZ-3532 (G3Ia), which can inhibit stress granule formation by targeting the specific domain NTF2 of G3BP1.

[0010] Furthermore, the pharmaceutically acceptable carrier includes but is not limited to saline, buffer, glucose, water, glycerol, ethanol and combinations thereof.

[0011] Furthermore, the dosage form of the pharmaceutical composition includes but is not limited to nasal drops, sprays, injections, etc., and the route of administration is selected according to the dosage form and the patient's condition.

[0012] By adopting the above technical scheme, the pharmaceutical composition can improve the pathological condition of the nasal mucosa, including reducing epithelial shedding, cell infiltration, exudation, and mucus secretion, reducing immune cell infiltration, cytokine production and serum allergen-specific IgE levels, and restoring macrophage efferocytosis and related receptor protein expression.

[0013] On the other hand, the present application also provides the use of the pharmaceutical composition in treating allergic rhinitis.

[0014] Furthermore, the pharmaceutical composition inhibits the assembly of stress granules in macrophages, thereby alleviating the symptoms of allergic rhinitis.

[0015] On the other hand, the present application also provides a macrophage-specific G3bp1 gene knockout mouse model for use in preparing a drug for treating allergic rhinitis or studying the pathogenesis of allergic rhinitis. The mouse model is constructed by knocking out G3bp1. f / f The mice were crossed with mice that express Cre recombinase specifically in macrophages.

[0016] Using the above technical scheme, the mouse model showed reduced macrophage stress granule assembly and alleviated allergic rhinitis symptoms, including reduced sneezing and scratching, reduced nasal mucosal epithelial shedding, cell infiltration, exudation, mucus secretion, inflammatory cell infiltration, cytokine expression, and serum OVA-specific IgE concentration, and a reduced number of apoptotic cells.

[0017] On the other hand, the present application also provides a combination of therapeutic targets for allergic rhinitis based on the regulation of macrophage stress granule assembly, which includes the G3bp1 gene in macrophages and molecular targets related to G3bp1 that regulate stress granule assembly and thereby affect the progression of allergic rhinitis.

[0018] Furthermore, the molecular target is Lrp1 mRNA involved in m7G modification and the protein QKI7 bound thereto.

[0019] Compared with the existing technology, this application provides a model and potential treatment technology for allergic rhinitis, specifically targeting the G3bp1 gene and related molecular targets in macrophages to regulate the assembly of stress granules (SG) to treat allergic rhinitis. Through experimental analysis of mouse models, this application comprehensively verifies the therapeutic effect of the G3BP1 inhibitor G3Ia on AR mouse models, as well as its related mechanism of action in nasal mucosal macrophages of AR patients, providing a solid experimental foundation for the further development of AR treatment methods based on SG regulation. BRIEF DESCRIPTION OF THE DRAWINGS

[0020] Figure 1 These are the results of the induction and evaluation of the mouse AR model and histological staining and analysis in Example 1; Figure a shows the number of sneezes and scratches per mouse in the control, OVA, and HDM groups within 15 minutes after the last intranasal challenge (n=5, biological replicates), using Tukey's HSD test; Figures b and c show H&E and PAS staining of the nasal mucosa and lung tissues of AR mice.

[0021] Figure 2 The results of nasal lavage fluid collection and cell analysis in Example 2 are shown. Figure d shows flow cytometric analysis of eosinophils and T cells in the nasal mucosa of AR mice (n=3, biological replicates), using Tukey's HSD test; Figure e shows flow cytometric analysis of eosinophils and neutrophils in nasal lavage fluid (NLF) of control and AR mice (n=3, biological replicates), using Tukey's HSD test.

[0022] Figure 3The results of nasal lavage cytokine detection in Example 3. Among them, Figure f shows the expression of the indicated cytokines, Prg2, Epx, and Mp mRNA in the nasal mucosa of AR mice by qRT-PCR (n=3, biological replicates), using Student's t test; Figure g shows the content of IL-4, IL-5, IL-6, and IL-13 in the NLF of the control group and AR mice by ELISA (n=3, biological replicates), using Tukey's HSD test; Figure h shows the IgE level in the serum of the control group and AR mice (n=3, biological replicates), using Tukey's HSD test. Data are expressed as mean ± standard deviation, or show representative photos from three independent experiments. *: p < 0.05; **: p < 0.01.

[0023] Figure 4 These are the results of the induction and evaluation of the mouse AR model and histological staining and analysis in Example 4; Figure a shows the number of sneezes and scratches per mouse within 15 minutes after the last intranasal challenge (n=5, biological replicates); Figure b shows hematoxylin and eosin (H&E) staining of the nasal mucosa and lung tissues of AR mice.

[0024] Figure 5 Flow cytometric detection of eosinophils, neutrophils and T cells in the nasal mucosa of AR mice in Example 5 (n=3, biological replicates).

[0025] Figure 6 The results of nasal lavage fluid collection and cell analysis and nasal lavage fluid cytokine detection in Example 6 are shown in Figure d. ELISA analysis of IL-4, IL-5, IL-6, and IL-13 in nasal lavage fluid (NLF) of AR mice (n=3, biological replicates); Figure e is the mRNA expression of cytokines, eosinophil major basic protein 2 (Prg2), eosinophil peroxidase (Epx), and myeloperoxidase (Mpo) in the nasal mucosa of AR mice detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) (n=3, biological replicates); Figure f is the level of IgE in the serum of R mice (n=3, biological replicates); a photograph of one representative experiment from three independent experiments, *: p<0.05; **: p<0.01. DETAILED DESCRIPTION

[0026] The present invention will be further described below in conjunction with specific examples. It should be understood that these examples are intended to illustrate the present invention only and are not intended to limit the scope of the invention. The experimental methods in the following examples, for which specific conditions are not specified, were generally performed under conventional conditions, conditions described in laboratory manuals, or conditions recommended by the manufacturer.

[0027] Example 1 1. Experimental materials and animal model construction Experimental animals were 6-8 week old C57BL / 6J mice purchased from Joint Ventures Sipper BK Experimental Animal Company (Shanghai, China). f / f The mice were constructed by Cyagen Biosciences Corporation (Suzhou, China), and Lyz2 Cre mice were obtained from The Jackson Laboratory. f / f Mice were crossed with Lyz2-Cre mice to obtain macrophage-specific G3bp1 knockout (G3bp1 mac- / - ) mice. G3bp1 was also set f / f Mice were used as controls. All animal experiments followed the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health and were approved by the Scientific Research Committee of the Second Military Medical University.

[0028] 2. AR model induction and evaluation 1) OVA-induced AR model G3bp1 f / f and G3bp1 mac- / - The mice were divided into two groups and subjected to OVA sensitization. On days 0, 7, and 14, 200 μL of PBS solution containing 0.1 mg OVA and 2 mg Imject Alum was intraperitoneally injected into the mice for sensitization. On days 21-27, 20 μL of PBS solution containing 2 mg OVA was instilled into the mice's nasal cavity every day for stimulation. On day 27, the AR symptoms of the mice were measured. The specific operation was to place each mouse alone in a cage for 15 minutes after the last nasal instillation, carefully count the number of scratches and sneezes of each mouse within these 15 minutes, and statistically analyze G3bp1 f / f and G3bp1 mac- / - Differences between mice.

[0029] 2) AR model induced by house dust mite (HDM) The two groups of mice were treated in the same way. On day 0, the mice were sensitized by intranasal instillation of 20 μL of PBS solution containing 1 μg HDM. From day 7 to day 11, the mice were challenged by intranasal instillation of 20 μL of PBS solution containing 10 μg HDM every day. On day 11, the AR symptoms of the mice were measured in the same way as in the OVA-induced model above. That is, after the last nasal instillation, the mice were left alone for 15 minutes and the number of scratching and sneezing was counted, and G3bp1 was statistically analyzed. f / f and G3bp1 mac- / - Differences between mice.

[0030] 3. Tissue sample collection and processing 1) After completing the symptom assessment, the mice were anesthetized. Nasal mucosa and lung tissues were carefully collected and quickly fixed in 4% paraformaldehyde solution for 24 hours.

[0031] 2) The fixed tissues were decalcified, dehydrated with graded alcohol, and embedded in paraffin, and then cut into 5 μm thick sections for subsequent H&E and PAS staining analysis.

[0032] 4. Textile dyeing and analysis 1) H&E staining The paraffin sections were dewaxed to water and sequentially stained with hematoxylin, differentiated, blued, and eosin according to conventional histological staining procedures.

[0033] Pathological changes in the nasal mucosa and lung tissue were observed using an optical microscope, with a focus on epithelial cell integrity, cellular infiltration, and structural changes. The pathological status of the nasal mucosa was scored according to a pre-established scoring system: normal epithelial cells were scored as 0, microvilli loss as 1, partial detachment as 2, and complete detachment as 3. Normal cellular infiltration was scored as 0, mild infiltration as 1, severe infiltration as 2, and extravasation into the lumen as 3. Two experienced pathologists independently performed the scoring, and the average score was used as the final result.

[0034] 2) PAS staining PAS staining was performed on nasal mucosal tissue sections to detect mucus secretion. After staining, the number of PAS-positive goblet cells was observed and counted under a microscope, and the expression of G3bp1 was compared. f / f and G3bp1 mac- / - Differences between mice.

[0035] The experimental results showed that the present invention successfully constructed macrophage-specific G3bp1 gene knockout mice (G3bp1 mac- / - ), the expression of G3BP1 protein in macrophages was effectively eliminated. Figure 1 , using immunofluorescence microscopy, we found that G3bp1 mac- / - The formation of stress granules (SG) in mouse macrophages was significantly weakened compared with normal conditions. OVA and HDM AR mouse models were used to investigate G3bp1 mac- / - Stimulation experiments were conducted on mice, and the results showed that the AR symptoms of the mice were significantly alleviated, as manifested by a significant reduction in the number of sneezing and scratching.

[0036] Example 2 The nasal cavity of the mouse obtained in Example 1 was rinsed three times with 1 mL of cold PBS containing 10 mM EDTA, and the lavage fluid was collected. The lavage fluid was centrifuged at 1500 rpm at 4°C for 10 minutes to collect the precipitated cells.

[0037] The precipitated cells were analyzed by flow cytometry and stained with antibodies against CD45, CD11b, F4 / 80, SiglecF, Ly6G, CD3, CD19, etc. to distinguish different cell types, such as eosinophils (CD11b + Ly6G - Siglec-F + ), neutrophils (CD11b + Ly6G + ), macrophages (CD11b + Ly6G - f / 4 / 80 + ), T cells (CD11b - CD3 + ) and B cells (CD11b - CD3 - CD19 + ). Analysis of G3bp1 f / f and G3bp1 mac- / - The infiltration of various cells in the nasal lavage fluid of mice and the comparison of the differences in cell numbers.

[0038] The experimental results show that Figure 2 As shown, G3bp1 was analyzed by flow cytometry. mac- / - The number of eosinophils, neutrophils and T cells in the nasal mucosa of mice was lower than that of normal mice, and the cell infiltration in the nasal lavage fluid (NLF) was also significantly improved. + There was no significant change in the number of infiltrating macrophages, but G3bp1 mac- / - The mice showed an increase in the number of macrophages produced, which was associated with the resolution of inflammation.

[0039] Example 3 The mouse nasal cavity was rinsed three times with 0.5 mL of cold PBS containing 10 mM EDTA, and the supernatant was collected. IL-4, IL-5, and IL-13 protein levels in the supernatant were measured using the LEGEND MAX™ Mouse IL-4 ELISA Kit, Mouse IL-13 Quantikine ELISA Kit, and Mouse IL-5 Quantikine ELISA Kit, respectively, according to the kit instructions. Absorbance was measured using a microplate reader, and cytokine concentrations were calculated using a standard curve. Differences between the two groups of mice were compared.

[0040] At the same time, mouse serum was collected by orbital bleeding and stored at 80°C for future use. The OVA-specific IgE level in serum was detected using a Mouse OVA-specific IgE ELISA Kit. Sample addition, incubation, washing, and color development were performed according to the kit's operating procedures. Finally, the absorbance was measured using a microplate reader, and the IgE concentration was calculated based on the standard curve. G3bp1 was analyzed. f / f and G3bp1 mac- / - Differences between mice.

[0041] Total RNA was isolated from macrophages using TRIzol reagent according to the manufacturer's instructions. Real-time quantitative reverse transcription PCR (qRT-PCR) was performed using the SYBR RT-PCR kit (RR430B, Takara Biotechnology (Dalian) Co., Ltd.) and LightCycler (Roche, Switzerland). The primer sequences are shown in Table 1. In each sample, 2 ΔΔCt The relative expression level of each gene was normalized to the relative expression level of the internal reference gene by the cycle threshold method.

[0042] Table 1 Primer sequences (5'-3') in real-time quantitative PCR The experimental results show that Figure 3 As shown, the detection of cytokine expression and production showed that G3bp1 mac- / - The expression of cytokines in the nasal lavage fluid of mice was lower, and the amount of cytokines produced in the nasal lavage fluid was also lower than that in normal mice. At the same time, the concentration of OVA-specific IgE in the serum was higher than that in G3bp1. mac- / - It also decreased in mice.

[0043] Example 4 1. AR model induction and evaluation G3bp1 f / f and G3bp1 mac- / -The mice were divided into two groups and subjected to OVA sensitization operation separately. On days 0, 7 and 14, 200 μL of PBS solution containing 0.1 mg OVA and 2 mg Imject Alum was intraperitoneally injected into the mice for sensitization. On days 21-27, the mice were stimulated by intranasal instillation of 20 μL of PBS solution containing 2 mg OVA every day. In addition, PBS, sodium arsenite (NaAsO2, 0.015 mg / kg) or G3Ia (0.05 mg / kg) were administered intranasally once a day, and the AR symptoms of the mice were measured on day 27. The specific operation was to place each mouse alone in a cage for 15 minutes after the last nasal instillation, carefully count the number of scratching and sneezing of each mouse within these 15 minutes, and statistically analyze G3bp1 f / f and G3bp1 mac- / - Differences between mice.

[0044] 2. Tissue Sample Collection and Processing 1) After completing the symptom assessment, the mice were anesthetized. Nasal mucosa and lung tissues were carefully collected and quickly fixed in 4% paraformaldehyde solution for 24 hours.

[0045] 2) The fixed tissues were decalcified, dehydrated with graded alcohol, and embedded in paraffin, and then cut into 5 μm thick sections for subsequent H&E and PAS staining analysis.

[0046] 3. Histological staining and analysis 1) H&E staining The paraffin sections were dewaxed to water and sequentially stained with hematoxylin, differentiated, blued, and eosin according to conventional histological staining procedures.

[0047] Pathological changes in the nasal mucosa and lung tissue were observed using an optical microscope, with a focus on epithelial cell integrity, cellular infiltration, and structural changes. The pathological status of the nasal mucosa was scored according to a pre-established scoring system: normal epithelial cells were scored as 0, microvilli loss as 1, partial detachment as 2, and complete detachment as 3. Normal cellular infiltration was scored as 0, mild infiltration as 1, severe infiltration as 2, and extravasation into the lumen as 3. Two experienced pathologists independently performed the scoring, and the average score was used as the final result.

[0048] 3) PAS staining PAS staining was performed on nasal mucosal tissue sections to detect mucus secretion. After staining, the number of PAS-positive goblet cells was observed and counted under a microscope, and the expression of G3bp1 was compared. f / f and G3bp1 mac- / - Differences between mice.

[0049] The experimental results show that Figure 4 As shown, the sodium arsenite group (stress granule inducer group) showed more severe allergic rhinitis symptoms, while G3Ia treatment effectively alleviated the progression of allergic rhinitis. At the same time, G3Ia treatment significantly improved mucosal integrity.

[0050] Example 5 The nasal cavity of the mouse obtained in Example 4 was rinsed three times with 1 mL of cold PBS containing 10 mM EDTA, and the lavage fluid was collected. The lavage fluid was centrifuged at 1500 rpm at 4°C for 10 minutes to collect the precipitated cells.

[0051] The precipitated cells were analyzed by flow cytometry and stained with antibodies against CD45, CD11b, F4 / 80, SiglecF, Ly6G, CD3, CD19, etc. to distinguish different cell types, such as eosinophils (CD11b + Ly6G - Siglec-F + ), neutrophils (CD11b + Ly6G + ), macrophages (CD11b + Ly6G - f / 4 / 80 + ), T cells (CD11b - CD3 + ) and B cells (CD11b - CD3 - CD19 + ). Analysis of G3bp1 f / f and G3bp1 mac- / - The infiltration of various cells in the nasal lavage fluid of mice and the comparison of the differences in cell numbers.

[0052] The experimental results show that Figure 5 As shown, treatment with G3Ia significantly inhibited the infiltration of immune cells.

[0053] Example 6 The mouse nasal cavity obtained in Example 4 was rinsed three times with 0.5 mL of cold PBS containing 10 mM EDTA, and the supernatant was collected. The protein levels of IL-4, IL-5, and IL-13 in the supernatant were detected using the LEGEND MAX™ Mouse IL-4 ELISA Kit, Mouse IL-13 Quantikine ELISA Kit, and Mouse IL-5 Quantikine ELISA Kit, respectively. The procedures were performed according to the kit instructions. The absorbance values were measured using a microplate reader, and the cytokine concentrations were calculated based on the standard curve. The differences between the two groups of mice were compared.

[0054] Mouse serum was collected by orbital bleeding and stored at 80°C for later use. The OVA-specific IgE level in serum was detected using a MouseOVA specific IgE ELISA Kit. Sample addition, incubation, washing, and color development were performed according to the kit's operating procedures. Finally, the absorbance was measured using a microplate reader. The IgE concentration was calculated based on the standard curve. G3bp1 was analyzed. f / f and G3bp1 mac- / - Differences between mice.

[0055] Total RNA was isolated from macrophages using TRIzol reagent according to the manufacturer's instructions. Real-time quantitative reverse transcription PCR (qRT-PCR) was performed using the SYBR RT-PCR kit (RR430B, Takara Biotechnology (Dalian) Co., Ltd.) and LightCycler (Roche, Switzerland). The primer sequences are shown in Table 1. In each sample, 2 ΔΔCt The relative expression level of each gene was normalized to the relative expression level of the internal reference gene by the cycle threshold method.

[0056] The experimental results show that Figure 6 As shown in the results, G3Ia treatment significantly inhibited the production of cytokines and the level of ovalbumin-specific immunoglobulin E (IgE) in the serum. In summary, the SG inducer NaAsO2 group aggravated AR symptoms, while G3Ia treatment effectively alleviated AR, specifically by significantly improving mucosal integrity and effectively inhibiting immune cell infiltration, cytokine production, and serum OVA-specific IgE levels.

[0057] Through the detailed operation and analysis of the above examples, the therapeutic effect of the G3BP1 inhibitor G3Ia on the AR mouse model and the related mechanism of action in the nasal mucosal macrophages of AR patients were fully verified, providing a solid experimental basis for the further development of AR treatment methods based on SG regulation.

[0058] This specific embodiment is merely an explanation of the present application and is not a limitation of the present application. After reading this specification, those skilled in the art may make non-creative modifications to the present embodiment as needed, but as long as they are within the scope of the claims of the present application, they are protected by the patent law.

Claims

1. A pharmaceutical composition for treating allergic rhinitis, characterized in that: The pharmaceutical composition comprises an active ingredient capable of inhibiting the assembly of stress granules in macrophages and a pharmaceutically acceptable carrier. The active ingredient inhibits the assembly of stress granules by inhibiting the activity of proteins or molecules related to the assembly of stress granules.

2. The pharmaceutical composition according to claim 1, characterized in that The stress granule assembly-related protein is G3BP1, and the active ingredient can specifically inhibit the function or expression of G3BP1, thereby reducing the stress granule assembly in macrophages.

3. The pharmaceutical composition according to claim 2, characterized in that The active ingredient is G3Ia FAZ-3532 (G3Ia), which can inhibit stress granule formation by targeting a specific domain of G3BP1, NTF2.

4. The pharmaceutical composition according to claim 1, characterized in that The pharmaceutically acceptable carrier includes, but is not limited to, saline, buffer, glucose, water, glycerol, ethanol, and combinations thereof.

5. The pharmaceutical composition according to claim 1, characterized in that The dosage form of the pharmaceutical composition includes but is not limited to nasal drops, sprays, injections, etc., and the administration route is selected according to the dosage form and the patient's condition.

6. Use of the pharmaceutical composition according to any one of claims 1 to 5 in the treatment of allergic rhinitis.

7. The use according to claim 6, characterized in that The pharmaceutical composition inhibits the assembly of stress granules in macrophages, thereby alleviating the symptoms of allergic rhinitis.

8. Use of a macrophage-specific G3bp1 gene knockout mouse model in preparing a drug for treating allergic rhinitis or studying the pathogenesis of allergic rhinitis, characterized in that: The mouse model is characterized by G3bp1 f / f The mice were crossed with mice that express Cre recombinase specifically in macrophages.

9. A combination of therapeutic targets for allergic rhinitis based on the regulation of macrophage stress granule assembly, characterized in that: The combination includes the G3bp1 gene in macrophages and molecular targets related to G3bp1 that regulate stress granule assembly and thereby affect the progression of allergic rhinitis.

10. The allergic rhinitis treatment target combination according to claim 9, characterized in that: The molecular targets are Lrp1 mRNA involved in m7G modification and the protein QKI7 bound thereto.

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