Loki Zupa alleviates inflammatory and fibrotic responses in cigarette smoke induced rat model of chronic obstructive pulmonary disease

Abstract BackgroundLoki zupa formula is kind of a traditional medicines which used to treat airway diseases, especially those caused by abnormal phlegm, such as cough, asthma and chronic bronchitis. The study was to explore the anti-inflammatory and anti-remodeling effects of Loki zupa using a cigarette-smoke induced rat model of chronic obstructive pulmonary disease.MethodsThe rats were divided into five groups: the normal group, the model group, the LZ 4 g/kg and LZ8g/kg group, and the positive control group. Rats were exposed to cigarette smoke for 24 weeks to induce a COPD rat model. Lung function was assessed. Histopathological changes were recorded using Haematoxylin-eosin. Mucus hypersecretion was evaluated by PAS staining. Inflammatory factors were measured in blood serum and bronchial alveolar lavage fluid using an enzyme-linked immunosorbent assay. Malondialdehyde and superoxide dismutase and glutathione S—transferase levels were tested by biochemical methods. Gene expression patterns were evaluated using GN-GeneChip Clariom S Array for rat from Affymetrix. And top upregulated and downregulated genes validated by qPCR. And these genes was also compared with gene transcriptomic data from smoker patients with emphysema and non-smokers in GEO dataset. IL-6/PLAGA2A signalling protein expression was assessed by western blot and immunohistochemistry. TGF-β1and smad2/3 signalling expressions were analysed by western Blot.Results Loki zupa improved COPD rats lung function as compared to the model group and pathological changes including inflammatory cell infiltration and goblet cell metaplasia was alleviated in rats treated with Loki zupa . Inflammatory factors IL-6, TNF-α, IL-1β and TGF-β1 decreased while significant increase was observed in blood serum IL-10 content in rats treated with Loki zupa . And IL-6 and TNF-α level in bronchial alveolar lavage fluid showed same expression trend in blood serum, while there was no change in MMP-9 content. It also increased antioxidant enzyme SOD activity while reducing the lipid peroxidation. Gene microarray analysis showed there were 355 differentially expressed gene in LZ treated COPD rat lung as compared to model group. Both microarray and qPCR results showed that top differentially expressed genes nxt1(up regulated ) and pla2g2a (down regulated) expression were also reversed by LZ treatment. And protein expression level of IL-6 and pla2g2a was also elevated in CS exposed rats while significant reduction was observed in LZ treated rats. Accordingly, Loki zupa inhibited Collagen-1 upstream protein expression of TGF-β/smad2/3 signalling pathway. Conclusion These results demonstrated that Loki zupa showed protective effects in the lung of the COPD rat model. This mainly because of Loki zupa exerts anti-inflammatory effects by blocking IL-6/pla2g2a signalling and inhibiting inflammatory gene expression and attenuates fibrotic responses by inhibiting TGF-β/smad2/3 signalling pathway.

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Loki Zupa alleviates inflammatory and fibrotic responses in cigarette smoke induced rat model of chronic obstructive pulmonary disease

10.21203/rs.3.rs-24856/v2 ◽

2020 ◽

Author(s):

Nabijan Mohammadtursun ◽

Qiuping Li ◽

Muhammadjan Abuduwaki ◽

Shan Jiang ◽

Hu Zhang ◽

...

Keyword(s):

Protein Expression ◽

Blood Serum ◽

Cigarette Smoke ◽

Rat Model ◽

Lavage Fluid ◽

Inflammatory Factors ◽

Chronic Obstructive ◽

Model Group ◽

Obstructive Pulmonary Disease ◽

Bronchial Alveolar Lavage Fluid

Abstract Background: Loki zupa formula is kind of a traditional medicines which used to treat airway diseases, especially those caused by abnormal phlegm, such as cough, asthma and chronic bronchitis. The study aim was to explore the anti-inflammatory and anti-remodeling effects of Loki zupa by using a cigarette-smoke induced rat model of chronic obstructive pulmonary disease.Methods: The rats were divided into five groups: the normal group, the model group, the LZ 4g/kg and LZ8g/kg group, and the positive control group. Rats were exposed to cigarette smoke for 24 weeks to induce a COPD rat model. Lung function was assessed. Histopathological changes were recorded using Haematoxylin-eosin and Masson’s tricrome staining. Mucus hypersecretion was evaluated by PAS staining. Inflammatory factors were measured in blood serum and bronchial alveolar lavage fluid using an enzyme-linked immunosorbent assay. Malondialdehyde and superoxide dismutase and glutathione S—transferase levels were tested by biochemical methods. Gene expression patterns were evaluated using GN-GeneChip Clariom S Array for rat from Affymetrix. And top upregulated and downregulated genes validated by qPCR. And these genes was also compared with gene transcriptomic data from smoker patients with emphysema and non-smokers in GEO dataset. IL-6/PLAGA2A signalling protein expression was assessed by western blot and immunohistochemistry. TGF-β1and smad2/3 signalling expressions were analysed by western Blot.Results Loki zupa improved COPD rats lung function as compared to the model group and pathological changes including inflammatory cell infiltration and goblet cell metaplasia was alleviated in rats treated with Loki zupa Inflammatory factors IL-6, TNF-α, IL-1β and TGF-β1 decreased while significant increase was observed in blood serum IL-10 content in rats treated with Loki zupa . And IL-6 and TNF-α level in bronchial alveolar lavage fluid showed same expression trend in blood serum, while there was no change in MMP-9 content. It also increased antioxidant enzyme SOD and GPX activity while reducing the lipid peroxidation. Gene microarray analysis showed that there were 355 differentially expressed gene in LZ treated COPD rat lung as compared to model group. Both microarray and qPCR results showed that top differentially expressed genes nxt1(up regulated ) and pla2g2a (down regulated) expression were also reversed by LZ treatment. And protein expression level of IL-6 and pla2g2a was also elevated in CS exposed rats while significant reduction was observed in LZ treated rats. Accordingly, Loki zupa inhibited Collagen-1 upstream protein expression of TGF-β/smad2/3 signalling pathway. Conclusion: These results demonstrated that Loki zupa showed protective effects in the lung of the COPD rat model. This mainly because of Loki zupa exerts anti-inflammatory effects by blocking IL-6/pla2g2a signalling and inhibiting inflammatory gene expression and attenuates fibrotic responses by inhibiting TGF-β/smad2/3 signalling pathway.

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The effects of menopausal hormone therapy on proinflammatory cytokines and immunoglobulins in perimenopausal patients with type 2 diabetes mellitus and chronic obstructive pulmonary disease (COPD)

Terapevticheskii arkhiv ◽

10.26442/terarkh201890104-83 ◽

2018 ◽

Vol 90 (10) ◽

pp. 79-83

Author(s):

A S Panevina ◽

N S Smetneva ◽

A M Vasilenko ◽

M V Shestakova

Keyword(s):

Blood Serum ◽

Hormone Therapy ◽

Proinflammatory Cytokines ◽

Lavage Fluid ◽

Menopausal Hormone Therapy ◽

Chronic Obstructive ◽

Menopausal Syndrome ◽

Obstructive Pulmonary Disease ◽

Tnf Α

Aim. To determine the effects of menopausal hormone therapy dosage on levels of proinflammatory cytokines and immunoglobulins in bodily fluids of patients with type 2 diabetes mellitus (DM) and chronic obstructive pulmonary disease (COPD) during perimenopause. Materials and methods. The study included 119 perimenopausal females with moderate type 2 DM and stable COPD with signs of menopausal syndrome. Cytokine levels in bronchoalveolar lavage fluid and blood serum were measured with flow cytofluorometry (Вeckman Coulter FC500, USA) using a multiplex kit for human cytokines (BMS810FF) in adherence to the manufacturer’s instructions. The lower limit of quantification was 2.5-52.7 pg/mL. The following cytokines were studied: IL-1β, IL-6, IL-8, TNF-α and IF-γ. The data was analyzed with Flow CytomixProver 3.0 manufacturer-licensed software package. IgМ, IgG and IgА in the blood serum (Vektor-Best, Russia) were detected using an immunoenzymatic assay (Stat Fax 3200Analyzer, Awareness Technology, USA). Menopausal hormone therapy (MHT) with 17 beta-estradiol/dydrogesterone (standard - 2 mg, low - 1 mg, ultralow - 0.5 mg): 0.5/2.5 (estradiol 0.5 mg/dydrogesterone 2.5 mg) - ultralow-dose MHT, 1/10 (estradiol 1 mg/dydrogesterone 10 mg) - low-dose MHT; 2/10 (estradiol 2 mg/dydrogesterone 10 mg) - standard-dose MHT. Саrbohydrate metabolism was assessed in three groups. Results and discussion. While 2/10 MHT yielded the most prominent decrease in IL-1β, IL-6, IL-8, TNF-α and IF-γ levels in bronchoalveolar lavage fluid and blood serum, the effect was statistically insignificant compared to 0.5/2.5 and 1/10 MHT. Initially decreased IgM, IgG and IgA levels were elevated in all the three dosage groups with no significant differences between them. As to carbohydrate metabolism target values of glycemia were achieved in all three groups taking MHT. Conclusion. Standard-, low - and ultralow-dose MHT has positive effects on levels of proinflammatory cytokines and immunoglobulins characteristic of the association between type 2 DM, COPD and menopausal syndrome. The differences between the three dosage groups were statistically insignificant. Different dosage of MHT with dydrogesterone provide for improving impaired carbohydrate metabolism.

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Baicalin Exerts Anti-Airway Inflammation and Anti-Remodelling Effects in Severe Stage Rat Model of Chronic Obstructive Pulmonary Disease

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2018/7591348 ◽

2018 ◽

Vol 2018 ◽

pp. 1-14 ◽

Cited By ~ 3

Author(s):

Genfa Wang ◽

Nabijan Mohammadtursun ◽

Yubao Lv ◽

Hongying Zhang ◽

Jing Sun ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Bronchoalveolar Lavage ◽

Cigarette Smoke ◽

Rat Model ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Chronic Obstructive ◽

Airway Remodelling ◽

Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a worldwide epidemic. Current approaches are disappointing due to limited improvement of the disease development. The present study established 36-week side stream cigarette smoke induced rat model of COPD with advanced stage feature and evaluted the effects of baicalin on the model. Fifty-four Sprague–Dawley rats were randomly divided into six groups including room air control, cigarette smoke exposure, baicalin (40 mg/kg, 80 mg/kg, and 160 mg/kg), and budesonide used as a positive control. Rats were exposed to cigarette smoke from 3R4F research cigarettes. Pulmonary function was evaluated and pathological changes were also observed. Cytokine level related to airway inflammation and remodelling in blood serum, bronchoalveolar lavage fluid, and lung tissue was determined. Blood gases and HPA axis function were also examined, and antioxidant levels were quantified. Results showed that, after treatment with baicalin, lung function was improved and histopathological changes were ameliorated. Baicalin also regulated proinflammatory and anti-inflammatory balance and also airway remodelling and anti-airway remodelling factors in blood serum, bronchoalveolar lavage fluid, and lung tissue. Antioxidant capacity was also increased after treatment with baicalin in COPD rat model. HPA axis function was improved in baicalin treated groups as compared to model group. Therefore, baicalin exerts lung function protection, proinflammatory and anti-inflammatory cytokine regulation, anti-airway remodelling, and antioxidant role in long term CS induced COPD model.

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Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

10.1101/2020.06.29.177345 ◽

2020 ◽

Author(s):

Yiping Ma ◽

Zhu Li ◽

Yalei Zhao ◽

Mo Sun ◽

Wuzhuang Sun ◽

...

Keyword(s):

Protein Expression ◽

Cigarette Smoke ◽

Rat Model ◽

Airflow Obstruction ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Chronic Obstructive ◽

Lung Pathology ◽

Airway Wall ◽

Tgf Β1

AbstractBackgroundRecently, some researchers have reported that PIgR expression is down-regulated in Chronic Obstructive Pulmonary Disease (COPD) and SIgA deficiency correlates with severity of airflow obstruction. What’ s more, some studies have demonstrated that 2 percent of hydrogen or hydrogen water is effective in treating and preventing various diseases.ObjectivesThe aim of this study was to observe the effect of hydrogen on the expression of SIgA, PIgR, IL-4, IL-5, TGF-β1 and IL-40 in lung tissue of COPD rats, to study the relationship between lung pathology parameter and SIgA, PIgR, therefore we can understand the effect of hydrogen on the development of COPD by changing SIgA expression of airway mucosal in COPD rats.MethodsA rat model of COPD was established by cigarette smoke exposure, and different concentrations of hydrogen were inhaled as intervention measures. After 4 months of cigarette smoke exposure, pathologic changes and airway wall remodeling of the lung were assessed by optical microscope. The protein expressions of SIgA, PIgR, IL-4, IL-5, TGF-β1 as well as IL-40 in the lung tissues were observed by immunohistochemistry or Western blot. The correlation between lung pathology parameter and the expression of SIgA, PIgR was analyzed. The correlation between SIgA and the expression of IL-4, IL-5, TGF-β1 and IL-40 was analyzed.ResultsThe results showed that hydrogen inhalation significantly ameliorated lung pathology and airway wall remodeling, increased the protein expression of SIgA, PIgR, IL-4, IL-5, and IL-40, and reduced the protein expression of TGF-β1.ConclusionsInhalation of 22% and 41.6% hydrogen showed a better effect than inhalation of 2% hydrogen. Hydrogen inhalation can significantly improve the expression of SIgA on the mucosal surface of COPD rats, which may be one of the mechanisms which hydrogen works on COPD pathogenesis.

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FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

BMC Pulmonary Medicine ◽

10.1186/s12890-021-01409-6 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ying Liu ◽

Jiawei Xu ◽

Tian Liu ◽

Jinxiang Wu ◽

Jiping Zhao ◽

...

Keyword(s):

Lung Function ◽

Airway Inflammation ◽

Cigarette Smoke ◽

Airway Remodeling ◽

Critical Factor ◽

Lavage Fluid ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Copd Patients ◽

Impaired Lung Function

Abstract Background Cigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulation, airway inflammation and remodeling. Methods Serum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1± mice and FSTL1flox/+ mice were exposed to room air or chronic CS. Additionally, 3-methyladenine (3-MA), an inhibitor of autophagy, was applied in CS-exposed WT mice. The lung tissues and serum from patients and murine models were tested for FSTL1 and autophagy-associated protein expression by ELISA, western blotting and immunohistochemical. Autophagosome were observed using electron microscope technology. LTB4, IL-8 and TNF-α in bronchoalveolar lavage fluid of mice were examined using ELISA. Airway remodeling and lung function were also assessed. Results Both FSTL1 and autophagy biomarkers increased in COPD patients and CS-exposed WT mice. Autophagy activation was upregulated in CS-exposed mice accompanied by airway remodeling and airway inflammation. FSTL1± mice showed a lower level of CS-induced autophagy compared with the control mice. FSTL1± mice can also resist CS-induced inflammatory response, airway remodeling and impaired lung function. CS-exposed WT mice with 3-MA pretreatment have a similar manifestation with CS-exposed FSTL1± mice. Conclusions FSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke-induced COPD.

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Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽

10.3390/medicines5030106 ◽

2018 ◽

Vol 5 (3) ◽

pp. 106 ◽

Cited By ~ 4

Author(s):

Yuanjun Deng ◽

Kairui Tang ◽

Runsen Chen ◽

Yajie Liu ◽

Huan Nie ◽

...

Keyword(s):

Signaling Pathway ◽

P38 Mapk ◽

Low Dose ◽

Serum Levels ◽

Inflammatory Factors ◽

Enzyme Linked Immunosorbent Assay ◽

High Dose ◽

Model Group ◽

Necrosis Factor Alpha ◽

Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

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Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling

Molecules ◽

10.3390/molecules23102489 ◽

2018 ◽

Vol 23 (10) ◽

pp. 2489 ◽

Cited By ~ 6

Author(s):

Na-Rae Shin ◽

Chul Kim ◽

Chang-Seob Seo ◽

Je-Won Ko ◽

Young-Kwon Cho ◽

...

Keyword(s):

Cigarette Smoke ◽

Inflammatory Cell ◽

Pulmonary Inflammation ◽

Water Extract ◽

Lavage Fluid ◽

Chronic Obstructive ◽

Necrosis Factor Alpha ◽

Obstructive Pulmonary Disease ◽

Cell Counts ◽

Oxide Synthase

Galgeun-tang water extract (GGWE) is used to treat various diseases such as the common cold, eczema and asthma in China and Korea. In this study, we investigated the anti-inflammatory effect of GGWE using a cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced induced pulmonary inflammation mouse model. The mice were exposed to CS for a total of seven days (eight cigarettes per day for 1 h) and LPS was administered intranasally to mice on day 4. GGWE was administered by oral gavage at doses of 50 mg/kg or 100 mg/kg 1 h before exposure to CS. GGWE decreased inflammatory cell counts, and expression of inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) in bronchoalveolar lavage fluid (BALF) from mice exposed to CS and LPS. GGWE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the phosphorylation of inhibitor of kappa-B subunit alpha (IκBα) and nuclear factor kappa-B (NF-κB) in CS- and LPS-exposed mice. Histological examinations revealed that GGWE suppressed inflammatory cell infiltration into lung tissue compared to untreated CS- and LPS-exposed mice. In conclusion, GGWE effectively suppressed CS- and LPS-induced pulmonary inflammation. Our results indicate that GGWE may be used as a protective drug to control pulmonary inflammation diseases such as chronic obstructive pulmonary disease.

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Matrine reduces cigarette smoke-induced airway neutrophilic inflammation by enhancing neutrophil apoptosis

Clinical Science ◽

10.1042/cs20180912 ◽

2019 ◽

Vol 133 (4) ◽

pp. 551-564 ◽

Cited By ~ 9

Author(s):

Xuhua Yu ◽

Huei Jiunn Seow ◽

Hao Wang ◽

Desiree Anthony ◽

Steven Bozinovski ◽

...

Keyword(s):

Cigarette Smoke ◽

Lung Inflammation ◽

Therapeutic Potential ◽

Proteolytic Enzymes ◽

Ex Vivo ◽

Lavage Fluid ◽

Airflow Limitation ◽

Chronic Obstructive ◽

Neutrophilic Inflammation ◽

Anti Inflammatory

AbstractChronic Obstructive Pulmonary Disease (COPD) is a major incurable global health burden and will become the third largest cause of death in the world by 2030. It is well established that an exaggerated inflammatory and oxidative stress response to cigarette smoke (CS) leads to, emphysema, small airway fibrosis, mucus hypersecretion, and progressive airflow limitation. Current treatments have limited efficacy in inhibiting chronic inflammation and consequently do not reverse the pathology that initiates and drives the long-term progression of disease. In particular, there are no effective therapeutics that target neutrophilic inflammation in COPD, which is known to cause tissue damage by degranulation of a suite of proteolytic enzymes including neutrophil elastase (NE). Matrine, an alkaloid compound extracted from Sophora flavescens Ait, has well known anti-inflammatory activity. Therefore, the aim of the present study was to investigate whether matrine could inhibit CS-induced lung inflammation in mice. Matrine significantly reduced CS-induced bronchoalveolar lavage fluid (BALF) neutrophilia and NE activity in mice. The reduction in BALF neutrophils in CS-exposed mice by matrine was not due to reductions in pro-neutrophil cytokines/chemokines, but rather matrine’s ability to cause apoptosis of neutrophils, which we demonstrated ex vivo. Thus, our data suggest that matrine has anti-inflammatory actions that could be of therapeutic potential in treating CS-induced lung inflammation observed in COPD.

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IL-33/ST2 axis promotes the inflammatory response of nasal mucosal epithelial cells through inducing the ERK1/2 pathway

Innate Immunity ◽

10.1177/1753425920918911 ◽

2020 ◽

Vol 26 (6) ◽

pp. 505-513

Author(s):

Yun-Qiu Li ◽

Yu Zhong ◽

Xu-Ping Xiao ◽

Dan-Dan Li ◽

Zheng Zhou ◽

...

Keyword(s):

Epithelial Cells ◽

Ar Model ◽

Inflammatory Factors ◽

Mrna Levels ◽

Model Group ◽

Protein Levels ◽

Tnf Α ◽

Der P1 ◽

The Relationship

Allergic rhinitis (AR) is a nasal mucosal inflammatory disease mediated by environmental allergens. At present, the relationship between the IL-33/ST2 axis, ERK1/2 pathway and AR progression needs further exploration. In our study, an AR model was constructed in vitro by treating HNEpC cells with Der p1. qRT-PCR was applied to assess the mRNA levels of IL-33, ST2, TNF-α, IL-6, and IL-8. Western blotting was used to measure the protein levels of IL-33, ST2, and the downstream proteins p-ERK1/2, ERK1/2, p-RSK, and RSK. IL-6, IL-8, IL-33, and TNF-α protein levels in cell supernatants were evaluated by ELISA. Flow cytometry was performed to check cell apoptosis of HNEpC in the presence or absence of Der p1. Our results indicate that the relative levels of IL-33, ST2, TNF-α, IL-6, and IL-8 were increased significantly in the AR model group. The above effects were notably reversed after transfection with shIL-33 or shST2. IL-33 stimulation further resulted in the increase in both ST2 and inflammation-associated cytokines, and these effects were restored after shST2 treatment. Also, the levels of inflammatory factors induced by IL-33 stimulation or ST2 overexpression were reversed after applying an ERK1/2 pathway blocker. In conclusion, IL-33/ST2 mediated inflammation of nasal mucosal epithelial cells by inducing the ERK1/2 pathway.

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