Sweat pores function is the ascending and descending of Qi. The human body maintains a continuous, holistic, and dynamic balance through the functioning of sweat pores as well as the Qi movement and transformation in the spleen, stomach, and triple energizer. Sweat pores play a crucial role in the generation and development of Zang-fu organs, essence and spirit, and body and orifices, as well as in the onset and progression of diseases. Oxidative stress significantly affects the regulation of inflammation in allergic rhinitis(AR), induces the pathological damage to nasal epithelial cells, and alters immune activity, serving as a key mechanism exacerbating AR symptoms. This mechanism closely aligns with the pathogenesis associated with dysfunction in the sweat pore-Qi-triple energizer system. In recent years, oxidative stress and antioxidants in AR have received increasing attention. Elevated levels of reactive oxygen species, fractional exhaled nitric oxide, and malondialdehyde have become key indicators for the early diagnosis of AR. Classical prescriptions, empirical prescriptions, and newly developed preparations of traditional Chinese medicine(TCM) for external use with anti-inflammatory, anti-allergic, and immune-regulatory effects via antioxidant pathways have demonstrated definite efficacy in treating AR. This provides a basis for understanding the pathogenesis of AR in TCM from a modern medical perspective. Therefore, this paper systematically examines the relationship between the sweat pore-Qi-triple energizer system and AR, incorporating the oxidative stress mechanism into the research on pathogenesis of the disorders. Furthermore, methods for treating AR in children are proposed with TCM preparations for external use which aimed at opening nasal sweat pores, dispersing, searching, channeling with aroma, warming, and dredging, regulating Qi movement in spleen, warming Yang Qi to promote urination, and clearing latent wind to inhibit liver depression.
Humans ; Oxidative Stress/drug effects* ; Rhinitis, Allergic/metabolism* ; Child ; Qi ; Sweat/metabolism* ; Drugs, Chinese Herbal/administration & dosage* ; Medicine, Chinese Traditional

Allergic rhinitis (AR) is a chronic non-specific inflammatory disease of the nasal mucosa caused by abnormal activation of the immune system, with alterations in macrophage polarization playing a crucial role in its occurrence and development. Non-coding RNA has been found to play a key role in the polarization of macrophages. This study aims to explore the latest developments in research on the role of non-coding RNA-regulated macrophage polarization in the pathogenesis of AR, with the goal of identifying new approaches and potential targets for the diagnosis and treatment of AR.
Humans ; Rhinitis, Allergic/immunology* ; Macrophages/metabolism* ; RNA, Untranslated/genetics* ; Animals ; Macrophage Activation/genetics* ; Cell Polarity/genetics*

Objective To explore the effect of Evodiamine (Evo) on the immune function of allergic rhinitis (AR) rats and the regulatory mechanism on C-C motif chemokine ligand 2 (CCL2)/ C-C motif chemokine receptor 2 (CCR2) pathway. Methods The related targets of Evo-AR-immune function were screened by network pharmacology, and the protein interaction network diagram of intersecting targets was constructed. The AR rat model was established by ovalbumin (OVA) combined with aluminium hydroxide, and the rats were divided into six groups: a normal control (NC) group, a model group, a Loratadine (LOR) group, an Evodiamine low dose (Evo-L) group, a Evodiamine high dose (Evo-H) groups, and an Evo-H combined with CCL2 group. After the last administration, the symptoms of rats in each group were scored; ELISA was applied to detect the levels of histamine, immunoglobulin E (IgE), interleukin 4 (IL-4), IL-13 and interferon γ (IFN-γ); Diff-Quick staining solution was applied to detecte the number of cells in the nasal lavage fluid (NALF); hematoxylin eosin (HE) staining was applied to observe the pathological changes of nasal mucosa tissue; real-time quantitative PCR was applied to detect the levels of CCL2 and CCR2 mRNA in tissue; Western blot was applied to detect the expression levels of CCL2, CCR2 and CXC motif chemokine ligand 8 (CXCL8) proteins in nasal mucosa. Results There were eight intersection targets of EVo-AR-immune function, and protein interaction network diagram showed that CXCL8 was the core target. Compared with the NC group, the score of nasal symptoms, the levels of histamine, IgE, IL-4 and IL-13, the numbers of eosinophil, macrophages, neutrophils, lymphocytes and total cells, the mRNA and protein expression levels of CCL2 and CCR2, and the expression of CXCL8 protein in the model group were increased, while the level of IFN-γ was decreased. Compared with the model group, the score of nasal symptoms, the levels of histamine, IgE, IL-4 and IL-13, the numbers of eosinophil, macrophages, neutrophils, lymphocytes and total cells, the mRNA and protein expression levels of CCL2 and CCR2, and the expression of CXCL8 protein in LOR and Evo groups were decreased, while the level of IFN-γ was increased. Further use of CCL2 recombinant protein for compensatory experiments revealed that the improvement effect of Evo on immune function in AR rats was reversed by CCL2. Conclusion Evo can improve the immune function of AR rats, and its mechanism may be related to the inhibition of the CCL2/CCR2 pathway.
Animals ; Receptors, CCR2/immunology* ; Signal Transduction/drug effects* ; Chemokine CCL2/immunology* ; Rats ; Rhinitis, Allergic/metabolism* ; Immunoglobulin E/blood* ; Quinazolines/pharmacology* ; Male ; Interferon-gamma ; Rats, Sprague-Dawley ; Interleukin-13 ; Histamine ; Interleukin-4/immunology* ; Disease Models, Animal

Objective To investigate the expression of blood basophil activation markers in patients with allergic rhinitis (AR) and the effects of allergens on their expression. Methods The blood samples were collected from the following four groups: healthy control (HC), AR patients with negative skin prick test (nAR), seasonal AR patients (sAR) and perennial AR patients (pAR). Flow cytometry was employed to analyze the expression of basophil activation markers Immunoglobulin E receptor I alpha(FcepsilonRIα), CD63 and CD203c in AR patients. Plasma levels of interleukin 4 (IL-4) and IL-8 were measured by liquid-phase chip technology, and their correlations with the percentages of activated basophils were further analyzed. An ovalbumin-induced AR mouse model was established, and the expression levels of FcepsilonRIα and CD63 on blood basophils were detected. Results The expression of FcepsilonRIα, CD203c and CD63 on basophils were increased in nAR, sAR and pAR patients. Allergens enhanced the mean florescence intensity expression of CD63 and CD203c on basophils of sAR and pAR patients. The plasma levels of IL-4 and IL-8 were elevated in nAR, sAR and pAR patients, showing moderate to high correlations with the expression levels of basophil activation markers. The FcepsilonRIαand CD63 expression on basophils of AR mice were increased. Conclusion Allergens may contribute to AR pathogenesis by upregulating the expression of FcepsilonRIα, CD63 and CD203c, as well as promoting the secretion of IL-4 and IL-8.
Basophils/metabolism* ; Humans ; Allergens/immunology* ; Animals ; Rhinitis, Allergic/blood* ; Female ; Male ; Adult ; Mice ; Biomarkers/blood* ; Tetraspanin 30/blood* ; Interleukin-4/blood* ; Interleukin-8/blood* ; Receptors, IgE/blood* ; Phosphoric Diester Hydrolases ; Young Adult ; Pyrophosphatases ; Middle Aged ; Mice, Inbred BALB C

One of the main pathological features of airway inflammatory diseases is hypersecretion of airway mucus, which is manifested by goblet cell hyperplasia and mucociliary clearance dysfunction. In recent years, it has been found that the molecular structure of calcium activated chloride ion channels, transmenbrane protein 16A（TMEM16A）, is closely related to airway mucus hypersecretion.TMEM16A not only mediates ion transepithelial transport and hydration, but also participates in the regulation of mucin secretion. TMEM16A is highly expressed in airway epithelium of a variety of inflammatory diseases of upper and lower airway, such as asthma, cystic fibrosis, allergic rhinitis, chronic sinusitis and so on. Understanding the expression level and regulation mechanism of TMEM16A in different airway diseases and revealing its physiological function and pathological mechanism is critical for targeted disease treatment. This paper summarizes the research status of the discovery process, structural characteristics and regulatory mechanism of TMEM16A, and then summarizes the expression level of TMEM16A in asthma, cystic fibrosis, allergic rhinitis and chronic sinusitis ant related pathological mechanisms, clarifies the potential value of TMEM16A as a therapeutic target for the above four diseases, in order to guide treatment of airway inflammatory diseases.
Humans ; Asthma/metabolism* ; Anoctamin-1 ; Cystic Fibrosis/metabolism* ; Neoplasm Proteins/metabolism* ; Sinusitis/metabolism* ; Chloride Channels/metabolism* ; Rhinitis, Allergic/metabolism* ; Inflammation

In recent years，with the increase in environmental pollution，organisms are exposed to more internal and external oxidative stress factors than ever before.Nuclear factor erythroid 2-related factor 2（nuclear factor erythroid 2-related factor 2，NRF2），as a core transcription factor in response to oxidative stress，maintains cellular redox homeostasis by inducing the expression of various antioxidant factors.The nasal cavity，as the "gateway" of the respiratory tract，is often accompanied by oxidative stress（oxidative stress，OS）damage，leading to the occurrence of allergic rhinitis（allergic rhinitis，AR）.Recent studies have revealed some associations between the NRF2 signaling pathway and the mechanism of AR development.Activation of NRF2 provides a potential protective effect against AR，and some natural NRF2 activators have shown therapeutic potential in clinical experiments.Therefore，this article briefly reviews the relationship between NRF2 and AR，aiming to provide a new therapeutic target and perspective for the treatment of AR.
NF-E2-Related Factor 2/metabolism* ; Humans ; Rhinitis, Allergic/metabolism* ; Signal Transduction ; Oxidative Stress

OBJECTIVE: To investigate the changes in percentage of GATA3⁺ regulatory T (Treg) cells in patients with allergic rhinitis (AR) and mouse models. METHODS: The nasal mucosa specimens were obtained from 6 AR patients and 6 control patients for detection of nasal mucosal inflammation. Peripheral blood mononuclear cells (PBMC) were collected from 12 AP patients and 12 control patients to determine the percentages of Treg cells and GATA3⁺ Treg cells. In a C57BL/6 mouse model of AR, the AR symptom score, peripheral blood OVA-sIgE level, and nasal mucosal inflammation were assessed, and the spleen of mice was collected for detecting the percentages of Treg cells and GATA3⁺ Treg cells and the expressions of Th2 cytokines. RESULTS: Compared with the control patients, AR patients showed significantly increased eosinophil infiltration and goblet cell proliferation in the nasal mucosa (P < 0.01) and decreased percentages of Treg cells and GATA3⁺ Treg cells (P < 0.05). The mouse models of AR also had more obvious allergic symptoms, significantly increased OVA-sIgE level in peripheral blood, eosinophil infiltration and goblet cell hyperplasia (P < 0.01), markedly lowered percentages of Treg cells and GATA3⁺ Treg cells in the spleen (P < 0.01), and increased expressions of IL-4, IL-6 and IL-10 (P < 0.05). CONCLUSION The percentage of GATA3⁺ Treg cells is decreased in AR patients and mouse models. GATA3⁺ Treg cells possibly participate in Th2 cell immune response, both of which are involved in the occurrence and progression of AR, suggesting the potential of GATA3⁺ Treg cells as a new therapeutic target for AR.
Animals ; Mice ; Cytokines/metabolism* ; Disease Models, Animal ; GATA3 Transcription Factor ; Inflammation ; Leukocytes, Mononuclear/metabolism* ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nasal Mucosa/metabolism* ; Ovalbumin ; Rhinitis, Allergic/therapy* ; T-Lymphocytes, Regulatory ; Th2 Cells/metabolism* ; Humans

Objective To investigate the role of microRNA-18a (miR-18a) in the pathogenesis of allergic rhinitis in mice. Methods Twenty-two BALB/c mice were randomly divided into a blank group, a model group and a miR-18a group. Mice in the model group and the miR-18a group were injected intraperitoneally with obumin (OVA) suspension to prepare allergic rhinitis models, and mice in the miR-18a group were simultaneously given lentiviral vector plasmid for overexpression of miR-18a. Allergy symptoms were evaluated by the behavioral score and HE staining. The plasma levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) were measured by ELISA. The distribution of CD45⁺ cells in nasal mucosa was measured by immunofluorescence histochemistry, and CD45⁺ cells in nasal lavage fluid were measured by flow cytometry. The mRNA expression levels of IL-1β, IL-6 and TNF-α in nasal mucosa tissues were measured by fluorescence quantitative PCR, and the protein expressions of Toll like receptor 4 (TLR4), nuclear factor κB p65 (NF-κB p65), inhibitor of NF-κB α (IκBα) and phosphorylated IκBα (p-IκBα) in nasal mucosa were measured by Western blot analysis. Results Compared with the blank group, the plasma levels of IL-1β, IL-6, and TNF-α in the model group increased significantly. The number of CD45⁺ cells in both nasal mucosa tissue and nasal irrigation fluid increased, and the mRNA levels of IL-1β, IL-6 and TNF-α and the protein expression levels of TLR4, NF-κB p65 and p-IκBα in nasal mucosa increased. Compared with the model group, the plasma levels of IL-1β, IL-6 and TNF-α in the miR-18a group decreased significantly. The number of CD45⁺ cells in both nasal mucosa tissue and nasal lavage fluid decreased, and the mRNA levels of IL-1β, IL-6 and TNF-α and the exprotein expression levels of TLR4, NF-κB p65 and p-IκBα in nasal mucosa decreased. Conclusion miR-18a can inhibit the occurrence and development of allergic rhinitis, and its molecular mechanism is related to the inhibition of TLR4/NF-κB pathway activation.
Animals ; Mice ; Disease Models, Animal ; Inflammation ; Interleukin-6/genetics* ; MicroRNAs/genetics* ; NF-kappa B/metabolism* ; NF-KappaB Inhibitor alpha ; Rhinitis, Allergic ; RNA, Messenger ; Toll-Like Receptor 4/metabolism* ; Tumor Necrosis Factor-alpha/genetics*

Objective To investigate the expressions of IL-18, IL-18 binding protein isoform a (IL-18BPa) and IL-18 receptor α (IL-18Rα) in blood CD4⁺ Th2 cells of patients with allergic rhinitis (AR) and the effects of allergens on their expressions. Methods Blood samples of AR patients and healthy control subjects (HCs) were collected. Peripheral blood mononuclear cells (PBMCs) and CD4⁺ T cells sorted by immunomagnetic beads were stimulated by crude extract of Artemisia sieversiana wild allergen (ASWE), Platanus pollen (PPE) and house dust mite extract (HDME). Flow cytometry was used to detect the expression of IL-18, IL-18BPa and IL-18Rα in CD4⁺ Th2 cells, and BioPlex was used to detect the level of plasma IL-4 and analyze its correlation with the proportion of IL-18⁺ Th2 cells. Results Compared with HCs, the proportion of IL-18⁺ cells was increased in Th2 cells of AR patients; MFI of IL-18 was increased, while that of IL-18Rα was decreased. Moreover, allergens induced IL-18 and IL-18Rα expression in sorted CD4⁺ Th2 cells of HCs and induced IL-18Rα in that of AR patients. Additionally, elevated plasma IL-4 level was found in AR patients, which was moderately correlated with the percentage of IL-18⁺ Th2 cells. Conclusion Allergens may be involved in the pathogenesis of AR by inducing expression of IL-18 in peripheral blood CD4⁺ Th2 cells.
Humans ; Th2 Cells ; Interleukin-18/metabolism* ; Up-Regulation ; Leukocytes, Mononuclear/metabolism* ; Interleukin-4/metabolism* ; Rhinitis, Allergic/metabolism* ; Allergens ; Cytokines/metabolism*

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected 660 million people and resulted in 6.7 million deaths. At present, a variety of risk factors related to the severity of COVID-19 have been identified, but whether allergic rhinitis and asthma will affect SARS-CoV-2 infection remains controversial. In general, there is no sufficient evidence to support that allergic rhinitis or asthma is a risk factor for increasing the rate of SARS-CoV-2 infection or aggravating the disease. Some studies even show that atopy may be a protective factor to alleviate SARS-CoV-2 infection, which is related to the decreased expression of angiotensin-converting enzyme 2, the receptor required for SARS-CoV-2 to enter cells, in atopic individuals. This paper reviews the influence of the severity and treatment of allergic rhinitis and asthma on SARS-CoV-2 infection, in order to provide some references for establishing strategies for prevention, risk stratification and treatment of COVID-19.
Humans ; COVID-19 ; SARS-CoV-2/metabolism* ; Peptidyl-Dipeptidase A/metabolism* ; Asthma/therapy* ; Rhinitis, Allergic