Search

Objective To investigate the expression characteristics of cysteamine leukotriene receptor 1 (CysLTR1) in the adenoid tissue of children with adenoid hypertrophy (AH), as well as the mechanism of action of CysLTR1 in the formation of AH and the influencing factors for CysLTR1 expression. Methods A total of 71 children who underwent adenoidectomy in Department of Otolaryngology, Weihai Municipal Hospital, from October 1, 2020 to October 1, 2021 were enrolled. Immunohistochemical staining was performed for CysLTR1 in the resected specimens, and according to the results of staining, the children were divided into high CysLTR1 expression group and low CysLTR1 expression group. The two groups were compared in terms of the data including sex, age, degree of adenoid hypertrophy, presence or absence of allergic rhinitis, and presence or absence of other comorbidities (secretory otitis media, chronic sinusitis, and sleep apnea syndrome), and a multivariate logistic regression analysis was used to identify the influencing factors for the expression of CysLTR1 in children with AH. Results Immunohistochemistry showed that CysLTR1 was expressed in the adenoid tissue of all 71 children with AH, and there were significant differences between the high and low expression groups in the degree of adenoid hypertrophy, the presence or absence of allergic rhinitis, and the presence or absence of other comorbidities (χ2=9.003-49.196,P

Introduction: Asthma has been attributed to Th1/Th2 imbalance and inappropriate Th2 responses to environmental allergens. MicroRNAs (miRNAs), 21 to 23 RNA molecules, are first found in mammals and have been implicated in various biological activities. Our previous study found that miR-410 effectively ameliorates airway inflammation in the ovalbumin (OVA)-induced asthma murine model. However, the role of miR-410 in regulating helper T (Th) cell differentiation is not clear. In the present study, we aimed to explore the regulatory effects of miR-410 on the differentiation of Th cells through both in vivo and in vitro studies. Methods: Dual-luciferase reporter assay was used to find if miR-410 has any direct binding position with VEGF mRNAs. PBMC and CD4+ T cells were isolated and stimulated with OVA. The miR-410 mimics and inhibitors were transfected into CD4+ T cells. The differentiation of Th cells was evaluated by enzyme-linked immunosorbent assay (ELISA) for the concentration of IL-4, IFN-γ, and TGF-β levels in supernatants. Western Blot was used to detect protein expression and phosphorylation of PI3K and AKT. BALB/c mice were kept in a specific pathogen-free condition and received sterile OVA-free food and water. OVA-induced asthmatic mice model was established. ELISA was used to measure the bronchoalveolar lavage fluid (BALF) concentrations of IL-4, IFN-γ, TGF-β, and VEGF. Hematoxylin and eosin staining and immunohistochemical staining were conducted to analyze inflammatory cell infiltration, pathological changes, and the expression of VEGF. Results: Dual-luciferase reporter assay showed that miR-410 has no direct binding position with VEGF mRNAs. In the OVA-primed mononuclear cells compared to normal cells, IFN-γ and TGF-β were decreased while IL-4 and VEGF were increased. This change was reversed while miRNA-410 mimics were transfected into CD4+ T cells. Besides, the OVA-primed CD4+ T cells treated with miR-410 decrease the proliferation of cytokine of Th2 cells as well as phosphorylation of PI3K, and AKT. In OVA-induced asthma mice, IFN-γ and TGF-β were decreased in BALF while the IL-4 and VEGF were increased. OVA-induced mice with asthma treated with miR-410 mimics showed marked reductions in the infiltration of inflammatory cells as well as IL-4 and VEGF in BALF. The immunohistochemical staining of the expression of VEGF also decreased in OVA-induced asthma mice with the instillation of miR-410. Conclusions: In this study, we revealed that miR-410 could regulate the differentiation of Th cells via the PI3K-AKT-VEGF signaling pathway in asthma. [ABSTRACT FROM AUTHOR]

Asthma is a common chronic inflammatory respiratory disease characterised by airway inflammation and hyperresponsiveness. The present study was designed to clarify the effect of intranasal miR-410 administration in an ovalbumin (OVA)-induced murine model of asthma. It was found that miR-410 expression was significantly decreased in the lungs of OVA-induced asthmatic mice (P<0.05) and miR-410 was overexpressed via intranasal instillation. Bioinformatics indicated that the 3′-untranslated regions of interleukin (IL)-4 and IL-13 messenger RNAs (mRNAs) contain miR-410 binding sites. The IL-4 and IL-13 genes were confirmed to be miR-410-regulated using the dual-luciferase reporter assay. Additionally, intranasal administration of miR-410 markedly attenuated airway inflammation and reduced infiltration of inflammatory cells into bronchoalveolar lavage fluid (P<0.05) as determined by bronchoalveolar lavage fluid analysis. Moreover, miR-410 significantly decreased the lung expression of IL-4 and IL-13 (P<0.05), although the levels of mRNAs encoding IL-4 and IL-13 in lungs did not change significantly as determined by real-time PCR analysis. In conclusion, we found that intranasal administration of miR-410 effectively inhibited airway inflammation in OVA-induced asthmatic mice by targeting IL-4 and IL-13 at the post-transcriptional level. miR-410 is thus a promising treatment for allergic asthma. [ABSTRACT FROM AUTHOR]

The obesity-asthma phenotype is characterized by increased asthma severity and decreased glucocorticoid responsiveness. To date, the mechanism underlying the association between obesity and asthma remain to be fully elucidated. The present study investigated the correlation between oxidative stress and the nuclear factor (NF)-κB pathway in obese asthmatic mice. The animals were divided into the following groups: Control (n=8), comprising C57BL/6J mice without exposure to a high-fat diet; non-obese asthma group (n=8), comprising mice of a normal weight subjected to the induction of asthma; obese control group (n=8), comprising C57BL/6J mice subjected to a high-fat diet; and obese asthmatic group (n=8), comprising obese mice subject to the induction of asthma. The levels of the malondialdehyde (MDA) oxidant and glutathione (GSH) antioxidant in the lungs and bronchoalveolar lavage fluid (BALF) were measured using ELISA. The expression levels of inhibitory κB kinase-β (IKK-β) and the inhibitor of κBα (IκB-α) in the pulmonary tissues was determined using western blot analysis. An electrophoretic mobility shift assay was performed to determine the transcription activity of NF-κB. The levels of MDA in the BALF and lung tissues increased significantly in the two asthmatic groups, compared with the control groups (P<0.01). The asthmatic mice showed significantly lower concentrations of GSH in the BALF and lung tissues, compared with the control groups (P<0.01). In the asthmatic animals, the expression of IκB kinase (IKK)-β and activation of NF-κB were upregulated in the pulmonary tissues, compared with those in the control groups (P<0.01). The expression of IKK-β and transcriptional activity of NF-κB were significantly higher the in obese asthmatic mice, compared with the non-obese asthmatic mice (P<0.01). On examining the expression levels of IκB-α in the pulmonary tissues, a significant reduction was found in the asthmatic animals, compared with the controls (P<0.01). In addition, the level of IκB-α was significantly lower in the obese asthmatics, compared with the non-obese asthmatics (P<0.01). MDA was positively correlated with NF-κB in the obese asthmatic group (R=0.83; P<0.05) and non-obese asthmatic group (R=0.82; P<0.05). Oxidative stress was upregulated in the pulmonary tissues of the asthmatic mice. This upregulation was more marked in the obese asthmatic mice, and was positively correlated with activation of the NF-κB signaling pathway in the pulmonary tissues. The results in the present study indicated that higher oxidative stress and activation of the NF-κB signaling pathway were observed in the lung tissues of the obese asthmatics. Furthermore, a positive correlation was identified between oxidative stress and NF-κB.

Objective: To evaluate the efficacy of sublingual immunotherapy with dermatophagoides farina drops on children with allergic rhinitis., Method: This was retrospective study analyzing the efficacy of dermatophaguides farinae drops SLIT in 110 patients (aged 4-14 years old) with house dust mites induced allergic rhinitis (without asthma). All the patients were divided into the SLIT group (n = 60) and drug group (n = 50). Patients in SLIT group received sublingual immunotherapy combined with symptomatic medication, and patients in drug group only received symptomatic medication. We recorded and evaluated the total nasal symptom scores (TNSS), total medication scores (TMS) and visual analogue scale (VAS) of the 2 groups at three time points, before the treatment, and the treatment for 1-year and 2-year., Result: After 1-year and 2-year treatment, compared with drug group, TMS, TNSS and VAS in SLIT group decreased significantly (P < 0.01). When compared with baseline, we got the similar result as compared with drug group. Besides, the TMS of drug group increased significantly after treatment (P < 0.01). And no significant difference was observed in TNSS and VAS. In addition, there was significant difference in the Proportion of patients withdrawing symptomatic medication in SLIT group and drug group (68.33%,16.00%, respectively; P < 0.01). There were 4 local adverse reactions occurred during the treatment and no serious adverse events occurred., Conclusion: Sublingual immunotherapy with Dermatophagoides farinae drops showed significant clinical efficacy in children with allergic rhinitis comparing with pharmacotherapy.