Effect of di-(2-ethylhexyl) phthalate (DEHP) on allergic rhinitis.

Allergic rhinitis (AR) is a common chronic inflammatory disease of the upper respiratory tract. Di(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer and belongs to environmental endocrine disruptors (EDCs). It can be entered the human body which is harmful to health. The relationship between DEHP and AR is still inconclusive. This study aims to investigate the effect of environmental pollutants DEHP on AR. By examining DEHP metabolites in the urine of AR patients and building an AR model. 24 BALB/c mice were used as the study subjects, and ovalbumin (OVA) and DEHP (3 mg/kg/body) were used for intragastric administration. They were divided into control group, DEHP group, OVA group and OVA + DEHP group. Examination, behavioral scoring, inflammatory factor testing, oxidative stress testing, detection of aryl hydrocarbon receptor (AhR) and signaling pathways CYP1A1 and CYP1B1 related proteins and mRNA. The concentrations of 3 metabolites of DEHP (MEHHP, MEOHP, and MEHP) in urine of AR patients were higher. And HE-staining showed that for the control group, many chronic inflammatory cell infiltration and nasal mucosal destruction were observed in the OVA + DEHP group and were more severe than the OVA group. Allergic symptom scores were obtained from sneezing, scratching, number of scratching, and nose flow. The scores of the OVA group and the OVA + DEHP group were higher than 7 points. Serum ELISA and nasal mucosal oxidative stress tests are more serious in the OVA + DEHP group. The expression of AhR protein and its mRNA was increased in the DEHP group, OVA group and OVA + DEHP group. The OVA + DEHP group was more significant in the OVA group and DEHP group. And the mRNAs of the AhR-related signaling pathways CYP1A1 and CYP1B1 were also more prominent in the OVA + DEHP group. DEHP may aggravate its inflammatory response through the AhR pathway closely related to the environment. When combined with OVA, DEHP can further aggravate the OVA-induced nasal inflammatory response and make the nasal cavity have undergone severe changes, and many inflammatory cells have infiltrated. DEHP has shown an adjuvant effect, and the AhR-related signaling pathways CYP1A1 and CYP1B1 may be critical.

The airway inflammation induced by nasal inoculation of PM2.5 and the treatment of bacterial lysates in rats.

Particulate matter (PM) is one of the most important environmental issues in China. This study aimed to explore the correlation between PM2.5 and airway inflammation in healthy rats. The PM2.5 group was given an intranasal instillation of PM2.5 suspension on 15 consecutive days, and each received oral saline from day 16 to 90. The BV intervention group was treated as the PM2.5 exposure group, except that BV instead of saline was given daily. A histopathologic examination was performed to evaluate the airway inflammation. The prevalence and function of Th1/Th2/Treg/Th17 cells were detected by flow cytometry and ELISA. The expression of AhR was detected by western blot and real-time PCR. We found that epithelial damage and increased infiltration of inflammatory cell were present in the airways after PM2.5 exposure; there was an immune imbalance of Th cells in the PM2.5 group; the expression of AhR was increased in the airways after PM2.5 exposure. In the PM2.5 + BV group, we demonstrated alleviated immune imbalance and reduced inflammatory cell infiltration in the airways. Our study showed that exposure to PM2.5 induced airway inflammation. The imbalance of Th1/Th2/Treg/Th17 in PM2.5-induced airway inflammation might be associated with activation of the AhR pathway. Oral BV reduces PM2.5-induced airway inflammation and regulates systemic immune responses in rats.

Exposure to air pollution and risk of prevalence of childhood allergic rhinitis: A meta-analysis.

OBJECTIVES: Allergic rhinitis (AR), a common chronic inflammatory disease in the upper airways. The prevalence of AR in children seems to be increasing recently, and the most significant causes of the increase are thought to be changes in environmental factors, especially air pollution. However, we could not find any meta-analysis on the risk of air pollution exposure on the prevalence of AR in childhood. The aim of this research was to carry out a meta-analysis on the results of recent studies (21 s t century) to present valid information about exposure to air pollution and risk of prevalence of childhood AR. METHODS: PubMed, Science, Google Scholar, Elsevier and MDPI web database were searched up to January 1, 2000 to February 28, 2018. Including of air pollution and AR in childhood related to the observation of literature. Meta-analysis, study quality assessment, heterogeneity analysis and publication bias test were using Stata-MP 14.1 and Review Manager version 5.3 software. RESULTS: 13 studies will be included in the meta-analysis (8 cross-sectional studies, 5 cohort studies). Exposure to NO2 (OREurope = 1.031, 95%CI [1.002,1.060], P = 0.033; ORAsia = 1.236, 95%CI [1.099,1.390], P = 0.000; ORoverall = 1.138, 95%CI [1.052,1.231], P = 0.001); Exposure to SO2 (OREurope = 1.148, 95%CI [1.030,1.279], P = 0.012; ORAsia = 1.044, 95%CI [0.954,1.142], P = 0.352; ORoverall = 1.085, 95%CI [1.013,1.163], P = 0.020); Exposure to PM10 (OREurope = 1.190, 95%CI [1.092,1.297], P = 0.000; ORAsia = 1.075, 95%CI [0.995,1.161], P = 0.066; ORoverall = 1.125, 95%CI [1.062,1.191], P = 0.000); Exposure to PM2.5 (OREurope = 1.195, 95%CI [1.050,1.360], P = 0.007; ORAsia = 1.163, 95%CI [1.074,1.260], P = 0.000; ORoverall = 1.172, 95%CI [1.095,1.254], P = 0.000). CONCLUSIONS: Exposed to air pollution probable is a risk of prevalence of childhood AR. And the prevalence of AR will be increase when exposed to NO2, SO2, PM10 and PM2.5, but maybe the relationship between SO2/PM10 and prevalence of AR are not closely in Asia.

Human urokinase-type plasminogen activator gene-modified bone marrow-derived mesenchymal stem cells attenuate liver fibrosis in rats by down-regulating the Wnt signaling pathway.

AIM: To evaluate the therapeutic effects of bone marrow-derived mesenchymal stem cells (BMSCs) with human urokinase-type plasminogen activator (uPA) on liver fibrosis, and to investigate the mechanism of gene therapy. METHODS: BMSCs transfected with adenovirus-mediated human urokinase plasminogen activator (Ad-uPA) were transplanted into rats with CCl4-induced liver fibrosis. All rats were sacrificed after 8 wk, and their serum and liver tissue were collected for biochemical, histopathologic, and molecular analyzes. The degree of liver fibrosis was assessed by hematoxylin and eosin or Masson's staining. Western blot and quantitative reverse transcription-polymerase chain reaction were used to determine protein and mRNA expression levels. RESULTS: Serum levels of alanine aminotransferase, aminotransferase, total bilirubin, hyaluronic acid, laminin, and procollagen type III were markedly decreased, whereas the levels of serum albumin were increased by uPA gene modified BMSCs treatment. Histopathology revealed that chronic CCl4-treatment resulted in significant fibrosis while uPA gene modified BMSCs treatment significantly reversed fibrosis. By quantitatively analysing the fibrosis area of liver tissue using Masson staining in different groups of animals, we found that model animals with CCl4-induced liver fibrosis had the largest fibrotic area (16.69% ± 1.30%), while fibrotic area was significantly decreased by BMSCs treatment (12.38% ± 2.27%) and was further reduced by uPA-BMSCs treatment (8.31% ± 1.21%). Both protein and mRNA expression of ß-catenin, Wnt4 and Wnt5a was down-regulated in liver tissues following uPA gene modified BMSCs treatment when compared with the model animals. CONCLUSION: Transplantation of uPA gene modified BMSCs suppressed liver fibrosis and ameliorated liver function and may be a new approach to treating liver fibrosis. Furthermore, treatment with uPA gene modified BMSCs also resulted in a decrease in expression of molecules of the Wnt signaling pathway.