Effect of Proparacaine in a Mouse Model of Allergic Rhinitis

OBJECTIVES: Lidocaine, a local anaesthetic is a treatment option in uncontrolled asthma due to its immunomodulatory effects. In the present study, proparacaine (PPC), a derivative of lidocaine was examined for its therapeutic application in a mouse model of allergic rhinitis. METHODS: The mice were grouped into 4 groups: control group, allergic rhinitis (AR) group, ciclesonide (CIC) group, and PPC group. Nasal symptom scores, eosinophil counts, goblet cell counts, and mast cells counts in the nasal mucosa were measured. Serum ovalbumin (OVA)-specific immunoglobulin (Ig) E, OVA-specific IgG1, OVA-specific IgG2a, interleukin (IL)-4, IL-5, and cortisol levels were measured. RESULTS: Intranasal administration of PPC significantly decreased nasal symptoms, number of eosinophils, goblet cells, and mast cells in the lamina propria of the nasal mucosa. Serum OVA-specific IgE, OVA-specific IgG1, OVA-specific IgG2a was significantly higher in the AR compared with the control group. Serum level of IL-4 was significantly lower in the CIC group and PPC group in comparison with AR group. Serum IL-5 showed no significant difference among all groups. No significant difference in serum cortisol levels was observed among the 4 groups. CONCLUSION: PPC appears to have a therapeutic potential in treatment of allergic rhinitis in a mouse model by reducing eosinophil, goblet cell, and mast cell infiltration in the nasal mucosa.

Immunoglobulin E to allergen components of house dust mite in Korean children with allergic disease

BACKGROUND: House dust mites (HDMs) are important sources of indoor allergens. Seventeen components have been identified from Dermatophagoides pteronyssinus (Der p). OBJECTIVE: Our aim was to define the prevalence of specific IgE to components of Der p in Korea and investigate the clinical features of them in children with allergic disease. METHODS: We performed a prospective evaluation of 80 HDM sensitized patients with history of allergic rhinitis (AR), atopic dermatitis (AD), asthma and urticaria (UC). Patients underwent ImmunoCAP for total IgE, Der p, Der f, Der p 1, Der p 2, and Der p 10. RESULTS: Seventy-nine patients had detectable serum IgE to Der p, 80 patients were sensitized to Der f, 66 patients were sensitized to Der p 1, 63 patients to Der p 2, and 7 patients were sensitized to Der p 10. Der p 1 specific IgE was significantly lower in the UC group compared with the AD and AR group. Total IgE was significantly higher in the Der p 10 sensitized group. Der p 10 serum IgE level was highly correlated with crab and shrimp specific IgE. There was a significant positive correlation between total IgE and specific IgE to Der p and its components and Der f. CONCLUSION: Sensitization to HDM and its components in Korea is similar to previous studies from temperate climate. The determination of Der p 1, Der p 2, and Der p 10 specific IgE helps in obtaining additional information in regards to allergic disease.

Rhinovirus-Infected Epithelial Cells Produce More IL-8 and RANTES Compared With Other Respiratory Viruses

PURPOSE: The environmental factors human rhinoviruses (HRVs) and house dust mites (HDMs) are the most common causes of acute exacerbations of asthma. The aim of this study was to compare the chemokine production induced by HRVs in airway epithelial cells with that induced by other respiratory viruses, and to investigate synergistic interactions between HRVs and HDMs on the induction of inflammatory chemokines in vitro. METHODS: A549 human airway epithelial cells were infected with either rhinovirus serotype 7, respiratory syncytial virus (RSV)-A2 strain, or adenovirus serotype 3 and analyzed for interleukin (IL)-8 and regulated on activation, normal T-cell expressed and secreted (RANTES) release and mRNA expression. Additionally, activation of nuclear factor (NF)-kappaB and activator protein (AP)-1 were evaluated. The release of IL-8 and RANTES was also measured in cells stimulated simultaneously with a virus and the HDM allergen, Der f1. RESULTS: HRV caused greater IL-8 and RANTES release and mRNA expression compared with either RSV or adenovirus. NF-kappaB and AP-1 were activated in these processes. Cells incubated with a virus and Der f1 showed an increased IL-8 release. However, compared with cells incubated with virus alone as the stimulator, only HRV with Der f1 showed a statistically significant increase. CONCLUSIONS: IL-8 and RANTES were induced to a greater extent by HRV compared with other viruses, and only HRV with Der f1 acted synergistically to induce bronchial epithelial IL-8 release. These findings may correspond with the fact that rhinoviruses are identified more frequently than other viruses in cases of acute exacerbation of asthma.

The effect of rhinovirus on airway inflammation in a murine asthma model / 소아과

PURPOSE: The aim of the present study was to investigate the differences in lower airway inflammatory immune responses, including cellular responses and responses in terms of inflammatory mediators in bronchoalveolar lavage fluid (BALF) and the airway, to rhinovirus (RV) infection on asthma exacerbation by comparing a control and a murine asthma model, with or without RV infection. METHODS: BALB/c mice were intraperitoneally injected with a crude extract of Dermatophagoides farinae (Df) or phosphate buffered saline (PBS) and were subsequently intranasally treated with a crude extract of Df or PBS. Airway responsiveness and cell infiltration, differential cell counts in BALF, and cytokine and chemokine concentrations in BALF were measured 24 hours after intranasal RV1B infection. RESULTS: RV infection increased the enhanced pause (Penh) in both the Df sensitized and challenged mice (Df mice) and PBS-treated mice (PBS mice) (P<0.05). Airway eosinophil infiltration increased in Df mice after RV infection (P<0.05). The levels of interleukin (IL) 13, tumor necrosis factor alpha, and regulated on activation, normal T cells expressed and secreted (RANTES) increased in response to RV infection in Df mice, but not in PBS mice (P<0.05). The level of IL-10 significantly decreased following RV infection in Df mice (P<0.05). CONCLUSION: Our findings suggest that the augmented induction of proinflammatory cytokines, Th2 cytokines, and chemokines that mediate an eosinophil response and the decreased induction of regulatory cytokines after RV infection may be important manifestations leading to airway inflammation with eosinophil infiltration and changes in airway responsiveness in the asthma model.

Effect of respiratory syncytial virus infection on regulated on activation, normal T-cells expressed and secreted production in a murine model of asthma / 소아과

PURPOSE: Synthesis of regulated on activation, normal T-cells expressed and secreted (RANTES) in the airway has previously been shown to be elevated after respiratory syncytial virus (RSV) infection. However, since few studies have examined whether RSV-infected asthma patients express a higher level of RANTES than do normal individuals, we used a murine model of asthma to address this question. METHODS: We prepared Dermatophagoides farinae-sensitized mice as an asthma model, and then infected them with RSV and analyzed the changes in airway responsiveness and the cell populations and cytokine levels of bronchoalveolar lavage fluid. RESULTS: RANTES synthesis increased in response to RSV infection in both control mice and in asthma model (D. farinae) mice. However, there was no significant difference in the amount of RANTES produced following RSV infection between control and D. farinae mice. RSV infection affected neither interferon-gammasynthesis nor airway responsiveness in either control or D. farinae mice. CONCLUSION: RSV infection did not induce more RANTES in a murine model of asthma than in control mice.

Effect of respiratory syncytial virus infection on regulated on activation, normal T-cells expressed and secreted production in a murine model of asthma / 소아과

PURPOSE: Synthesis of regulated on activation, normal T-cells expressed and secreted (RANTES) in the airway has previously been shown to be elevated after respiratory syncytial virus (RSV) infection. However, since few studies have examined whether RSV-infected asthma patients express a higher level of RANTES than do normal individuals, we used a murine model of asthma to address this question. METHODS: We prepared Dermatophagoides farinae-sensitized mice as an asthma model, and then infected them with RSV and analyzed the changes in airway responsiveness and the cell populations and cytokine levels of bronchoalveolar lavage fluid. RESULTS: RANTES synthesis increased in response to RSV infection in both control mice and in asthma model (D. farinae) mice. However, there was no significant difference in the amount of RANTES produced following RSV infection between control and D. farinae mice. RSV infection affected neither interferon-gammasynthesis nor airway responsiveness in either control or D. farinae mice. CONCLUSION: RSV infection did not induce more RANTES in a murine model of asthma than in control mice.