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BACKGROUND: There is no trial to make a diagnostic tool of allergic rhinitis (AR) utilizing biomarkers from nasal fluid. Base on previous studies, we selected following five biomarkers in nasal fluids that represent the characteristics of allergic reactions: tryptase, eosinophil cationic protein (ECP), interleukin 5 (IL-5), Clara cell protein 16 (CC16) and CC16-to-albumin ratio. OBJECTIVE: This study aimed to identify biomarkers in nasal discharge that may be used in biosensors to diagnose AR as an additional diagnostic tool. METHODS: Patients showed rhinorrhea and tested positive on allergic skin and specific immunoglobulin E (IgE) tests were included in the AR group. The non-AR group included individuals no dominant nasal symptoms and tested negative on allergy tests. Nasal lavage fluid samples were collected from all participants. Biomarkers in the samples were quantified using enzyme-linked immunosorbent assay. RESULTS: Forty-five patients with AR and 28 non-AR subjects were enrolled in this study. Comparing the concentrations of biomarkers, the concentrations of tryptase and IL-5 were significantly higher in the AR group than in the NAR group. And CC16 level and CC16-to-albumin ratio were significantly lower in the AR group. In the combination of tryptase or CC16-to-albumin ratio, the sensitivity was 90.7% and the specificity was 64.3% (p = 0.013). CONCLUSION: The combination of "tryptase or CC16-to-albumin" could be used as a screening tool for AR. Although this diagnostic method could not replace conventional diagnostic tools, we could consider the method we proposed as an additional screening tool for patients who could not undergo allergy tests.
Asunto(s)
Rinitis Alérgica , Triptasas/análisis , Uteroglobina/análisis , Albúminas , Humanos , Líquido del Lavado Nasal , Mucosa Nasal , Rinitis Alérgica/diagnósticoRESUMEN
Objective To explore the anti-inflammatory effect of antiflammin-2 (AF2) and recombinant peptide sequence 2(R2) on acute lung injury of mouse. To observe the expression of clara cell 16000 protein (CC16) and surfactant protein A (SP-A) in the lung of mouse inoculated with lipopolysaccharide (LPS) and the impact of AF2,R2,and glucocorticoids(hydrocortisone,HC) may have on the expression of the CC16 and SP-A in the lung of mice with acute lung injury. Methods Balb/c mice were inoculated with LPS (5 mg/kg) by intraperitoneal injection to set up ALI mice model. Mice weighed from 15 g to 16 g were grouped into control group, model group and treated groups respectively treated with AF2, R2 or HC. Mice in the control group were injected with physiological saline solution, while mice in the other four groups were inoculated with LPS to induce acute lung injury. Then animals in the treated groups were treated with AF2, R2 or HC each on a dose of 2 mg/kg also through intraperitoneal injection,while those of the control group and the model group, were given equivalent physiological saline solution as a placebo. The respiratory rate of all of these animals were recorded 6 hours after the injection. And at the time point of 12 hour,all the mice were sacrificed for a preparation of the whole lung tissue for the sake of a pathological investigation ,or for extractions of RNA for a semiquantitative analysis of the expression of CC16 and SP-A within the lungs. Results (1) An obvious attenuation of the respiratory rates of the three treated groups were observed when comparing with that of the mice in the model group without any anti-inflammatory treatment. (2) Remarkable extenuation of the extent of intra-alveolar and intersticial hemorrhage and infiltration of inflammatory cells were observed within the treated groups comparing with that of the model group. (3) An attenuate expressions of CC16 or SP-A were observed in the model group,while obvious uptrend of CC16 expression was observed in AF2 treated groups and increase of SP-A expressions were found in R2 and HC treated groups. Conclusion The anti-inflammatory effect of the peptide, AF-2 or R2, has been conformed on ALI mice model induced by LPS.
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BACKGROUND: Arsenic from drinking water has been associated with malignant and nonmalignant respiratory illnesses. The association with nonmalignant respiratory illnesses has not been well established because the assessments of respiratory symptoms may be influenced by recall bias or interviewer bias because participants had visible skin lesions. OBJECTIVES: We examined the relationship of the serum level of Clara cell protein CC16--a novel biomarker for respiratory illnesses--with well As, total urinary As, and urinary As methylation indices. METHODS: We conducted a cross-sectional study in nonsmoking individuals (n = 241) selected from a large cohort with a wide range of As exposure (0.1-761 microg/L) from drinking water in Bangladesh. Total urinary As, urinary As metabolites, and serum CC16 were measured in urine and serum samples collected at baseline of the parent cohort study. RESULTS: We observed an inverse association between urinary As and serum CC16 among persons with skin lesions (beta = -0.13, p = 0.01). We also observed a positive association between secondary methylation index in urinary As and CC16 levels (beta = 0.12, p = 0.05) in the overall study population; the association was stronger among people without skin lesions (beta = 0.18, p = 0.04), indicating that increased methylation capability may be protective against As-induced respiratory damage. In a subsample of study participants undergoing spirometric measures (n = 31), we observed inverse associations between urinary As and predictive FEV(1) (forced expiratory volume measured in 1 sec) (r = -0.37; FEV(1)/forced vital capacity ratio and primary methylation index (r = -0.42, p = 0.01). CONCLUSIONS: The findings suggest that serum CC16 may be a useful biomarker of epithelial lung damage in individuals with arsenical skin lesions. Also, we observed the deleterious respiratory effects of As exposure at concentrations lower than reported in earlier studies.