Perturbation of the microbiome has numerous associations with the phenotypes and progression in chronic airways disease. However, the differences in the nasal microbiome in asthma and allergic rhinitis (AR) have not been defined. We examined whether the nasal microbiome would vary among different comorbidities in asthma and AR and that those differences may be associated with the severity of asthma. Nasal lavage fluid was collected from 110 participants, including 20 healthy controls, 30 subjects with AR, 30 subjects with asthma and 30 subjects with combined asthma + AR. The Asthma Control Questionnaire (ACQ-7) was used to evaluate asthma control status. Using 16S rRNA bacterial gene sequencing, we analyzed nasal microbiome in patients with asthma, AR, combined asthma + AR, and healthy controls. Bacterial diversity was analyzed in corresponding with α diversity indices (Chao and Shannon index). Compared with healthy controls, the Chao index tended to be lower in subjects with AR (P = 0.001), asthma (P = 0.001), and combined asthma + AR (P = 0.001) when compared with healthy controls. Furthermore, the Shannon index was significantly lower in subjects with asthma (P = 0.013) and comorbid asthma with AR (P = 0.004) than the control subjects. Disparity in the structure and composition of nasal bacteria were also observed among the four groups. Furthermore, patients with combined asthma + AR and isolated asthma were divided into two groups according to the level of disease control: partially or well-controlled and uncontrolled asthma. The mean relative abundance observed in the groups mentioned the genera of Pseudoflavonifractor were dominated in patients with well and partially controlled disease, in both isolated asthma and combined asthma + AR. In subjects with uncontrolled asthma and combined asthma + AR, a lower evenness and richness (Shannon index, P = 0.040) was observed in nasal microbiome composition. Importantly, lower evenness and richness in the nasal microbiome may be associated with poor disease control in combined asthma + AR. This study showed the upper airway microbiome is associated with airway inflammation disorders and the level of asthma control.
Objective: The aim of the present study was to explore the diagnostic value and safety of color Doppler ultrasound (US)-guided transthoracic core needle biopsy (CNB) of peripheral lung, chest wall and mediastinal lesions using automated biopsy guns. Materials and methods: We analyzed clinical and image data, histopathologic and microbiologic details and complications from 121 patients with peripheral lung, chest wall and mediastinal lesions who underwent color Doppler US-guided transthoracic CNB in Ningbo First Hospital between January 2015 and June 2018. Results: Color Doppler US-guided transthoracic CNB performed with a freehand technique using automated biopsy guns had a sensitivity of 93.94%, a specificity of 100%, a positive predictive value of 100%, a negative predictive value of 78.57%, and a diagnostic accuracy of 95.04%. Lesion size did not affect the diagnostic rate (P=0.40). No serious complications of the procedure were noted. Conclusion: Color Doppler US-guided transthoracic CNB of peripheral lung, chest wall and mediastinal lesions is a safe and inexpensive procedure. The diagnostic accuracy of color Doppler US-guided transthoracic CNB was higher than that of color Doppler US-guided transthoracic fine needle aspiration biopsy (FNAB).
Background: Because minimizing future risk is the goal of asthma chronic asthma management, it is particularly important to identify risk factors. We conducted this 3-year single-center prospective cohort study to determine the independent risk factors of asthma exacerbations (AEs).Methods: We performed this prospective, longitudinal, observational study with a 3-year follow-up on 257 patients aged 18-81 years with at least a 1-year history of asthma. Follow-up visits are conducted through regular annual phone calls, and the primary endpoints were AE. Results:The uncontrolled group was more likely to develop AE than the well-controlled group [odds ratio (OR): 6.34, 95% confidence interval (CI): 1.14-35.21, P<0.05]. Patients with low Asthma Quality of Life Questionnaire (AQLQ) scores were more likely to develop AE than these with high AQLQ scores (OR: 0.59, 95% CI: 0.35-0.99, P<0.05). AQLQ and Asthma Control Questionnaires (ACQ) were both strong independent risk factors within 3 years of enrollment; the cut-off values (COV) of the AQLQ and the ACQ (uncontrolled) that better evaluated the risk with the AE were ≤5.4 and >1, respectively. The AQLQ scores had a sensitivity of 79.07% and a specificity of 59.09% [area under curve (AUC): 0.70, P<0.0001], and the ACQ (uncontrolled) had a sensitivity of 81.4% and a specificity of 52.29% (AUC 0.68, P<0.0001). Conclusions:The findings of this study suggest that patients with uncontrolled asthma and a diminished health-related quality of life had an increased risk of exacerbations in the future. Defining these risk factors associated with AE is important as it will identify these at the highest risk to patients and may guide future interventions.
The relationship between fine particulate matter (PM2.5) and chronic airway inflammatory diseases, such as chronic obstructive pulmonary disease and asthma, have garnered public attention, while the detailed mechanisms of PM2.5‐induced airway inflammation remain unclear. This study reveals that PM2.5 induces airway inflammation both in vivo and in vitro, and, moreover, identifies DNA damage and DNA damage repair (DDR) as results of this exposure. Ataxia telangiectasia‐mutated heterozygous (ATM+/−) and wild‐type C57BL/6 (WT) mice were exposed to PM2.5. The results show that, following exposure to PM2.5, the number of neutrophils in broncho alveolar lavage fluid and the mRNA expression of CXCL‐1 in lung tissues of the ATM+/− mice were lower than those of the WT mice. The mRNA expression of FANCD2 and FANCI were also down‐regulated. Human bronchial epithelial (HBE) cells were transfected with ATM‐siRNA to induce down‐regulation of ATM gene expression and were subsequently stimulated with PM2.5. The results show that the mRNA expression of TNF‐α decreased in the ATM‐siRNA‐transfected cells. The mRNA expression of CXCL‐1 and CXCL‐2 in peritoneal macrophages, derived from ATM‐null mice in which experiments showed that the protein expression of FANCD2 and FANCI decreased, were also decreased after PM2.5 exposure in ATM‐siRNA‐transfected HBE cells. In conclusion, PM2.5‐induced airway inflammation is alleviated in ATM+/− mice compared with WT mice. ATM promotes PM2.5‐induced airway inflammation, which may be attributed to the regulation of DNA damage and DDR.
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