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Background: Eosinophil activation is associated with asthma. Whether air pollution affects the activation of blood eosinophils in patients with asthma remains unknown. In this study, we investigated the correlation between transcriptional activity in eosinophils and air pollutant exposure in patients receiving different levels of Global Initiative for Asthma (GINA) treatment. Methods: We evaluated the expression levels of activation‐ and function‐related genes in eosinophils from patients with GINA 4 or 5 (n = 20), those with GINA 3 (n = 12), and normal individuals (n = 7); the eosinophils were activated with interleukin (IL)−5 or IL‐17. A land use regression model was used to estimate air pollutant exposure. The correlations between mRNA expression, lung function, and air pollutant exposure were investigated. Results: The expression levels of TGFB1, IL7R, and TLR3 were significantly higher for patients with GINA 4 or 5 than for those with GINA 3 or normal individuals. The expression of certain genes, particularly in IL‐17‐activated eosinophils, was correlated with lung function decline in patients with GINA 4 or 5. For patients with GINA 4 or 5, NO2 exposure was correlated with upregulated TGFB1 expression in IL‐5‐activated eosinophils. For patients with GINA 3, O3 exposure was correlated with upregulated CCR5, IL5RA, IL7R, and TGFB1 expression in IL‐17‐activated eosinophils and upregulated IL7R expression in IL‐5‐activated eosinophils. Conclusion: Patients with GINA 4 or 5 may exhibit elevated transcriptional activity in eosinophils; this elevation is correlated with lung function decline. Air pollution may affect eosinophil mRNA expression in patients with asthma. [ABSTRACT FROM AUTHOR]

Background: Non-cystic fibrosis bronchiectasis is associated with airway pathogen colonization. We planned to investigate the inflammatory markers in patients with different airway pathogens and their correlation with disease severity. Methods: We enrolled patients aged between 20 and 75 from October 2021 to August 2022. All patients had sputum evaluation for bacterial and fungal cultures before enrollment, and were classified into four groups according to the culture results. Results: Forty-four patients with non-CF bronchiectasis and six controls were enrolled and categorized as follows: Group 1, no pathogens identified in sputum cultures (n = 14); Group 2, positive fungal culture results (n = 18); Group 3, positive P. aeruginosa culture results (n = 7); and Group 4, positive culture results for both fungi and P. aeruginosa (n = 5). Group 4 had significantly higher serum defensin α 1, IL-6 and tissue inhibitors of MMP (TIMP)-1 levels than group 1 patients. The serum levels of IL-6 and TIMP-1 were positively correlated with the FACED score and negatively correlated with distance-saturation product. Conclusion: Significantly higher levels of serum IL-6 and TIMP-1 were found in the patients who had concomitant fungal and P. aeruginosa colonization, and were closely related to clinical severity and may have important roles in disease monitoring. [ABSTRACT FROM AUTHOR]

In this third of three cousin articles on the call for disruptive qualitative research approaches, further treatment is proffered on the concerns and irritations that "soft science"/"subtle science" social scientists (and humanists, and posthumanists) are troubled by today. While the opening article (by Hollinshead, Suleman, and Nair here in Tourism, Culture & Communication) laid out the general case for the fit of disruptive qualitative research advances cum dissident interpretive research overtures in Tourism Studies to help atone for the field's long-recognized biases towards highly economic/linear/ empirical outlooks, the second article (by Hollinshead, Suleman, and Vellah) constituted a consolidation of the advanced social justice orientations being aired across the trio of articles. In this third of the three bedfellow articles, the authors (Hollinshead, Suleman, and Lo) now provide further critique on the soft science constructions and the subtle science thinking that have been promoted within the landmark text on advanced qualitative and interpretive praxis by Brown, Carducci, and Kuby (entitled Disrupting Qualitative Inquiry). In this third article, the need for such dissident developments within Tourism Studies is provided with respect to a number (10) of common ontological issues encountered in research into tourism/travel today, such as the difficulty in researching the shadowy and indistinct "unique ways" in which foreign peoples differ from each other. At the end of this article, a further 15 terms are made manifest for the cumulative glossary being developed across the three companion articles. These terms include "critical ethnography" (vis-à-vis the revised cognitive practices of tourism) and "unsettlement" (vis-à-vis the rhetorics of futurity of tourism). This third article—like its two predecessors—is notably Deleuzian in hue, although readers should spot the conceptual mark of (Arturo) Escobar (and considerations of pluriversality that emanate from "The South") in places. [ABSTRACT FROM AUTHOR]

Background: Toll‐like receptor (TLR)‐7‐associated rhinovirus (RV) activation is involved in the pathogenesis of asthma. Plasmacytoid dendritic cells (pDCs) are the main interferon‐α‐producing cells against viruses. Objective: To determine whether asthmatic patients and control subjects differ in terms of interferon‐α expression in pDCs under TLR‐7 or RV stimulation. Methods: pDCs were identified in BDCA‐2+ and HLA‐DR+ peripheral blood mononuclear cells. Interferon‐α expression of pDCs was analyzed after TLR‐7 stimulation with or without interleukin 4 (IL‐4)/IL‐13 pretreatment. Interferon‐α expression was also analyzed after RV stimulation over periods of 24, 48, or 96 h with or without IL‐4 pretreatment. RV detection and molecular typing were assayed from throat swabs. Results: Following TLR‐7 stimulation, the expression of intracellular interferon‐α was higher in the pDCs of normal subjects than those of asthmatic patients; however, pretreatment with IL‐4 was shown to reduce this effect. After 48‐ and 96‐h RV stimulation, we observed a notable increase in the production of interferon‐α of pDCs in normal subjects but not in asthmatic patients. Baseline interferon‐α expression in pDCs and the incidence of asthma exacerbation to emergency was higher among the 13% of patients identified as rhinovirus+ than among their RV counterparts. Conclusion: Our study discovered the response to TLR‐7 stimulation in pDCs was compromised and the sustainability of interferon‐α expression to RV stimulation was reduced in pDCs of asthmatic patients, which provide further evidence of defective innate response and subspeciality to RV infection in asthma. The high exacerbation history founded in RV+ patients agrees with these findings. Further research is required for the modulatory effect of IL‐4 on TLR‐7 stimulated pDCs. [ABSTRACT FROM AUTHOR]

Background: Patients with severe asthma have increased airway remodelling and elevated numbers of circulating fibrocytes with enhanced myofibroblastic differentiation capacity, despite being treated with high doses of corticosteroids, and long acting β2-adrenergic receptor (AR) agonists (LABAs). We determined the effect of β2-AR agonists, alone or in combination with corticosteroids, on fibrocyte function.Methods: Non-adherent non-T cells from peripheral blood mononuclear cells isolated from healthy subjects and patients with non-severe or severe asthma were treated with the β2-AR agonist, salmeterol, in the presence or absence of the corticosteroid dexamethasone. The number of fibrocytes (collagen I+/CD45+ cells) and differentiating fibrocytes (α-smooth muscle actin+ cells), and the expression of CC chemokine receptor 7 and of β2-AR were determined using flow cytometry. The role of cyclic adenosine monophosphate (cAMP) was elucidated using the cAMP analogue 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) and the phosphodiesterase type IV (PDE4) inhibitor, rolipram.Results: Salmeterol reduced the proliferation, myofibroblastic differentiation and CCR7 expression of fibrocytes from healthy subjects and non-severe asthma patients. Fibrocytes from severe asthma patients had a lower baseline surface β2-AR expression and were relatively insensitive to salmeterol but not to 8-Br-cAMP or rolipram. Dexamethasone increased β2-AR expression and enhanced the inhibitory effect of salmeterol on severe asthma fibrocyte differentiation.Conclusions: Fibrocytes from patients with severe asthma are relatively insensitive to the inhibitory effects of salmeterol, an effect which is reversed by combination with corticosteroids. [ABSTRACT FROM AUTHOR]