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Abstract: Interleukin (IL)‐17 is a major contributor to the pathogenesis of allergic asthma. Developmental endothelial locus‐1 (Del‐1) is an endothelial cell‐secreted protein known to inhibit IL‐17 expression. However, little is known about the association between Del‐1 and IL‐17 in the pathogenesis of allergic asthma. Using bronchoalveolar lavage fluid (BALF) and peripheral blood samples collected from allergic asthmatic patients and controls, we explored the role of Del‐1 in relation to IL‐17 in allergic asthma. We found that the negative correlation between Del‐1 and IL‐17 was significant in BALF of allergic asthmatics. Del‐1 treatment inhibited the expression of IL‐17, the differentiation of IL‐17‐secreting leukocytes and associated cytokines. Contrarily, IL‐17 levels were increased after treatment with anti‐Del‐1 mAb. Consistent with this, Del‐1 treatment led to downregulation of IL‐5, CCL5 and IL‐4, thus reducing secretion of eosinophil cationic protein. Furthermore, Del‐1 significantly downregulated the expression of ICAM‐1 and may have the potential to reduce leukocyte transendothelial migration. Our data demonstrate that Del‐1 can negatively regulate IL‐17 and its proinflammatory function, thereby limiting airway inflammation in allergic asthmatics, and suggest Del‐1 as a potential candidate for prevention and treatment of allergic asthma. [ABSTRACT FROM AUTHOR]

Abstract: Background: Treatment non‐adherence is a challenge to achieve asthma control. However, few prospective studies were done for exploring asthma patient adherence in real world. Objectives: To evaluate treatment adherence and causes of non‐adherence in a large asthma Chinese population. To analyze newly‐diagnosed patients' adherence first time. Methods: About 1582 asthma patients' data were collected from 12 study centers in China from February, 2012 to October, 2012. Disease and treatment information of subjects were collected were at first clinic visit, at 4, 12, and 24 weeks after that, follow‐up phone calls were carried out for recording subjects' treatment adherence based on their self‐reports. Subjects who reported non‐adherence were additionally asked to choose the primary non‐adherence cause from a list of nine potential causes. Results: Treatment adherence rate of all subjects markedly decreased from 83.3% at week 4 to 42.0% at week 24 after the first clinic visit. Significantly, at week 24, good treatment adherence rate in newly‐diagnosed patients was lower than those patients with asthma history (22.9% vs. 63.9%, P < .001). Newly‐diagnosed patients were three times more likely to become non‐adherence than those patients with asthma history. Female patients had lower treatment adherence rate than male patients (38.3% vs. 45.6%, P = .006). Subjects in 30‐39 year age group had the worst treatment adherence (27.3%). The most commonly chosen cause for non‐adherence was “relief of symptoms after short‐term controller medication use” (43.8%). Conclusions: Asthma patients' treatment adherence could be improved by improving patient education, doctor/patient partnership, and level of medical service in Chinese population. [ABSTRACT FROM AUTHOR]

Cytomegalovirus ( CMV) IgG antibodies have been associated with inflammaging and immunosenescence. We aimed to assess the presence of CMV DNA in the blood of adult and elderly patients with bronchial asthma to establish potential association of CMV DNAemia with asthma and asthma characteristics. Eighty-five elderly asthmatics, 74 younger asthma patients, and 114 age-matched controls were recruited. The CMV DNA was detected using commercial artus assay in 10.7% of asthma patients, but was negative in all control individuals. The secondary assay identified CMV DNA in 41.5% of asthmatics and 13.3% of control subjects ( P < .001). Presence of CMV DNA was associated with an increased risk of asthma and CMV DNA copy numbers correlated with some asthma traits, including respiratory parameters and exhaled breath nitric oxide. We conclude that CMV infection is associated with asthma and may contribute to the pathogenesis of asthmatic inflammation. [ABSTRACT FROM AUTHOR]

Asthma is a heterogeneous disease characterized by numerous phenotypes relating to age of onset, triggers, comorbidities, severity (assessed by multiple exacerbations, lung function pattern) and finally the inflammatory cells involved in the pathophysiologic pathway. These phenotypes can vary over time in relation to changes in the principal triggers involved in the aetiology of the disease. Nevertheless, in a patient with multiple allergies and early-onset disease (defined as multiple sensitizations and allergic comorbidities), the prognosis of asthma is poor with a high risk of persistence and severity of the disease during childhood. Future research will focus on classifying phenotypes into groups based on pathophysiologic mechanisms (endotypes) and the biomarkers attached to these endotypes, which could predict prognosis and lead to targeted therapy. Currently, these biomarkers are related to inflammatory cells associated with the asthma endotype, essentially eosinophils and neutrophils (and related cytokines) attached to Th-2 and non Th-1 pathways, respectively. The most severe asthma (refractory asthma) is linked to neutrophil-derived inflammation (frequently associated with female sex, obesity and possibly disorganized airway microbiota) encountered in very young children or teenagers. Severe asthma is also linked to or a marked eosinophil inflammatory process (frequently associated with multiple atopy and, more rarely, with non-atopic hypereosinophilic asthma in children) and frequently encountered in teenagers. Severe phenotypes of asthma could also play a role in the origin of chronic obstructive pulmonary disease in adult life. [ABSTRACT FROM AUTHOR]

Background Disinfectant use among healthcare workers has been associated with respiratory disorders, especially asthma. We aimed to describe disinfectants used by U.S. nurses, and to investigate qualitative and quantitative differences according to workplace characteristics and region. Methods Disinfectant use was assessed by questionnaire in 8,851 nurses. Hospital characteristics were obtained from the American Hospital Association database. Results Working in a hospital was associated with higher disinfectant use (OR: 2.06 [95%CI: 1.89-2.24]), but lower spray use (0.74 [0.66-0.82]). Nurses working in smaller hospitals (<50 beds vs. ≥200 beds) were more likely to use disinfectants (1.69 [1.23-2.32]) and sprays (1.69 [1.20-2.38]). Spray use was lower in the West than in the Northeast (0.75 [0.58-0.97]). Conclusion Disinfectant use was more common among nurses working in smaller hospitals, possibly because they perform more diverse tasks. Variations in spray use by hospital size and region suggest additional targets for future efforts to prevent occupational asthma. Am. J. Ind. Med. 60:131-140, 2017. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objective We investigate the association between adult asthma and wealth, testing whether the disease impairs wealth accumulation (social selection model) or if wealth protects against asthma (social causation model). Methods We use the National Longitudinal Survey of Youth ( n = 7,644) and linear and logistic regressions to estimate the association between wealth and asthma. Changes in relative wealth following an asthma diagnosis and asthma status by increases in wealth through inheritance provide evidence on the causal direction. Results Asthma, particularly severe asthma, is associated with lower wealth. Wealth ranking does not change after a diagnosis of asthma, but inheriting a substantial sum is associated with a lower risk of severe asthma. Conclusion Wealth appears to protect against severe asthma, supporting the social causation model of disease. [ABSTRACT FROM AUTHOR]

Introduction: Humidity is commonly associated with increased airway hyperresponsiveness in asthma. Objective: To examine mold sensitization in patients with allergic asthma or allergic rhinitis and self-reports of humidity as exacerbating factors of clinical symptoms. Methods: A retrospective, cross-sectional study at a University hospital outpatient allergy and asthma clinic was performed. A total of 106 patients with either allergic asthma or allergic rhinitis completed standard prick-puncture skin testing with 17 allergens and controls and completed standardized forms addressing trigger factors for clinical symptoms. Results: Allergic asthmatics sensitized to Cladosporium were more likely to have a more severe asthma severity class (odds ratio = 4.26, confidence interval = 1.30-16.93). Sensitization to Alternaria, Cladosporium, Helminthosporium, Aspergillus and Dermatophagoides pteronyssinus in asthma was associated with higher likelihood for previous hospitalization, while sensitization to Cladosporium, Helminthosporium, Aspergillus, Dermatophagoides pteronyssinus and cockroach in asthma was associated with higher likelihood of having reduced pulmonary function based on forced expiratory volume in 1 s. Furthermore, allergic asthmatics more commonly reported humidity as an exacerbating factor of symptoms than did patients only with allergic rhinitis (68.42% vs 42.86%, respectively; P < 0.05). Conclusion: Mold sensitization is highly associated with more severe asthma, while humidity is more of an exacerbating factor in patients with allergic asthma as compared with allergic rhinitis alone. Further delineation between mold sensitization and humidity is needed to determine whether these are independent factors in asthma. Please cite this paper as: Hayes D Jr, Jhaveri MA, Mannino DM, Strawbridge H and Temprano J. The effect of mold sensitization and humidity upon allergic asthma. Clin Respir J 2013; 7: 135-144. [ABSTRACT FROM AUTHOR]

Adherence in asthma is an important cause for concern. Although nearly 50% of asthma patients are considered poorly adherent to therapeutic advices, adherence is still difficult to assess, understand and improve despite major medical consequences. In this review, we revisited the literature of the last 10 years related to adherence in severe asthma. The concepts have changed and 'compliance' is usually replaced by 'adherence'. Assessment of adherence is addressing ethical issues, but provides important insight into difficult-to-treat asthma. Different tools have been used but none is routinely recommended. Health-related outcomes (poor control, exacerbations, hospitalizations, lung function decline), which are clearly associated with severe asthma, are often worsened by non-adherence with consequences also on patient related outcomes (quality of life). The potential behaviour associated with non-adherence and all other related factors including easy-to-recognize psychological traits can help for patient's future management. Therapeutic educational interventions have been recognized with a scientifically proven efficiency even though evolution and improvements are needed. A multidisciplinary approach is required in severe asthma. Therapeutic adherence for a given patient is always a prerequisite to any other aspects when addressing severe asthma phenotypes. Severe asthma should be considered only in those who still experienced poor asthma outcomes despite optimal adherence. At a glance, poor adherence and severe asthma should be considered antinomic. Better understanding of the causes and customised management are potential future directions. [ABSTRACT FROM AUTHOR]

Allergy to rodents in the workplace is an important occupational health problem affecting research, pharmaceutical and toxicological sectors and can have a serious impact on employees working in this area. Despite measures to reduce aeroallergen exposures to rodents in the workplace, there are few signs that this occupational health problem is declining. Rodent allergens are well characterized and exposure-response relationships have been demonstrated to be complex. More recently, the importance of rodent allergens outside of the workplace has been demonstrated in several studies of individuals with asthma. This review focuses on rodent allergy both in the workplace and in the home and examines the complex exposure-response relationships between allergen exposure and sensitization and asthma. Risk factors for rodent allergy and mechanisms of tolerance to rodent allergens are discussed. Cite this as: H. Jeal and M. Jones, Clinical & Experimental Allergy, 2010 (40) 1593-1601. [ABSTRACT FROM AUTHOR]

Background The role in allergic asthma development of the immune response against fungi with concomitant exposure to other common aeroallergens has yet to be determined. In particular, there is little understanding of how inhaled fungi affect the host response to mite allergens. Objective To characterize the in vitro and in vivo effects of concurrent exposure of Aspergillus fumigatus ( Af) and Dermatophagoides farinae ( Derf) on dendritic cells (DCs) in the development of allergic asthma. Methods Murine bone marrow-derived DCs were pulsed with Derf and/or live or heat-inactivated Af. Cytokine production and the expression of pathogen recognition receptors (PRRs) were determined in vitro. Subsequently, these DCs were inoculated into the airway of naïve mice to assess the development of allergic airway inflammation in vivo. The effect of antibodies against PRRs was also evaluated. Results Live Af significantly enhanced IL-10 production and the expression of Toll-like receptor (TLR) 2 and Dectin-1 in Derf-pulsed DCs. Live Af infection significantly attenuated Derf-pulsed DC-induced allergic airway inflammation in vivo. Antibodies against either TLR2 or Dectin-1 significantly reversed the inhibitory effects of live Af in the development of Derf-pulsed DC-induced allergic airway inflammation. Conclusion Concurrent exposure of DCs to fungal antigens has profound influences on the subsequent mite allergen-induced allergic airway inflammation. Live Af could regulate the functions of airway DCs in the development of mite allergen-induced allergic airway inflammation via regulation of their PRRs. Our results suggest that concurrent exposure to pathogens such as fungi and mite allergens has profound influences on the subsequent allergen-induced allergic airway inflammation. Furthermore, modulating PRR signalling could provide a therapeutic regimen for the development of asthma. Cite this as: S. Fukahori, H. Matsuse, T. Tsuchida, T. Kawano, S. Tomari, C. Fukushima and S. Kohno, Clinical & Experimental Allergy, 2010 (40) 1507–1515. [ABSTRACT FROM AUTHOR]

A letter to the editor regarding clinical pharmacology study of formoterol fumarate dry powder inhalers and inhaled beclometasone dipropionate in asthmatic adolescents is presented.

The author reflects on the study conducted by C. D. Thomson and colleagues regarding asthma in children. The author states that there had been no evidence in the relationship of dietary selenium levels with asthma which was tackled in the study and the effect of nutritional antioxidants to the development of asthma in children. An overview of the occurrence of allergic asthma in children is presented.

A correction to the article "Innate lymphoid cells in asthma phenotypes," by Leyla Pur Ozyigit and colleagues that was published in September 15, 2015 issue is presented.