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With the recent approval of the first eosinophil-depleting therapeutic agents targeting the IL-5 pathway for treatment of severe eosinophilic asthma, eosinophils and eosinophilic disorders are in the limelight. Indeed, setbacks during clinical development of these compounds have revealed how much remains to be known about eosinophil biology in vivo, and have nurtured profuse research both on basic eosinophil biology and on pathogenic disease mechanisms, in order to better delineate the most meaningful targets for innovative therapeutic strategies. On one hand, variable degrees of eosinophil depletion observed in some compartments during IL-5-targeted treatment indicate that certain eosinophil subsets may not rely on this cytokine and/or that other important pro-eosinophilic mediators and signaling pathways are operative in vivo. On the other hand, it is increasingly clear that disorders involving eosinophils such as asthma are the final outcome of complex interactions between diverse cell types and mediators, beyond eosinophils and IL-5. These include type 2 helper T (Th2) cells and innate lymphoid cells, mast cells, and a variety of factors that either activate eosinophils or are released by them. Although a considerable amount of research has focused on asthma because it is a common condition and because management of severe asthma remains a major challenge, several rare eosinophilic disorders with more homogenous features have proven to be extremely useful models to reach a better understanding of the involvement of eosinophils in tissue damage and dysfunction, and of the micro-environmental interactions operating within the complex network of eosinophilic inflammation. Unraveling this interplay has resulted in advances in the development of molecular tools to detect disease subsets and to monitor therapeutic responses, and in identification of promising new therapeutic targets. This Research Topic dedicated to eosinophilic conditions covers aspects of the biology of eosinophils and closely related cells of particular relevance for drug development, reports on translational research investigating pathogenic mechanisms of specific eosinophilic disorders in humans that will likely result in significant changes in the way patients are managed, and presents an overview of the current advancement of targeted drug development for these conditions, with a special focus on asthma.

ILC2 --- Hypereosinophilic Syndrome --- mast cell --- Th2 cell --- Eosinophil Biology --- Asthma --- Eosinophilic Esophagitis

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Asthma is a common complex and heterogeneous respiratory disease with an increasing prevalence in developed countries. Asthma is a disease consisting of different phenotypes that are driven by different mechanistic pathways (endotypes). The recognition of these phenotypes and endotypes is central to asthma management entailing prognostic and therapeutic implications. It is acknowledged that despite optimal treatment, many patients are poorly controlled, highlighting the need for phenotype-guided treatments. In this context, the emergence of novel therapies (monoclonal antibody therapy, bronchial thermoplasty) is paving the way for personalized asthma therapy. A better understanding of disease pathogenesis may enable the identification of biomarkers, mediators, novel therapeutic targets, and treatable traits. Further molecular phenotyping or endotyping of asthma will be necessary to tailor new therapeutic strategies. The present Special Issue on Asthma aims to provide the current knowledge on phenotypes and endotypes in appreciating and managing the heterogeneous condition that is asthma.

asthma --- lactic acidosis --- hyperchloremic acidosis --- hypocapnia --- hypercapnia --- wheezing --- bronchial biopsies --- symptom persistence --- clinical remission --- eosinophil --- adhesion --- viability --- proliferation --- airway smooth muscle cell --- pulmonary fibroblast --- phenotype --- acute severe asthma exacerbation --- near fatal asthma --- severe asthma --- inflammation --- interleukin-5 (IL-5) --- anti-IL-5 --- interleukin-4 --- airway remodeling --- matrix metalloproteinases-9 --- tissue inhibitor of metalloproteinase-1 --- alveolar macrophages --- lung function --- bronchodilation --- resistance --- obstruction --- reproducible --- spirometry --- obstructive sleep apnea --- bronchial asthma --- alternative overlap syndrome --- exacerbation --- reactive oxygen species --- PBMC --- mitochondrial function --- innate immunity --- immune regulation --- NLRP3 --- IL-1β --- allergic airway inflammation --- microbiome --- pathogenesis --- immune responses --- PreDicta --- preschool --- FeNO --- asthma-specific quality of life --- chronic rhinitis --- disease-specific quality of life --- health-related quality of Life (HRQLQ) --- children --- longitudinal study

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The book “Integrated human exposure to air pollution” aimed to increase knowledge about human exposure in different micro-environments, or when citizens are performing specific tasks, to demonstrate methodologies for the understanding of pollution sources and their impact on indoor and ambient air quality, and, ultimately, to identify the most effective mitigation measures to decrease human exposure and protect public health. Taking advantage of the latest available tools, such as internet of things (IoT), low-cost sensors and a wide access to online platforms and apps by the citizens, new methodologies and approaches can be implemented to understand which factors can influence human exposure to air pollution. This knowledge, when made available to the citizens, along with the awareness of the impact of air pollution on human life and earth systems, can empower them to act, individually or collectively, to promote behavioral changes aiming to reduce pollutants’ emissions. Overall, this book gathers fourteen innovative studies that provide new insights regarding these important topics within the scope of human exposure to air pollution. A total of five main areas were discussed and explored within this book and, hopefully, can contribute to the advance of knowledge in this field.

Personal Air Pollution Exposure (PAPE) --- air pollution monitoring --- IoT --- Air Quality Decision Support System --- health impact --- air pollution --- public concern --- air quality index --- Baidu index --- Shanghai --- air quality --- crowd-sensing --- crowd-sourced sensing --- environmental analysis --- pollution --- particulate matter --- dust sensor --- human exposure --- Arduino --- wireless networks --- oxides --- traffic --- state space --- milan --- area b --- cross validation --- policy intervention analysis --- counter-factual --- unobservable components --- PM2.5 --- population exposure --- tier-models --- health burden misclassification --- BenMap-CE --- tuberculosis --- infectious disease --- time-series --- Poisson regression --- kriging --- road dust --- PM10 emission factors --- enrichment index --- human health risk --- atmospheric aerosols --- bioaerosols --- culturable bacteria --- long-term trends --- hazard for human --- indoor air quality --- e-cigarettes --- heat-not-burn tobacco --- traditional smoking products --- tobacco smoke --- passenger cars --- lung inflammation --- allergy --- indoor pollutants --- biomarkers --- FeNO --- eosinophil --- neutrophil --- fine particulate matter --- economic growth --- urbanization --- industrialization --- Granger causality test --- air pollutants --- monitoring --- seasonality --- chemical characterization --- source apportionment --- particulate matters (PM) --- air purifier --- experiment --- real-time monitoring unit --- transfer unit --- occupant --- breathing zone --- cooking fuel --- household air pollution --- preterm births --- perinatal mortality --- low birth weight --- stillbirth --- Nigeria --- n/a