Post-viral lung diseases: the microbiota as a key player.

Viral infections of the respiratory tract can lead to chronic lung injury through immunopathological mechanisms that remain unclear. Communities of commensal bacteria colonising the respiratory tract, known as the respiratory tract microbiota, are altered in viral infections, which can contribute to inflammation, lung epithelial damage and subsequent development of lung disease. Emerging evidence on post-viral lung injury suggests an interplay between viral infections, immune responses and airway microbiota composition in the development of viral-induced lung diseases.

Skin barrier immunology from early life to adulthood.

Our skin has a unique barrier function, which is imperative for the body's protection against external pathogens and environmental insults. Although interacting closely and sharing many similarities with key mucosal barrier sites, such as the gut and the lung, the skin also provides protection for internal tissues and organs and has a distinct lipid and chemical composition. Skin immunity develops over time and is influenced by a multiplicity of different factors, including lifestyle, genetics, and environmental exposures.

Highlights of the ERS Lung Science Conference 2022.

https://bit.ly/3tarCXc.

Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.

Chronic exposure to environmental pollutants is a major contributor to the development and progression of obstructive airway diseases, including asthma and COPD. Understanding the mechanisms underlying the development of obstructive lung diseases upon exposure to inhaled pollutants will lead to novel insights into the pathogenesis, prevention and treatment of these diseases. The respiratory epithelial lining forms a robust physicochemical barrier protecting the body from inhaled toxic particles and pathogens.

ERS ECM Awardee 2021, a preview of LSC 2022 and a brief overview of the Respiratory Channel.

https://bit.ly/2XTylbK.

Highlights of the ERS Lung Science Conference and Sleep and Breathing Conference 2021 and the new ECMC members.

https://bit.ly/2RSDP40.

Storage conditions of high-fat diets affect pulmonary inflammation.

Obesity alters the risks and outcomes of inflammatory lung diseases. It is important to accurately recapitulate the obese state in animal models to understand these effects on the pathogenesis of disease. Diet-induced obesity is a commonly used model of obesity, but when applied to other disease models like acute respiratory distress syndrome, pneumonia, and asthma, it yields widely divergent.

In the spotlight: Early Career Member Awardee 2020, ERS Lung Science Conference 2021, and Sleep and Breathing 2021.

https://bit.ly/3fUXs1M.

Early Career Members at the ERS Lung Science Conference 2020: metabolic alterations in lung ageing and disease.

https://bit.ly/2XZ5YGQ.

A sneak peek into the Early Career Members' session at the ERS International Congress and the experience of organising an ERS Research Seminar.

http://bit.ly/39yncgO.

Microbiome-induced antigen-presenting cell recruitment coordinates skin and lung allergic inflammation.

Background: Allergic skin inflammation often presents in early childhood; however, little is known about the events leading to its initiation and whether it is transient or long-term in nature.

Objective: We sought to determine the immunologic rules that govern skin inflammation in early life.

Methods: Neonatal and adult mice were epicutaneously sensitized with allergen followed by airway allergen challenge.

ERS International Congress, Madrid, 2019: highlights from the Basic and Translational Science Assembly.

In this review, the Basic and Translational Sciences Assembly of the European Respiratory Society (ERS) provides an overview of the 2019 ERS International Congress highlights. In particular, we discuss how the novel and very promising technology of single cell sequencing has led to the development of a comprehensive map of the human lung, the lung cell atlas, including the discovery of novel cell types and new insights into cellular trajectories in lung health and disease. Further, we summarise recent insights in the field of respiratory infections, which can aid in a better understanding of the molecular mechanisms underlying these infections in order to develop novel vaccines and improved treatment options.

Early Career Members at the Lung Science Conference and the Sleep and Breathing Conference 2019.

http://bit.ly/2XNX6V6.

AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation.

Acute respiratory distress syndrome (ARDS) is characterized by an excessive pulmonary inflammatory response. Removal of excess cholesterol from the plasma membrane of inflammatory cells helps reduce their activation. The secreted apolipoprotein A-I binding protein (AIBP) has been shown to augment cholesterol efflux from endothelial cells to the plasma lipoprotein HDL.

Hyperleptinemia is associated with impaired pulmonary host defense.

We have previously reported that obesity attenuates pulmonary inflammation in both patients with acute respiratory distress syndrome (ARDS) and in mouse models of the disease. We hypothesized that obesity-associated hyperleptinemia, and not body mass per se, drives attenuation of the pulmonary inflammatory response and that this e_ect could also impair the host response to pneumonia. We examined the correlation between circulating leptin levels and risk, severity, and outcome of pneumonia in 2 patient cohorts (NHANES III and ARDSNet-ALVEOLI) and in mouse models of diet-induced obesity and lean hyperleptinemia.

A Comparative Study of Lung Host Defense in Murine Obesity Models. Insights into Neutrophil Function.

We have shown that obesity-associated attenuation of murine acute lung injury is driven, in part, by blunted neutrophil chemotaxis, yet differences were noted between the two models of obesity studied. We hypothesized that obesity-associated impairment of multiple neutrophil functions contributes to increased risk for respiratory infection but that such impairments may vary between murine models of obesity. We examined the most commonly used murine obesity models (diet-induced obesity, db/db, CPE(fat/fat), and ob/ob) using a Klebsiella pneumoniae pneumonia model and LPS-induced pneumonitis.

Muscle-specific GSK-3β ablation accelerates regeneration of disuse-atrophied skeletal muscle.

Muscle wasting impairs physical performance, increases mortality and reduces medical intervention efficacy in chronic diseases and cancer. Developing proficient intervention strategies requires improved understanding of the molecular mechanisms governing muscle mass wasting and recovery. Involvement of muscle protein- and myonuclear turnover during recovery from muscle atrophy has received limited attention.

The role of leptin in the development of pulmonary neutrophilia in infection and acute lung injury.

Objectives: One of the hallmarks of severe pneumonia and associated acute lung injury is neutrophil recruitment to the lung. Leptin is thought to be up-regulated in the lung following injury and to exert diverse effects on leukocytes, influencing both chemotaxis and survival. We hypothesized that pulmonary leptin contributes directly to the development of pulmonary neutrophilia during pneumonia and acute lung injury.

Leptin as regulator of pulmonary immune responses: involvement in respiratory diseases.

Leptin is an adipocyte-derived hormone, recognized as a critical mediator of the balance between food intake and energy expenditure by signalling through its functional receptor (Ob-Rb) in the hypothalamus. Structurally, leptin belongs to the long-chain helical cytokine family, and is now known to have pleiotropic functions in both innate and adaptive immunity. The presence of the functional leptin receptor in the lung together with evidence of increased airspace leptin levels arising during pulmonary inflammation, suggests an important role for leptin in lung development, respiratory immune responses and eventually pathogenesis of inflammatory respiratory diseases.