How eating makes asthma worse
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Type 2 immunity in allergic diseases
Significant advancements have been made in understanding the cellular and molecular mechanisms of type 2 immunity in allergic diseases such as asthma, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis (EoE), food and drug allergies, and atopic dermatitis (AD). Type 2 immunity has evolved to protect against parasitic diseases and toxins, plays a role in the expulsion of parasites and larvae from inner tissues to the lumen and outside the body, maintains microbe-rich skin and mucosal epithelial barriers and counterbalances the type 1 immune response and its destructive effects. During the development of a type 2 immune response, an innate immune response initiates starting from epithelial cells and innate lymphoid cells (ILCs), including dendritic cells and macrophages, and translates to adaptive T and B-cell immunity, particularly IgE antibody production. Eosinophils, mast cells and basophils have effects on effector functions. Cytokines from ILC2s and CD4+ helper type 2 (Th2) cells, CD8 + T cells, and NK-T cells, along with myeloid cells, including IL-4, IL-5, IL-9, and IL-13, initiate and sustain allergic inflammation via T cell cells, eosinophils, and ILC2s; promote IgE class switching; and open the epithelial barrier. Epithelial cell activation, alarmin release and barrier dysfunction are key in the development of not only allergic diseases but also many other systemic diseases. Recent biologics targeting the pathways and effector functions of IL4/IL13, IL-5, and IgE have shown promising results for almost all ages, although some patients with severe allergic diseases do not respond to these therapies, highlighting the unmet need for a more detailed and personalized approach.
Relationships of eating behaviors with psychopathology, brain maturation and genetic risk for obesity in an adolescent cohort study
Unhealthy eating, a risk factor for eating disorders (EDs) and obesity, often coexists with emotional and behavioral problems; however, the underlying neurobiological mechanisms are poorly understood. Analyzing data from the longitudinal IMAGEN adolescent cohort, we investigated associations between eating behaviors, genetic predispositions for high body mass index (BMI) using polygenic scores (PGSs), and trajectories (ages 14–23 years) of ED-related psychopathology and brain maturation. Clustering analyses at age 23 years (N = 996) identified 3 eating groups: restrictive, emotional/uncontrolled and healthy eaters. BMI PGS, trajectories of ED symptoms, internalizing and externalizing problems, and brain maturation distinguished these groups. Decreasing volumes and thickness in several brain regions were less pronounced in restrictive and emotional/uncontrolled eaters. Smaller cerebellar volume reductions uniquely mediated the effects of BMI PGS on restrictive eating, whereas smaller volumetric reductions across multiple brain regions mediated the relationship between elevated externalizing problems and emotional/uncontrolled eating, independently of BMI. These findings shed light on distinct contributions of genetic risk, protracted brain maturation and behaviors in ED symptomatology.
CXCL16 knockout inhibit asthma airway inflammation by suppressing H2-DM molecular mediated antigen presentation
The inflammatory microenvironment influences dendritic cell-mediated antigen presentation to regulate asthma Th2 inflammation. The scavenger receptor is expressed on DCs and regulates antigen presentation and T priming. However, whether the transmembrane scavenger receptor (SR-PSOX/CXCL16) regulates the phenotype and antigen presentation function of DCs remains unclear. We found that CXCL16 is mainly expressed on DCs in the lung tissues of asthma patients and asthma mice. CXCL16 knockout led to the suppression of airway inflammation, mucus overproduction, and airway hyperresponsiveness in Aspergillus-induced asthma. In addition, the adoptive transfer of Aspergillus-pulsed DCs shows the CXCL16+ DCs exerted a promoting role in airway inflammation, the CXCL16− DCs inhibit airway inflammation. Additionally, RNA sequencing and flow cytometry data revealed that CXCL16 knockout inhibits airway inflammation by suppressing the antigen processing and presentation function of DCs, which was mediated by MHC II chaperone H2-DM. Furthermore, we found CXCL16 knockout suppressed dendritic cells differentiated forward to cDC2b subtype which is mainly charged with antigen presentation to T cell. In conclusion, we found that CXCL16 downregulated the capacity of DC antigen processing and presentation to suppress airway inflammation by reducing H2-DM expression which mediated DC differentiation. The study suggested that inhibition of CXCL16 can be a potential therapy for asthma.
Single-cell RNA transcriptomic analysis identifies Creb5 and CD11b-DCs as regulator of asthma exacerbations
Immune responses that result in asthma exacerbation are associated with allergen or viral exposure. Identification of common immune factors will be beneficial for the development of uniformed targeted therapy. We employed a House Dust Mite (HDM) mouse model of asthma and challenged allergic HDM mice with allergens (HDM, cockroach extract (CRE)) or respiratory syncytial virus (RSV). Purified lung immune cells underwent high-dimensional single-cell RNA deep sequencing (scRNA-seq) to generate an RNA transcriptome. Gene silencing with siRNA was employed to confirm the efficacy of scRNA-seq analysis. scRNA-seq UMAP analysis portrayed an array of cell markers within individual immune clusters. SCENIC R analysis showed an increase in regulon number and activity in CD11b– DC cells. Analysis of conserved regulon factors further identified Creb5 as a shared regulon between the exacerbation groups. Creb5 siRNAs attenuated HDM, CRE or RSV-induced asthma exacerbation. scRNA-seq multidimensional analysis of immune clusters identified gene pathways that were conserved between the exacerbation groups. We propose that these analyses provide a strong framework that could be used to identify specific therapeutic targets in multifaceted pathologies.
The interplay between positive lifestyle habits and academic excellence in higher education
Systematically examining the correlation between the lifestyle habits of undergraduate students and their academic performance holds significant practical implications in advancing higher education. This study adopts an integrated perspective and analyzes a substantial dataset (3,123,840 data points) of 3499 undergraduates at a Chinese university. This study employs a Long short-term memory neural network to identify eating behavior indicators and develops a comprehensive model to evaluate the relationship between students’ lifestyle habits and academic performance; the lifestyle habits cover eating, hygiene, and studying habits. The findings challenge conventional wisdom by revealing that stringent eating schedules do not consistently correlate with superior academic performance. Instead, a higher degree of inertia in eating behavior (e.g., waking up early) correlates with better academic outcomes. Positive correlations also exist between students’ hygiene and studying habits and their academic performance. These results provide valuable insights into the relationship between students’ behavior and academic performance. This work carries implications for promoting the digitalization of higher education and enhancing education management for undergraduate students.
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