Background: The impact of physical activity (PA) on immune response is a hot topic in exercise immunology, but studies involving asthmatic children are scarce. We examine the level of PA and TV attendance (TVA) in asthmatic children to assess the role on asthma control and immune response to various stimulants. Methods: Weekly PA and daily TVA were obtained from questionnaires at inclusion of the PreDicta study. PBMC cultures were stimulated with phytohemagglutinin (PHA), R848, poly I:C and zymosan. Cytokines were measured and quantified in cell culture supernatants using luminometric multiplex immunofluorescence beads-based assay. Results: Asthmatic preschoolers showed significantly more TVA than their healthy peers (58.6% vs. 41.5% 1-3h daily and only 25.7% vs. 47.2% ≤ 1h daily). Poor asthma control was associated with less frequent PA (75% no or occasional activity in uncontrolled vs. 20% in controlled asthma; 25% ≥ 3x weekly vs. 62%). Asthmatics with increased PA exhibited elevated cytokine levels in response to stimulants, suggesting a readiness of circulating immune cells for type-1, -2 and -17 cytokine release compared to low-PA and high-TVA subjects. Low PA and high TVA were associated with increased proinflammatory cytokines. Proinflammatory cytokines were correlating with each other in in-vitro immune responses of asthmatic children, but not healthy controls. Conclusion: Asthmatic children show more sedentary behavior than healthy subjects, while poor asthma control leads to a decrease in PA. Asthmatic children profit from exercise, as elevated cytokine levels in stimulated conditions indicate an immune system prepared for a strong response in case of infection.

Staphylococcal Enterotoxins sensitization and response of Omalizumab in severe atopic and non atopic asthma Nicolas Migueres1,2, Anh Poirot1, Nan Zhang ,3,4, Claus Bachert 3,4, Frédéric de Blay1 ,51: Chest Diseases Department, Strasbourg University Hospital, Strasbourg France.2: UMR 7357 Laboratoire des sciences de l’ingénieur, de l’informatique et de l’imagerie ICUBE3: Upper Airways Research Laboratory, Ghent University, Ghent, Belgium4: Division of ENT diseases, CLINTEC, Karolinska Institute, University of Stockholm, Sweden5: EA 3072, Fédération de médecine translationnelle, université de Strasbourg, 67000 Strasbourg, FranceCorresponding author: Nicolas Migueres, [email protected] Diseases DepartmentNouvel Hôpital CivilHopitaux Universitaires de Strasbourg67093 STRASBOURG CEDEXtel: 00 33 6 07 60 51 86,Total word count ( 570 words)Author Contributions: All investigators contributed to the conception and design of the study. All authors contributed to the acquisition, analysis and interpretation of the data. They provided input into the drafting of the manuscript, critical feedback, and final approval for submission of the manuscript for publication. NM is the guarantor of the final content of the manuscript.The authors have no conflicts of interest to declare.

In the airway, IgE is traditionally regarded as a key mediator in allergic diseases, such as AR and allergic asthma. However, growing evidence demonstrates the importance of local IgE in airway inflammatory diseases, irrespective of the presence of allergy. In this review, we discuss the most recent evidence for IgE in chronic rhinosinusitis with nasal polyps(CRSwNP), including the local IgE’s characteristics, the modulation of its synthesis, and function. The levels of local IgE are significantly elevated in polyps independently of IgE serum levels and atopic status. Local IgE is polyclonal and functional, which is correlated with type 2 inflammation. IgE is produced by active B cells and is dependent on the classing switch recombination(CSR). In NPs, this process is triggered by not only allergens but also microbial colonization, especially the superantigen- Staphylococcus aureus. The production of local IgE is modulated by lymphocytes(such as Tfh, ILC2s, iTreg), cytokines(such as IL-4, IL-13, IFN-γ, TGF-β, IL-2, IL-21), transcription factors, and B cell intrinsic factor. Due to the central role of IgE in NPs, it is regarded as an ideal target for therapy and has been proved to be clinically successful. Based on this knowledge, we believe that exploring the trigger and regulatory factors for the activation of local B cells and CSR to IgE will provide more valuable information for us to recognize the pathological mechanisms of local IgE and offer the possible option for new [therapeutic](#/javascript:;) targets of NPs.