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Allergic diseases are rising worldwide, especially in childhood, and their clinical diversity increasingly exposes the limits of traditional phenotype-based classifications. Genetic susceptibility, environmental exposures, epithelial barrier biology, and immune pathways interact to shape highly variable disease trajectories and treatment responses. In this context, precision medicine is no longer only an aspirational concept, but a practical effort to define meaningful endotypes, identify clinically useful biomarkers, and connect biological insight to prevention and care.
Type 1 interferons (T1IFNs) are typically expressed in low concentrations under homeostatic conditions, but upon pathogenic insult or perturbation of the pathway, these critical immune signaling molecules can become either protectors from or drivers of pathology. While essential for initiating antiviral defense and modulating inflammation, dysregulation of T1IFN signaling can contribute to immunopathology, making it and its associated pathways prime targets for immune evasion and disruption by pathogens.
The airway epithelium is the primary structural and functional airway barrier and orchestrates innate immunity. Some children may have underlying epithelial vulnerabilities that contribute to the pathogenesis of acute wheeze and asthma.
Elexacaftor/tezacaftor/ivacaftor(ELX/TEZ/IVA) was safe and efficacious in children with CF 2-5y with at least one F508del allele in 24-week phase 3 Trial 445-111. Children who completed 445-111 were eligible for the long-term safety and efficacy extension trial.
Rhinoviruses (RVs) can cause severe wheezing illnesses in young children and patients with asthma. Vaccine development has been hampered by the multitude of RV types with little information about cross-neutralization. We previously showed that neutralizing antibody (nAb) responses to RV-C are detected twofold to threefold more often than those to RV-A throughout childhood. Based on those findings, we hypothesized that RV-C infections are more likely to induce either cross-neutralizing or longer-lasting antibody responses compared with RV-A infections.
Citation: Rossetto V, Moore-Machacek A, Woods DF, ……. O’Gara F, McGlacken GP, Jerry Reen F. Structural modification of the Pseudomonas aeruginosa
Persistent respiratory bacterial infections are a clinical burden in several chronic inflammatory airway diseases and are often associated with neutrophil infiltration into the lungs. Following recruitment, dysregulated neutrophil effector functions such as increased granule release and formation of neutrophil extracellular traps (NETs) result in damage to airway tissue, contributing to the progression of lung disease.
Here, we present the complete genome sequence of Pseudomonas aeruginosa phages Kara-mokiny 1, Kara-mokiny 2, and Kara-mokiny 3. These phages have lytic capabilities against P. aeruginosa and belong to the myovirus morphotype. The genomes of Kara-mokiny 1 and Kara-mokiny 2 are 67,075 bp while that of Kara-mokiny 3 is 66,019 bp long.
Many publications have demonstrated the detrimental effects of school closures on children, families and communities in the past two years of the COVID-19 pandemic. Currently, there is a surge of Omicron cases as children prepare to return to school around the world. While many children are asymptomatic or have mild disease, it is nevertheless an important problem.
We identified a double-stranded DNA (dsDNA) bacteriophage appearing to belong to Herelleviridae, genus Kayvirus. The bacteriophage, Biyabeda-mokiny 1, was isolated from breast milk using a clinical isolate of Staphylococcus aureus.