The respiratory tract antimicrobial defense system is a multilayered defense mechanism that relies upon mucociliary clearance and components of both the innate and adaptive immune systems to protect the lungs from inhaled or aspirated microorganisms. One of these potential pathogens, nontypeable Haemophilus influenzae (NTHi), adopts several, multifaceted redundant strategies to successfully colonize the lower airways and establish a persistent infection. NTHi can impair mucociliary clearance, express multiple multifunctional adhesins for various cell types within the respiratory tract and evade host defenses by surviving within and between cells, forming biofilms, increasing antigenic drift, secreting proteases and antioxidants, and by host‐pathogen cross‐talk, impair macrophage and neutrophil function. NTHi is recognized as an important pathogen in several chronic lower respiratory disorders, such as protracted bacterial bronchitis, bronchiectasis, cystic fibrosis, and primary ciliary dyskinesia. The persistence of NTHi in human airways, including its capacity to form biofilms, results in chronic infection and inflammation, which can ultimately injure airway wall structures. The complex nature of the molecular pathogenetic mechanisms employed by NTHi is incompletely understood but improved understanding of its pathobiology will be important for developing effective therapies and vaccines, especially given the marked genetic heterogeneity of NTHi and its possession of phase‐variable genes. Currently, no vaccine candidates are ready for large phase III clinical trials.

Asthma is a clinical syndrome caused by heterogeneous underlying mechanisms with some of them having a strong genetic component. It is known that up to 82% of atopic asthma has a genetic background with the rest being influenced by environmental factors that cause epigenetic modification(s) of gene expression. The interaction between the gene(s) and the environment has long been regarded as the most likely explanation of asthma initiation and persistence. Lately, much attention has been given to the time frame the interaction occurs since the host response (immune or biological) to environmental triggers, differs at different developmental ages. The integration of the time variant into asthma pathogenesis is appearing to be equally important as the gene(s)–environment interaction. It seems that, all three factors should be present to trigger the asthma initiation and persistence cascade. Herein, we introduce the importance of the time variant in asthma pathogenesis and emphasize the long‐term clinical significance of the time‐dependent gene–environment interactions in childhood.

The fast-spreading coronavirus disease 2019 (COVID-19) pandemic forced countries to apply restrictive measures to counteract it. School closure was quickly adopted by health authorities. We aimed to investigate the compliance of children aged 4 to 12 years with the COVID-19 lockdown restrictions and evaluate the impact of school closure on the children’s educational, social, economic, and psychological outcomes. An online survey was distributed through a social networking platform to parents of pre-primary and primary school-age children. The study period was defined as from 27 November 2020 to 3 December 2020, two weeks after the school closure due to the general lockdown in Greece. This study showed that the school units were well-informed and complied with the protection measures against COVID-19. The pupils quickly adopted the protection measures, even those whose parents suggested masks were less effective. The quarantine-forced school closure highly impacted primary school children’s physical activity, quality of sleep, psychological status, eating habits, academic performance, and household income. Web use showed an increase, with the children over-spending extracurricular time in web activities. Our study highlights the need for long term monitoring of these aforementioned indices, and the development of COVID-19 mitigation measures that carefully incorporate effectiveness and societal impact.

Calprotectin (CP) is a non-covalent heterodimer formed by the subunits S100A8 (A8) and S100A9 (A9). When neutrophils become activated, undergo disruption, or die, this abundant cytosolic neutrophil protein is released. By fervently chelating trace metal ions that are essential for bacterial development, CP plays an important role in human innate immunity. It also serves as an alarmin by controlling the inflammatory response after it is released. Extracellular concentrations of CP increase in response to infection and inflammation, and are used as a biomarker of neutrophil activation in a variety of inflammatory diseases. Although it has been almost 40 years since CP was discovered, its use in daily pediatric practice is still limited. Current evidence suggests that CP could be used as a biomarker in a variety of pediatric respiratory diseases, and could become a valuable key factor in promoting diagnostic and therapeutic capacity. The aim of this study is to re-introduce CP to the medical community and to emphasize its potential role with the hope of integrating it as a useful adjunct, in the practice of pediatric respiratory medicine.