Most severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in children are mild, yet neurological complications can occur. Host immune variability is partly determined by human leukocyte antigen (HLA) polymorphisms and may influence susceptibility. This study investigates whether specific HLA-B alleles are associated with neurological involvement in pediatric coronavirus disease 2019 (COVID-19).

This retrospective study spanned over one year, including children with confirmed SARS-CoV-2 infection. Patients were classified into two groups: patients with COVID-19 with neurological disease (neuro-COVID-19), and those with COVID-19 without neurological disease (non-neuro COVID-19). A control group of 120 healthy children was included to represent baseline allele distribution. HLA-B class I allele typing was performed using polymerase chain reaction with sequence-specific oligonucleotide probes (PCR-SSOP).

HLA-B49 represented the most common allele among children suffering from neurological COVID-19 (10.4%). None of the alleles reached statistical significance when compared in patients with and without neurological disease. A possible, but not statistically significant, lower frequency of the HLA-B52 allele was observed in cases with neurological manifestations (p = 0.088). However, in exploratory unadjusted analyses, HLA-B53 showed higher odds of neurological involvement when compared with children without neurological disease and healthy controls (OR = 6.29; 95% CI: 1.23-32.13; nominal p = 0.027), while HLA-B45 demonstrated a positive trend (OR = 3.75; 95% CI: 0.87-16.22; nominal p = 0.077). These allele-level findings were not corrected for multiple comparisons and should therefore be interpreted as exploratory and hypothesis-generating.

This study suggests a possible immunogenetic contribution to neurological complications in pediatric COVID-19, with a nominal unadjusted signal for HLA-B53. Given the small sample size, multiple-allele testing, and the absence of adjusted modelling, this finding should be considered exploratory and hypothesis-generating. Validation in larger multicenter cohorts with correction for multiple comparisons and adjustment for relevant confounders is required.

Public health measures during COVID-19 were associated with reduced respiratory syncytial virus cases in Hong Kong, China. Mask wearing was associated with a 35% reduction; avoidance behaviors and hand hygiene were also associated with reductions. After the mask mandate was lifted in March 2023, we observed resurgence in RSV activity.

The COVID-19 pandemic prompted lifestyle changes and increased parental stress and food insecurity, raising concern for single-parent households. This study investigates disparities in schoolchildren's diet quality in single-parent and two-parent households in Japan before, during and after the April 2020 state of emergency, considering financial status and parental meal preparation skills.

Data from a nationwide cross-sectional study conducted in December 2020 were analysed. A stratified two-stage cluster sampling design was used to select households with fifth-grade and eighth-grade students. Parents reported their child's dietary intake before, during and after the state of emergency and their knowledge about food. 'Poor dietary quality' was defined as failing to consume any of the following food categories at least twice a day: 'milk and dairy products', 'meat, fish or eggs', 'vegetables' and 'fruits'. Multilevel modified Poisson models were used to estimate prevalence risk ratios and differences in dietary quality.

Among 1534 parents, single-mother households exhibited higher risk of poor dietary quality during and after the state of emergency (univariate prevalence differences 13.4% (95% CI 3.5% to 23.2%) and 8.3% (95% CI 1.8% to 14.8%), respectively) compared with two-parent households. This difference persisted after adjusting for child sex and grade but substantially diminished after accounting for food literacy and financial status. No significant increase was observed in single-father households.

Single-mother households, marked by lower food literacy and income, experience a higher prevalence of poor dietary quality. Targeted support is crucial to improve diet quality in single-mother households compared with their two-parent counterparts.

Determine patients' and physiotherapists' prospective acceptability of using a shared decision-making (SDM) intervention to support patient choice of airway clearance technique (ACT) prescription for adults with bronchiectasis.

We conducted a qualitative study using focus groups and interviews.

Participants were recruited throughout the UK. All interviews and focus groups were conducted from the researcher's private home or Research Team office at Newcastle University. Face-to-face focus groups or interviews were conducted in a university conference room.

21 physiotherapists and 21 patients living with bronchiectasis participated.

12 themes were identified covering all seven domains of the theoretical framework of acceptability. Themes included: adherence, cultural challenges, education, empowerment, engagement, flexibility, health literacy, overwhelming information, participant understanding, resources, supportive of preferences and time.

A SDM intervention to support patient choice of ACT in bronchiectasis appears to be acceptable to both stakeholder groups. Additionally, we identified novel factors informing the design and implementation of a future SDM intervention. Future research should consider the systematic development of an SDM intervention to support patient choice of ACT in bronchiectasis.

Asthma, a chronic inflammatory airway disease characterized by wheezing, imposes a substantial global health burden on children. Given the potential of early-life omega-3 polyunsaturated fatty acid (omega-3 PUFA) supplementation as an anti-inflammatory intervention to prevent childhood asthma and wheezing, this meta-analysis aims to clarify its efficacy and investigate dose-dependency.

This systematic review and meta-analysis was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Three reviewers independently evaluated the studies, extracted data, and assessed bias using the Jadad scale. The outcomes included the risk of asthma/wheezing: pooled odds ratios (ORs) were calculated using fixed-effects models, along with sensitivity/subgroup analyses and dose-response meta-regression.

Twelve randomized controlled trials (RCTs) involving 4,156 participants showed no overall association between omega-3 PUFA and a reduced risk of asthma/wheezing (odds ratio [OR]: 1.00; 95% confidence interval [CI]: 0.84-1.18). However, high-dose supplementation (≥1,200 mg/day) significantly decreased the risk (OR: 0.66; 95% CI: 0.46-0.94). Similarly, high-dose eicosapentaenoic acid (EPA≥1,000 mg/day) also significantly reduced the risk (OR: 0.67; 95% CI: 0.46-0.97). Dose-response analysis confirmed a linear relationship (p=0.002), indicating a 26.6% reduction in risk for every 1,000 mg/day increase in dose (OR: 0.734; 95% CI: 0.602-0.896). Subgroup analyses revealed no heterogeneity with respect to study location, allergy risk, or follow-up duration.

Early-life omega-3 PUFA supplementation reduces childhood asthma/wheezing risk in a dose-dependent manner. High-dose regimens, particularly those involving EPA, provide substantial protection, suggesting a potential clinical strategy for prevention, although further validation is required.

Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease driven by fibroblast activation and extracellular matrix deposition. Endothelial-to-mesenchymal transition (EndMT) critically contributes to vascular injury and fibrotic remodeling in IPF. Legumain (LGMN), a lysosomal cysteine protease involved in excessive extracellular matrix processing and signaling modulation, has been implicated in vascular remodeling and fibrosis. This study aimed to investigate whether LGMN influences pulmonary fibrosis by regulating the EndMT process. Independent transcriptomic analyses revealed LGMN is significantly upregulated in IPF and associated with poor prognosis. Publicly available single-cell RNA sequencing datasets identify endothelial cells as a major source of elevated LGMN in human IPF and murine fibrosis, with LGMN expression positively correlating with disease severity. Our studies demonstrated that LGMN knockdown in endothelial cells inhibited EndMT and enhanced migratory and tube formation capabilities; conversely, LGMN overexpression promoted EndMT and suppressed these functions. Transcriptomic profiling indicated that LGMN knockdown significantly influenced the p38 MAPK signaling pathway. To validate the mechanism, pharmacological inhibition of p38 MAPK reduced EndMT and partially reversed LGMN overexpression-induced EndMT. In conclusion, these results indicate LGMN promotes pulmonary fibrosis by activating the p38 MAPK pathway to regulate EndMT, suggesting its potential as a therapeutic target for pulmonary fibrosis.

Efficient regeneration of the alveolar epithelium is essential for restoring lung function after injury, yet the mechanisms that govern alveolar type II cell (AT2) behavior remain insufficiently defined. Here, we identify the m⁶A RNA demethylase Alkbh5 as a pivotal regulator of AT2 cell activation and lineage progression. Conditional deletion of Alkbh5 in AT2 cells markedly enhances their proliferation and differentiation across diverse lung injury contexts-including fibrotic (bleomycin), inflammatory (LPS), mechanical (pneumonectomy), and oxidative (BHT) insults. Loss of Alkbh5 increases m⁶A modification on Amphiregulin (Areg) transcripts, stabilizing its mRNA and elevating Areg expression specifically within transitional AT2 populations. The resulting amplification of EGFR signaling drives accelerated AT2-to-AT1 differentiation and epithelial repair. Supplementation of recombinant Areg phenocopies the regenerative effects of Alkbh5 deletion, whereas Areg neutralization abrogates these responses, establishing Areg as a key downstream effector of Alkbh5. Importantly, ALKBH5 ablation or pharmacologic inhibition in human ESC-derived alveolar organoids similarly promote proliferation, differentiation, and AREG upregulation, demonstrating evolutionary conservation of this regulatory axis. Together, our findings reveal an Alkbh5-Areg-EGFR circuit that orchestrates alveolar epithelial regeneration and suggest new therapeutic opportunities for enhancing lung repair following injury.

Inflammatory bowel disease (IBD)-associated pulmonary injury is one of the frequently underestimated extraintestinal manifestations in clinical practice. It can present as subclinical pulmonary function abnormalities, radiographic changes, or overt inflammatory pulmonary diseases and often overlaps with infection- and treatment-related pulmonary toxicity, complicating early recognition and differential diagnosis. Growing evidence indicates that IBD-associated pulmonary injury is not an isolated pulmonary event but rather a cross-organ pathological process jointly driven by disruption of the intestinal mucosal barrier, dysbiosis, and aberrant microbial metabolites, systemic inflammation, and abnormal immune cell trafficking. This article provides a comprehensive review of current basic and clinical research evidence regarding intestinal barrier dysfunction, bidirectional gut-lung axis regulation, immune remodeling mediated by microbial metabolites, such as short-chain fatty acids (SCFAs), and the mechanisms and differential diagnosis of drug-induced pulmonary injury in IBD treatment. Existing studies suggest that SCFAs, tryptophan metabolites, immune cell homing, and alterations in the local pulmonary microbiota may represent key regulatory nodes in IBD-associated pulmonary injury; however, prospective studies integrating intestinal inflammatory activity, circulating biomarkers, pulmonary phenotypes, and drug exposure are still lacking. In the future, emphasis should be placed on establishing a stratified diagnostic framework for distinguishing pulmonary involvement intrinsic to the disease, infection, and drug-induced pulmonary injury, and on evaluating precision intervention strategies targeting microbial function, metabolite supplementation, and barrier repair to advance the translational application of mechanistic research on IBD-associated pulmonary injury into clinical practice.

Despite the presence of licensed vaccines and therapeutics, influenza viruses remain a major public health concern, as they cause seasonal respiratory infections and pose a pandemic threat through the emergence of zoonotic strains. Although neutralizing antibodies elicited by seasonal vaccination constitute a primary defense against infection, their protective capacity is often limited because they frequently target the epitopes that are highly susceptible to structural changes through viral evolution. To overcome this challenge, broadly protective antibodies have been intensively investigated in both humans and animal models. These antibodies recognize conserved epitopes and confer protection through multiple mechanisms beyond conventional neutralization. Recent advances in antibody discovery technologies and structural biology have enabled high-resolution mapping of conserved epitopes and the on-target antibodies that bind them. Furthermore, although broadly protective antibodies are typically elicited only at low frequencies following standard vaccination, several settings have been reported in which their induction is enhanced. Those findings increase the feasibility of epitope-focused vaccine strategies for enhancing the breadth and durability of antibody responses. In this review, we summarize current knowledge of broadly protective flu antibodies and discuss how mechanistic and structural insights can guide the development of next-generation influenza vaccines that offer broad-spectrum protection against antigenically diverse viruses.

Mycoplasma pneumoniae is the primary pathogen of community-acquired bacterial pneumonia in humans. Children and adolescents are particularly susceptible, and a dry cough is the most common clinical symptom. In severe cases, this may progress to acute respiratory distress syndrome. To determine the anti-M. pneumoniae and anti-inflammatory activities of a novel pleuromutilin derivative, 22-(4-((2-furan-1-yl)acetamido)phenyl)thio) deoxypleuromutilin (p-furoylamphenmulin, or PFAPM).

We utilized M. pneumoniae-infected mice to conduct in vivo pharmacokinetic (PK) and pharmacodynamic (PD) studies. The recommended dose was calculated based on PK/PD analysis, and treatment trials were performed at this dose to validate the fitted outcomes and investigate the anti-inflammatory effects.

The PK/PD results indicated that PFAPM exhibited an absorption half-life (T1/2ka) of 0.07 h and an elimination half-life (T1/2kel) of 0.87 h, with corresponding AUC values ranging from 1.18 to 8.33 μg·h/mL at doses of 10-80 mg/kg. When the mycoplasma load decreased by 3 log10 cfu/mL, the corresponding AUC48h/MIC and Cmax/MIC values were 7617.62 h and 1256.76, respectively, at a dose of 67.66 mg/kg. ELISA and flow cytometry analysis revealed that drug treatment significantly reduced cytokines and inflammatory cells associated with T helper 1 (Th1) and T helper 2 (Th2) immune responses.

AUC48h/MIC was the best parameter to describe the PK/PD relationship. The bactericidal effect was achieved at a dose of 67.66 (∼68) mg/kg. Pleuromutilins can reduce Th1 and Th2 inflammation.