Population aging increases the risk of severe respiratory infections and their complications in older adults, largely because of immunosenescence. Beyond pneumonia, these infections can lead to cardiac and respiratory decompensation, acute cardiovascular events, loss of functional independence, and institutionalization. Vaccination remains the cornerstone of prevention. This review provides an update on four vaccine-preventable respiratory infections that are particularly common or severe in older adults: coronavirus disease 2019 (COVID-19), respiratory syncytial virus (RSV) infection, seasonal influenza, and pneumococcal disease. For each infection, we review the epidemiological burden, associated complications-particularly cardiovascular and functional outcomes-as well as recent real-world evidence on vaccine effectiveness and the 2026 French recommendations. The evidence is consistent: safe and effective vaccines are available for all four infections, yet vaccination coverage remains far below target among older adults and is even lower among healthcare workers, a situation that has worsened since the COVID-19 pandemic. The pandemic has durably reshaped attitudes towards vaccination, shifting from initial acceptance to growing hesitancy. Improving information and education for both the public and healthcare professionals, particularly those working in geriatric care settings, appears to be the most effective strategy for reducing this preventable burden. Clear, consistent communication and the integration of vaccination into personalized care plans are essential to translate well-established recommendations into effective protection.

Severe inflammatory lung disease, including acute respiratory distress syndrome (ARDS), is life-threatening with diverse causes and few targeted therapies. Inborn errors of immunity (IEIs) underlie a subset of cases. We describe a novel IEI caused by biallelic loss-of-function variants in PTPN6, encoding the immunoregulatory phosphatase SHP1. Seven children from five families developed early-onset anemia and severe inflammatory lung disease, at times presenting as ARDS. The causative variants were shown to destabilize SHP1 and abolish its phosphatase activity. These findings expand the genetic landscape of inflammatory lung disease and suggest SHP1 activation as a potential therapeutic strategy for immune-mediated pulmonary pathology.

Checkpoint inhibitor pneumonitis (CIP) is an uncommon but potentially life-threatening immune-related adverse event that may interrupt effective anticancer therapy and require prolonged immunosuppression. Its clinical presentation, radiographic appearance, inflammatory biology, and response to corticosteroids vary substantially, while infection, radiation pneumonitis, tumor progression, pulmonary embolism, and pre-existing interstitial lung disease may produce overlapping findings. Conventional severity grading remains important for communication and triage but does not fully capture this heterogeneity.

This narrative review synthesizes clinical, radiographic, immunological, and treatment-response evidence to develop a framework for phenotype-guided CIP management. We conceptualize CIP as a dynamic pulmonary immune syndrome and organize its assessment across four dimensions: clinical severity, radiographic phenotype, inflammatory and immune phenotype, and corticosteroid responsiveness. Emerging evidence involving CD4+ and CD8+ memory and tissue-resident T cells, Th17.1 and Tfh-like programs, pro-inflammatory monocytes and macrophages, cytokine networks, and humoral responses is linked to clinically relevant questions while remaining hypothesis-generating. Three patterns are emphasized: low-inflammatory-burden, steroid-responsive disease; high-risk progressive disease; and persistent immune-activation or steroid-refractory disease. The framework connects these patterns with diagnostic reassessment, multidisciplinary evaluation, corticosteroid treatment, recognition of treatment failure, immunomodulatory escalation, chronic pulmonary follow-up, and individualized immune checkpoint inhibitor rechallenge.

CIP should not be managed as a single toxicity defined by grade alone. Joint interpretation of clinical trajectory, imaging, inflammatory signals, and corticosteroid response may improve risk stratification and support more proportionate diagnostic and therapeutic decisions. This framework is a clinically grounded heuristic rather than a validated algorithm and requires prospective multicenter evaluation.

Maternal smoking during pregnancy impairs lung immune responses and leads to a higher frequency of respiratory infection in children. This study aims to assess the association of maternal smoking around birth with respiratory tract infection in adult offspring, using Mendelian randomization (MR).

This is an MR study based on the Integrative Epidemiology Unit (IEU) open Genome-Wide Association Study (GWAS) data. The exposure was maternal smoking around birth; the outcomes were upper respiratory tract infection (URTI), lower respiratory tract infection (LRTI), coronavirus disease 2019 (COVID-19), acute bronchitis, pneumonia, bacterial pneumonia, viral pneumonia, influenza pneumonia, and pneumonia death. The inverse variance weighted, weighted median, and MR-Egger methods were used as the main methods of MR analysis. Heterogeneity and pleiotropic analysis were performed to ensure the accuracy of the results.

After removing single-nucleotide polymorphisms (SNPs) related to smoking by the offspring, maternal smoking around birth was associated with an increased risk of LRTI (OR=2.68; 95% CI: 1.29-5.58; p=0.008), COVID-19 (OR=2.32; 95% CI: 1.30-4.14; p=0.004), acute bronchitis (OR=7.14; 95% CI: 2.54-20.06; p<0.001), pneumonia (OR=1.90; 95% CI: 1.07-3.38; p=0.030), and bacterial pneumonia (OR=2.96; 95% CI: 1.14-7.69; p=0.026). No significant correlation was detected between maternal smoking and URTI (OR=4.29; 95% CI: 0.72-25.68; p=0.111).

This Mendelian randomization study provides evidence that maternal smoking around birth is associated with an increased risk of LRTIs, particularly acute bronchitis, pneumonia, and bacterial pneumonia, along with COVID-19, in adult offspring. These findings suggest that the detrimental impact of early-life tobacco smoke exposure on respiratory health persists into adulthood, likely mediated by long-term alterations in pulmonary development and immune system programming.

Dogs can harbor a range of respiratory tract helminths which can cause clinical signs varying from asymptomatic to serious diseases. Lately, these parasites, notably Eucoleus spp. and Angiostrongylus vasorum, received considerable attention because of their spread in previously nonendemic regions, likely facilitated by several factors such as increased animal movements changes in the distribution and urbanization of wild canid reservoirs, along with climatic and environmental changes. This study aimed to assess the presence and dissemination of these helminths by investigating, for the first time in Morocco, the seroprevalence of A. vasorum and the fecal occurrence of Eucoleus spp. eggs in dogs. Overall, 318 fecal samples collected from dogs across different geographical areas of Morocco were examined using two fecal flotation techniques, centrifugal flotation with 33% zinc sulfate (ZnSO₄) and simple flotation with Sheather's sugar solution. Additionally, A. vasorum antigen detection was performed on 286 blood samples using an in-clinic serological test (Angio Detect Test, IDEXX Laboratories). A complete blood count was subsequently performed in dogs that tested positive. Results revealed the occurrence of Eucoleus boehmi eggs in three military working dogs (0.94%), with two being asymptomatic and one showing a mucous nasal discharge. All had mild to moderate eosinophilia (1.33-3.18 K/μL). With regard to the serological assays, all dogs tested negative for A. vasorum antigens. These preliminary findings provide initial evidence of the geographic spread of E. boehmi, suggesting that veterinarians in Morocco should include this infection in the differential diagnosis of dogs displaying upper respiratory tract symptoms. By contrast, despite the absence of dogs seropositive to A. vasorum, the disease cannot be excluded until a better understanding of its distribution is established. Hence, further studies involving larger canine populations across different regions and combining multiple diagnostic methods, including advanced molecular techniques, are highly recommended.

Legionella pneumonia (LP), primarily caused by Legionella pneumophila, is a clinically important subtype of community-acquired pneumonia (CAP) associated with substantial morbidity and mortality. However, the microbial characteristics and functional profiles of LP remain insufficiently understood.

In this study, metagenomic next-generation sequencing (mNGS) was used to compare airway microbial communities between patients with LP and those with non-Legionella CAP.

A total of 60 patients were included, comprising 23 patients with LP patients and 37 patients with non-Legionella CAP patients. Airway microbial diversity and composition differed between groups, although the between-group effect size was modest and residual confounding could not be excluded. The LP group showed higher relative abundance of Legionella pneumophila and selected opportunistic species, whereas several oral commensal-associated species were relatively enriched in non-Legionella CAP. In the pooled 60-patient cohort, selected microbial species were associated with inflammatory and clinical severity markers; these associations were not disease-specific and do not imply causality. Inferred functional profiles also differed between groups. Exploratory machine-learning models showed high internal discriminatory performance, with XGBoost yielding the highest mean AUC, but the small cohort and lack of external validation limit conclusions regarding diagnostic utility.

In this small retrospective cohort, LP was associated with differences in airway microbial composition and inferred functional potential compared with a heterogeneous non-Legionella CAP group. Because the study was observational, the groups differed in important clinical characteristics, and the pooled association analyses were not disease-specific, the findings should be considered exploratory and hypothesis-generating. The reproducibility and diagnostic value of microbiota-derived features require confirmation in larger, prospectively collected, independent cohorts.

Empirical evidence indicates that societal crises and adverse conditions can negatively impact population mental health. The Big Five personality traits - neuroticism, extraversion, openness, agreeableness, and conscientiousness -significantly influence stress responses. In this article, we examine how personality traits were associated with mental distress during and in the aftermath of the COVID-19 pandemic. Based on data from the Understanding America Study, we find that, since the pandemic began, individuals with high levels of neuroticism were more likely to experience mental distress. By contrast, the remaining personality traits exhibited weaker, inconsistent, or statistically insignificant associations with mental health trajectories. Further analyses indicate that the heightened vulnerability among individuals high in neuroticism was accompanied by elevated risk perceptions, differential adoption of protective behaviors, and less adaptive coping patterns. Taken together, these findings suggest that personality-linked differences, particularly driven by the level of neuroticism, help explain heterogeneity in mental health responses to large-scale societal stressors. Our findings point to the relevance of personality traits (particularly neuroticism) for identifying individuals who may benefit from targeted mental health support during future crises.

The role of guideline-directed medical therapy for heart failure (HF) is unclear in transthyretin amyloid cardiomyopathy (ATTR-CM). Dapagliflozin has demonstrated beneficial effects across HF phenotypes, and retrospective studies suggest potential benefit in ATTR-CM; however, prospective data are lacking. This pilot study evaluated the effect and tolerability of dapagliflozin in patients with ATTR-CM to inform the design of a larger randomized trial.

Participants were followed for 30 weeks over three study periods: 8 weeks baseline without study medication, 12 weeks intervention with dapagliflozin 10 mg once daily, and 10 weeks withdrawal without study medication. The study was open-label and nonrandomized. Vital signs and NT-proBNP were assessed every second week, while Kansas City Cardiomyopathy Questionnaire total symptom score (KCCQ-TSS) and 6-minute walking test (6MWT) were assessed every 4 weeks. Results were analyzed using linear mixed-effects models.

Seven of ten enrolled patients completed the trial. One participant discontinued because of genitourinary adverse effects, and two withdrew for reasons unrelated to the intervention. The estimated intervention-versus-baseline difference was -142 pg/mL (95% CI -324-41) for NT-proBNP, 24.3 m (95% CI -2.8 to 51.5) for 6MWT distance, and 0.4 points (95% CI -4.0 to 4.8) for KCCQ-TSS. Sitting SBP was 8.8 mmHg lower during intervention than during baseline (95% CI -13.2 to -4.4). No increase in hypotensive symptoms or cardiovascular adverse events was detected.

Dapagliflozin was generally well tolerated in this pilot study of patients with ATTR-CM. The estimated differences in NT-proBNP, 6MWT distance, and KCCQ-TSS were imprecise and did not provide conclusive evidence of treatment effects. SBP was lower during treatment, without a detected increase in hypotensive symptoms. These exploratory findings support further evaluation in an adequately powered randomized trial.

This study was registered with clinical trial number EudraCT no 2021-003674-32.

Baseline intracavitary haemodynamic measurements frequently demonstrate an inconsistent relationship with exertional performance. This may reflect an incomplete interpretation of left ventricular (LV) filling pressures. LV transmural pressure difference (ΔPTM = LV end-diastolic pressure [LVEDP]-right atrial pressure [RAP]) integrates LV filling pressure with right ventricular/pericardial constraint and may provide a composite representation of resting haemodynamic conditions. Ventilatory efficiency, assessed by the minute ventilation-carbon dioxide production (VE/VCO2) slope during cardiopulmonary exercise testing (CPET), is a leading representation of cardiopulmonary reserves and a powerful prognostic marker in heart failure (HF). Whether ΔPTM is associated with exercise ventilatory efficiency beyond conventional resting filling pressure measurements remains unclear.

We retrospectively studied 422 patients with advanced HF (LVEF ≤25%) who underwent right-heart catheterization and CPET. ΔPTM was analysed both continuously and by tertiles. The primary outcome was VE/VCO2 slope; peak VO2 was a secondary outcome. Bayesian multivariable regression models were adjusted using a directed acyclic graph-derived confounder set. Sensitivity analyses compared ΔPTM with LVEDP and RAP modelled individually and jointly.

Among 422 patients (mean age 51.3 ± 10.8 years; 62 [14.7%] female), higher ΔPTM was independently associated with a lower VE/VCO2 slope (posterior mean β = -0.34 per mmHg; 95% credible interval [CrI] -0.58 to -0.11; 99.7% posterior probability of a negative association). Unadjusted VE/VCO2 slope decreased from 40.2 (31.7-67.1) in the lowest ΔPTM tertile to 34.9 (30.6-44.8) in the highest tertile (P = .029). The adjusted posterior predictive difference between the highest and lowest ΔPTM tertiles was -4.42 units (95% CrI -7.85 to -0.62). Following multivariable adjustment, ΔPTM showed no significant association with peak VO2 (posterior mean β = +0.06; 95% CrI -0.02 to +0.14). Neither LVEDP nor RAP, modelled individually or jointly, demonstrated independent associations with ventilatory efficiency.

Resting ΔPTM was inversely associated with the VE/VCO2 slope during exercise, whereas no independent association was observed with peak VO2. Compared with individual left- or right-sided filling pressures, ΔPTM provides a parsimonious summary of the balance between left-sided distending pressure and right-sided constraint associated with ventilatory efficiency in advanced HF.

The optimal revascularization strategy for patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and multivessel disease remains uncertain. This meta-analysis aimed to evaluate the impact of one-time versus staged multivessel percutaneous coronary intervention (PCI) on clinical outcomes.

PubMed, Embase, and the Cochrane Library were searched for randomized controlled trials and cohort studies comparing one-time and staged PCI in NSTE-ACS patients with multivessel disease from January 1, 2000 to June 4, 2026. Study quality was assessed, data were extracted independently by two reviewers, and pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated using R software and the meta package.

Ten studies involving 6,749 patients (4,235 one-time PCI; 2,514 staged PCI) were included. In randomized trials, one-time PCI significantly reduced repeat revascularization (RR = 0.71, 95% CI 0.51-0.98, p = 0.037) versus staged PCI, with no differences in mortality or recurrent myocardial infarction. Cohort studies and the pooled analysis showed no significant differences across outcomes.

For NSTE-ACS patients with multivessel disease, multivessel revascularization in a single procedure may reduce repeat revascularization compared with staged PCI, but the evidence remains limited.