The COVID-19 pandemic has been associated with various autoimmune manifestations. Several studies have suggested a potential association between COVID-19 and thyroid diseases (TDs); however, findings remain inconclusive and are primarily based on relatively small studies. Population-level data examining the differential impact of the pandemic on specific thyroid conditions are scarce.

To examine the incidence patterns of Hashimoto's Thyroiditis (HT), Graves' Disease (GD), and Subacute Thyroiditis (SAT) during the COVID-19 pandemic compared to the pre-pandemic period.

We conducted a population-based retrospective cohort study using interrupted time series analysis of adults (≥16 years) in the Clalit Health Services southern district of Israel from January 2018 to December 2022. New cases of TDs were identified using either ICD-9 codes, laboratory results, medication dispensing data or a combination of them. Monthly disease-specific incidence rates were compared between pre-pandemic (January 2018-February 2020) and pandemic (March 2020-December 2022) periods, with adjustment for seasonal variations.

Among 4,765 incident TD cases identified, 3,731 (78.3%) had HT, 698 (14.6%) had GD, and 336 (7.1%) had SAT. The mean age was similar across groups (43-45 years) with consistent female predominance (77%). Interrupted time series analysis revealed a significant 30% increase in HT incidence during the pandemic period (IRR 1.30, 95% CI 1.04-1.64, p=0.023), which began prior to the national vaccination campaign. GD showed a non-significant upward trend suggestive of a possible increased incidence (IRR 1.66, 95% CI 0.99-2.79, p=0.054). Conversely, SAT demonstrated a significant 54% reduction in incidence (IRR 0.46, 95% CI 0.21-0.99, p=0.049).

The COVID-19 pandemic was associated with a significant increase in HT incidence and an unexpected decrease in SAT. These findings highlight the heterogeneous impact of the pandemic on different TDs.

To compare the effects of nasal versus buccal breathing on non-invasive indices of vascular function under standardized resting conditions.

This observational crossover study included 45 young healthy Caucasian male volunteers (mean age 21.3 ± 2.3 years). Each participant completed two breathing protocols: nasal breathing (NB) and buccal breathing (BB), in randomized order, separated by a washout period. Vascular responses were assessed using several non-invasive methods: Digital Plethysmography (DP) and UltraSound Flow-Mediated Dilation (US-FMD). Pulse Propagation Time (PPT) and Reflection Index (RI) were derived from DP, while brachial artery diameter was measured with US-FMD at rest and following each breathing condition.

Nasal breathing significantly increased PPT (6.35% ± 1.51) and reduced RI (4.6% ± 1.25) compared with buccal breathing, indicating changes consistent with increased vascular relaxation (p < 0.05). Ultrasound assessment demonstrated a significant increase in brachial artery diameter (4.46% ± 0.05) during nasal breathing (p < 0.001), an effect absent during buccal breathing. These findings indicate that nasal breathing is associated with enhanced vasodilation and differences in non-invasive vascular indices compared with buccal breathing.

In healthy young adults, nasal and buccal breathing were associated with distinct patterns in non-invasive indices of vascular function. These findings highlight the physiological relevance of breathing route under resting conditions and warrant further investigation.

Lung transplantation is a definitive lifesaving option for end-stage lung disease; however, its role in rapidly progressive interstitial lung disease (RP-ILD) associated with anti-melanoma differentiation-associated gene 5 (anti-MDA5) antibodies remains debated. We retrospectively analyzed two anti-MDA5-positive RP-ILD (MDA5⁺ RP-ILD) patients who underwent bilateral lung transplantation and synthesized pertinent literature to evaluate clinical value and the impact of therapeutic interventions. Both patients recovered postoperatively and were discharged after symptomatic management and supportive care. One patient subsequently developed cerebral infarction and died approximately 8 months after transplantation, whereas the other remains clinically stable under regular follow-up. Given the limited efficacy of conventional therapies and the overall poor prognosis of anti-MDA5-positive dermatomyositis (MDA5⁺ DM) with RP-ILD, our observations-together with prior reports-support lung transplantation, with extracorporeal membrane oxygenation (ECMO) as a bridge when necessary, as a promising and reliable therapeutic strategy. Lung transplantation may offer definitive treatment in carefully selected patients, underscoring its important clinical value.

Bronchiolitis obliterans syndrome (BOS) is a severe, often fatal pulmonary manifestation of chronic graft-versus-host disease (cGVHD) following allogeneic hematopoietic stem cell transplantation (HSCT). Its progression to air-leak syndrome (ALS) signifies a critical deterioration with exceedingly high mortality. Lung transplantation (LTx) remains a rare salvage option, especially in children, with scarce reports of successful outcomes in those with this complication cascade.

We report the case of a 7-year-old girl with Diamond-Blackfan anemia (DBA) who developed BOS complicated by ALS after allo-HSCT. She developed acute GVHD involving the skin and liver on +100d, which improved following immunosuppressive therapy. On +231d, pulmonary function tests showed severe mixed ventilatory dysfunction (FEV₁ 37% of predicted value, FEV₁/FVC 52%), and high-resolution computed tomography (HRCT) revealed mosaic perfusion and bronchial wall thickening, contributing to the diagnosis of BOS. Despite intensive immunosuppressive therapy, she developed ALS on +360d and type II respiratory failure on +475d. Sequential bilateral LTx was performed on October 28, 2025. Postoperatively, the patient recovered following the management of multidrug-resistant bacterial infections and respiratory complications, with no rejection or recurrence of cGVHD during follow-up.

This report presents the youngest documented DBA case of successful LTx for BOS complicated by ALS after allo-HSCT globally. It demonstrates that dynamic multimodal monitoring is crucial for early BOS detection. LTx is a viable therapy for end-stage pulmonary cGVHD in children. This case underscores the need for proactive monitoring in high-risk patients and provides a paradigm for managing this complex complication.

Seasonal influenza virus infections represent a global health threat, especially in high-risk groups, including patients with liver cirrhosis that are considered to be immunocompromised, in particular in decompensated stages. Although vaccination is the most cost-efficient tool to prevent infectious diseases, information about vaccine performance in these patients is scarce. This study aimed to dissect the immunological responses to seasonal influenza vaccines in patients suffering from compensated or decompensated liver cirrhosis.

Prospective, observational studies during the influenza seasons 2019-2020 (1^st season) and 2020-2021 (2^nd season) were performed. Participants received the WHO recommended seasonal tetravalent inactivated influenza vaccine. Samples taken before and after vaccination were subjected to in-depth analyses by serology, cytokine immunoprofiling, multi-parametric flow cytometry, and metabolomics. Patients with liver cirrhosis showed stronger vaccine-induced immune responses in comparison to healthy individuals, including hemagglutination-inhibiting and neutralizing antibodies. Furthermore, enhanced cell-mediated immune responses were observed in the cirrhosis patients as compared to healthy subjects after vaccination. Surprisingly, vaccination response was even stronger in more advanced, decompensated stages of liver cirrhosis. Distinct serum cytokine and metabolite profiles associated with systemic inflammation differentiated patients with decompensated from compensated cirrhosis as well as from the healthy individuals and were linked to vaccine response.

Patients with liver cirrhosis can mount an efficient response to seasonal influenza vaccines that is even superior in more advanced stages of cirrhosis. Systemic inflammation caused by liver cirrhosis may contribute to distinct humoral and cellular vaccine responses.

The gut-lung axis links early-life microbial programming to long-term respiratory health, offering a pivotal framework for understanding childhood asthma pathogenesis. This review synthesizes current evidence on how disruptions in microbial-immune crosstalk during critical developmental windows shape asthma susceptibility. Perinatal determinants-including maternal diet, delivery mode, antibiotic exposure, and breastfeeding-establish gut microbial communities that educate the developing immune system. Distinguishing itself from recent reviews, this review offers three novel contributions: (i) an integrated multi-omics framework linking early-life microbial maturation trajectories to specific asthma endotypes; (ii) a systematic synthesis of the molecular mechanisms by which microbial metabolites-including short-chain fatty acids, tryptophan derivatives, and bile acids-orchestrate gut-lung immune crosstalk; and (iii) a clinically actionable precision medicine algorithm that translates multi-omics profiling into personalized risk prediction, endotype-driven therapy selection, and targeted preventive strategies. Dysbiosis, characterized by delayed microbial maturation and depletion of short-chain fatty acid-producing taxa, compromises epithelial barrier integrity and skews immune homeostasis toward pro-allergic type-2 responses. Microbial metabolites, particularly short-chain fatty acids (acetate, propionate, butyrate) and tryptophan derivatives (indole-3-lactic acid, indole-3-propionic acid), serve as key molecular mediators that regulate regulatory T cells differentiation, reinforce mucosal barriers, and modulate distal airway inflammation. Microbial signatures correlate with specific asthma endotypes, offering opportunities for patient stratification. We critically evaluate emerging microbiome-targeted interventions-including strain-specific probiotics, prebiotics, postbiotics, and fecal microbiota transplantation-highlighting both therapeutic promise and the need for rigorous, well-powered clinical trials. Integrating multi-omics microbial profiling with host genetics and clinical phenotyping holds potential for microbiome-informed precision medicine, enabling personalized risk prediction, endotype-driven therapy selection, and novel preventive strategies targeting the gut-lung axis from the earliest stages of life.

Sepsis remains a life-threatening complication of severe pneumonia in infants and young children, yet early biomarkers are lacking. The gut microbiota modulates host immunity, but the association between the gut microbiota and pediatric pneumonia-associated sepsis is unclear due to confounding factors.

In this prospective, 1:1 matched case-control study, we enrolled 100 infants and young children (28 days-36 months) with severe pneumonia, stratifying them into sepsis (n=50) and non-sepsis (n=50) groups matched for age and antibiotic exposure. Fecal samples collected within 48 hours of PICU admission underwent 16S rRNA gene sequencing. Diversity, taxonomic composition, and differential taxa were analyzed.

The sepsis group exhibited significantly reduced alpha diversity (Shannon index: 2.30 ± 1.50 vs. 2.83 ± 1.36, P = 0.027), increased Enterobacteriaceae (18.97% vs. 9.44%, P = 0.046), and decreased Lachnospiraceae (2.01% vs. 8.11%, P = 0.010). LEfSe (Linear discriminant analysis Effect Size) further revealed distinct microbial signatures: the sepsis group exhibited enrichment of Lactobacillaceae and Clostridium butyricum, while the non-sepsis group was characterized by higher abundance of Lachnospiraceae and Segatella.

Sepsis in infants and young children with severe pneumonia is associated with a specific gut microbiota signature, independent of major confounders. This dysbiotic profile, involving taxa associated with endotoxin production and short-chain fatty acid metabolism, may serve as an early biomarker for risk stratification and could inform microbiota-targeted interventions in critically ill infants and young children.

Advances in antiretroviral therapy (ART) have substantially improved the lives of people with HIV (PWH) and reduced HIV acquisition through pre-exposure prophylaxis (PrEP). However, the long-term effect of ART on the physiological state of cells remains poorly understood and PWH are currently suffering from a disproportionate burden of non-AIDS comorbidities, including lung diseases.

Given the central function of alveolar macrophages (AM) in pulmonary immunity, we evaluated the impact of ART on AM of PWH and people on PrEP using a systems immunology approach.

We showed that continuous ART induces a progressive senescence-like pro-inflammatory state in AM characterized by increased constitutive epigenetic and transcriptomic priming of genes involved in cell-cycle arrest and senescence. At the AM single nucleus level, we discovered a coordinated gene regulatory network linking key pro-inflammatory transcription factors to the alterations induced by ART. The senescence ART-linked changes were strongly dependent on the duration of ART and irrespective of HIV infection. A secondary time independent ART-effect was observed for interferon signaling which impaired the AM response to ex vivo challenge with SARS-CoV-2.

Our data indicated that continuous ART promoted a dysregulated physiological state in AM. The results of our study advocate for optimized or adjuvant therapies to mitigate potential long-term adverse ART-effects.

The significant bidirectional comorbidity risk and extensive subclinical involvement observed between chronic obstructive pulmonary disease (COPD) and inflammatory bowel disease (IBD) underscore the pivotal role of the "gut-lung axis" in cross-organ pathological crosstalk. Here, we comprehensively review the molecular and immunological mechanisms driving this comorbidity. Genome-wide association studies (GWAS) have substantiated genetic pleiotropy that underpins a shared susceptibility to mucosal defense deficits. The "common mucosal immune system" (CMIS), rooted in embryonic homology, constitutes the anatomical basis for this pathological interplay, wherein aberrant immune cell homing, Th17/Treg imbalance, and the cross-organ trafficking of innate lymphoid cells (ILCs) mediate the distal dissemination of inflammation. Furthermore, gut dysbiosis-induced depletion of short-chain fatty acids (SCFAs), acting in concert with systemic hypoxia and the IL-23/IL-17 axis, potentiates synergistic injury to the gut-lung barriers. We highlight the reciprocal, bidirectional causality of this "hypoxic loop" and its testable mechanistic predictions for barrier dysfunction. Furthermore, we evaluate pharmacological evidence from drug repositioning, alongside a critical examination of the "hidden axis" of clinical therapies as profound iatrogenic confounders. Elucidating these mechanisms is critical for establishing systemic diagnostic and therapeutic strategies; interventions targeting shared molecular targets and the microbiota hold promise for achieving a simultaneous treatment approach for these distinct pathologies.

Long COVID (LC) presents persistent symptoms that pose a major clinical challenge. Identification of reliable biomarkers to evaluate LC pathophysiology is needed.

To investigate whether serum S- and N-antibody titers against SARS-CoV-2 spike and nucleocapsid proteins reflect the clinical features of LC.

This retrospective observational study included patients diagnosed with Omicron variant-related LC who attended a post-COVID-19 outpatient clinic between July 2023 and November 2024 and provided informed consent for antibody testing.

Among 275 patients (129 men and 146 women), 57 (21%) were unvaccinated. Median S- and N-antibody titers in vaccinated versus unvaccinated patients were 20,963 U/mL and 24.8 cut-off index (COI) versus 24 U/mL and 44.5 COI, respectively. S-antibody titers were associated with the number of vaccine doses received, whereas N-antibody titers correlated with disease severity during the acute phase of COVID-19 infection, with females having higher titers by multivariable analysis. N-antibody titers in unvaccinated patients with LC were negatively correlated with time interval from infection to clinic visit, with an estimated daily decline of 0.34% in measured N-antibody levels. Patients with LC having memory impairment had low S-antibody titers by multivariable logistic regression analysis, and low S-antibody levels were associated with reduced quality of life (QOL). Additionally, N-antibody titers positively correlated with lymphocyte counts and immunoglobulin levels.

Serum N-antibody titers reflect immune responses to COVID-19, although they are affected by gender differences and interval between infection and evaluation. Lower S-antibody titers were associated with brain fog symptoms and reduced QOL in patients with LC.