Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are pathologically characterized by disruption of the alveolar-capillary barrier, excessive inflammatory responses, and dysregulated intra-pulmonary coagulation. Although inflammatory and thrombotic cascades have been extensively studied, endogenous epithelial-derived signaling mechanisms coordinating barrier stabilization with immunothrombotic restraint remain undefined. Here, we identify fibroblast growth factor 20 (FGF20) as a constitutive epithelial regulator suppressed in alveolar barrier-associated cells during sepsis-induced ALI. In a CLP rat model, both prophylactic and therapeutic administration of recombinant human FGF20 (rhFGF20) improved 7-day survival, attenuated pulmonary edema and inflammation, restored gas exchange, and preserved alveolar-capillary integrity. rhFGF20 restrained procoagulant and antifibrinolytic mediators tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) while suppressing NF-κB activation. Mechanistically, FGF20 acted through fibroblast growth factor receptor 1 (FGFR1) to engage the FGFR1-PI3K-AKT cascade. AKT activation bifurcated into two axes: (i) inhibition of NF-κB phosphorylation and nuclear translocation, restraining TF/PAI-1 transcription; and (ii) inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser9, stabilizing epithelial and endothelial junctional proteins (E-cadherin, VE-cadherin, ZO-1). Pharmacological inhibition of FGFR1 or AKT abolished both barrier-protective and anticoagulant effects, confirming pathway dependency. Clinically, serum and bronchoalveolar lavage fluid FGF20 levels were reduced in ARDS patients and positively correlated with PaO₂/FiO₂ ratios, linking reduced FGF20 to disease severity. Collectively, these findings position FGF20 as an upstream integrator of structural and immunothrombotic homeostasis within the alveolar-capillary unit. Restoration of the FGF20-FGFR1 axis reconstitutes a proximal checkpoint stabilizing barrier architecture and constraining NF-κB-dependent procoagulant activation, highlighting FGF20 as a mechanistically grounded therapeutic target in sepsis-induced ALI/ARDS. CLINICAL SIGNIFICANCE.

Severe pulmonary leptospirosis (SPFL), characterized by diffuse alveolar haemorrhage (DAH) and acute respiratory distress syndrome (ARDS), carries a high mortality, often due to diagnostic delays and complex management. We report a case of a 42-year-old male with outdoor occupational exposure who presented with fever and hemoptysis, rapidly progressing to severe respiratory failure and thrombocytopenia. Chest imaging confirmed DAH/ARDS. For refractory hypoxemia, veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated without systemic anticoagulation due to active pulmonary haemorrhage. Metagenomic next-generation sequencing (mNGS) of bronchoalveolar lavage fluid rapidly identified Leptospira interrogans, enabling targeted antimicrobial therapy alongside multidisciplinary support. The patient gradually improved, was successfully weaned from ECMO and ventilator support, and was discharged without residual organ dysfunction. This case demonstrates that early application of anticoagulation-free VV-ECMO combined with mNGS-based rapid diagnosis and multidisciplinary care can improve outcomes in SPFL, highlighting the importance of considering this diagnosis in febrile patients with DAH and environmental exposure.

Acute respiratory distress syndrome (ARDS) remains a major challenge in trauma care, with high morbidity and mortality. Current management emphasizes lung-protective ventilation, careful fluid balance, and a multidisciplinary approach. New areas of discovery, such as ARDS phenotyping, precision medicine, ECMO innovations, and evolving adjunctive therapies, are reshaping practice and offering opportunities for improved outcomes. This comprehensive review highlights the current understanding of ARDS and management essentials and underscores the importance of emerging therapies that offer the clearest path to further reduce ARDS morbidity and mortality.

Acrolein is a highly toxic chemical substance commonly found in industrial production. This article analyzes the clinical data of 5 patients suspected of acute acrolein poisoning. The patients presented symptoms such as bilateral bronchitis, cyanosis of the lips and face, pharyngalgia, chest tightness, shortness of breath, etc. Severe poisoning patients also experienced acute respiratory failure and acute respiratory distress syndrome (ARDS). After comprehensive treatments including high-flow humidified oxygen inhalation, corticosteroid pulse therapy, and blood purification, 4 of the moderate-to-severe poisoning patients gradually improved and were discharged from the hospital, while 1 severe poisoning patient significantly improved after treatment with extracorporeal membrane oxygenation (ECMO), but died later due to secondary infection. This article provides valuable experience for clinicians in identifying, diagnosing, and treating acrolein poisoning, and highlights the risk of secondary infection in severe patients during treatment, which is significant for improving the success rate of treatment.

Prolonged intensive care unit (ICU) hospitalization due to acute respiratory distress syndrome results in reduced muscle strength and increased fatigability. This study investigated the central and peripheral neuromuscular mechanisms underlying these impairments in sixty COVID-19 patients up to 12 months post-ICU discharge. Muscle strength (maximal voluntary contraction; MVC), functional exercise capacity (six-minute walk test; 6MWT), and perceived fatigue (Fatigue Severity Scale; FSS) were assessed at each follow-up. High-Density surface electromyography was collected from the Tibialis anterior muscle at 30%, 50%, and 70% MVC. 6MWT distance increased from 3 to 6 months, but not 6-12. FSS declined from 6 to 12 months, while MVC increased across both intervals. Motor unit (MU) discharge rate decreased from 6 to 12 months at all contraction intensities and from 3 to 6 months at 50% and 70% MVC. MU discharge variability decreased at all levels except 70% MVC from 3 to 6 months. MU action potential amplitude increased from 3 to 6 months but not 6-12. Central MU properties correlated with voluntary force at 3-6 months and with fatigue scores at 6-12 months. These interval-based analyses indicate that associations between neural adaptations and muscle strength were more prominent between 3 and 6 months following ICU discharge, whereas associations with perceived fatigue were more evident between 6 and 12 months.

The class Bunyaviricetes encompasses a diverse group of vector- and rodent-borne viruses, many of which are major human pathogens causing severe and often lethal diseases worldwide. These include Lassa fever virus (Arenaviridae), hantaviruses such as Hantaan and Andes viruses (Hantaviridae), Crimean-Congo hemorrhagic fever virus (Nairoviridae), La Crosse and Oropouche viruses (Peribunyaviridae), and Rift Valley fever, severe fever with thrombocytopenia syndrome, and Toscana viruses (Phenuiviridae). Clinical syndromes range from hemorrhagic fever with multiorgan failure, vascular leak, and shock to acute encephalitis and severe respiratory distress. Despite their public health impact, safe and effective vaccines or targeted therapeutics are lacking for most bunyaviricetes diseases, leaving supportive care as the primary intervention. This review provides a comparative analysis of the immunopathogenesis of major human-pathogenic bunyaviricetes, highlighting shared and virus-specific strategies for innate immune evasion, cytokine modulation, and host cell targeting. Severe disease often arises from viral interference with key sensing pathways, such as RIG-I/MDA5 and downstream IRF and NF-κB signaling, which either suppresses interferon responses or leads to dysregulated inflammation. By integrating molecular, immunological, and clinical insights, we outline how these immune-virus interactions shape disease trajectory and severity. Understanding these mechanisms is critical for guiding the rational design of vaccines, antivirals, and immunomodulatory therapies, and for strengthening preparedness against these persistent zoonotic threats.