This case report describes a rare instance of drug-induced acute lung injury in a 16-year-old male patient following circumcision performed under sevoflurane-based general anesthesia. Although sevoflurane is a widely used inhalational anesthetic with a favorable safety and tolerability profile, this case demonstrates that it may, in rare instances, precipitate acute lung injury. The clinical features, imaging findings, and laboratory findings of this case were analyzed alongside a systematic review of the relevant literature to clarify the diagnostic basis and differential diagnoses. This case report aims to raise clinicians' awareness of sevoflurane-induced acute lung injury.

Acute respiratory distress syndrome (ARDS) is a critical illness with high incidence and mortality in the intensive care unit (ICU). Recent studies have demonstrated that the "gut-lung axis", a bidirectional regulatory network between the gut and the lungs, plays a pivotal role in the pathophysiology of ARDS. This review focuses on the "homing" mechanisms underlying the directed migration of gut-derived immune cells, particularly ILC2s, ILC3s, and γδ T17 cells, from the gut to the lungs. It also discusses the critical mediating role of the "gut-lymph-lung" pathway in gut-derived lung injury. Furthermore, this article summarizes interventional strategies targeting the gut-lung axis, including modulation of the gut microbiota (probiotics and fecal microbiota transplantation), supplementation with metabolites (such as short-chain fatty acids), and novel nanoparticle-based drug delivery systems. A deeper understanding of this immunoregulatory network will provide new insights and therapeutic targets for precision treatment and clinical translation of ARDS.

Patients with acute respiratory distress syndrome (ARDS) frequently develop a series of neurological complications that occur not only during the acute phase of the disease but may also persist for months or even years after discharg, leading to increased long-term mortality and disability. This article systematically reviews the clinical manifestations of neurological complications associated with ARDS, and examines in depth their complex pathophysiological mechanisms, aiming to provide a theoretical basis and clinical guidance for the early identification of high-risk patients and for the development of individualized, neuroprotection-oriented treatment strategies, with the goal of reducing mortality, and improving long-term cognitive function and quality of life.

Isoliquiritigenin ameliorates Pseudomonas aeruginosa-induced acute lung injury through inhibiting lung epithelial cell ferroptosis via PPARγ/Nrf2/GPX4 axis.

Emerging evidence links veno-venous extracorporeal membrane oxygenation (VV-ECMO) to right ventricular (RV) dysfunction, but the relative contribution of ECMO versus underlying disease progression remains unclear. We conducted a multicenter, retrospective, propensity-matched study including 408 intubated acute respiratory distress syndrome (ARDS) patients who were admitted between January 2020 and October 2024 in a quaternary referral hospital network within the United States and underwent at least two transthoracic echocardiograms (TTEs) after intubation. Using 1:2 propensity score matching, we adjusted for baseline comorbidities, baseline hemoglobin, lactate, and worst PaO2/FiO2 ratio (P/F). Longitudinal echocardiographic changes were analyzed with a cumulative link mixed model (CLMM), evaluating RV size and function as ordinal outcomes. Within 408 patients (112 received ECMO support), propensity matching identified 55 ECMO and 110 non-ECMO patients with balanced baseline characteristics. Among 469 serial echocardiograms, RV size and function worsened more frequently in ECMO patients. In longitudinal modeling, ECMO use alone was not associated with RV dilation (p = 0.23) or dysfunction (p = 0.43). However, longer ECMO duration was associated with RV dilation (OR: 1.04 per day, p = 0.004) and dysfunction (odds ratio [OR]: 1.04 per day, p < 0.001). Higher ECMO circuit flow had a trend toward progressive RV dilation and dysfunction but did not reach statistical significance. These findings highlight the need for vigilant RV monitoring during ECMO support.

Biological subphenotypes in severe acute hypoxaemic respiratory failure and acute respiratory distress syndrome using rapid prospective classification (SPARC) in the USA: a multicentre, observational, study.

Diallyl trisulfide activates Nrf2 by promoting S-sulfhydration of Keap1 to attenuate acute hypobaric hypoxia-induced lung injury.

Acute lung injury (ALI) is a common inflammatory pulmonary disorder, with increasing evidence implicating ferroptosis as a critical type of cell death in its pathogenesis. Ubiquitin-specific protease 43 (USP43) is an important deubiquitinating enzyme that plays a significant role in both inflammation and ferroptosis regulation. In this study, we mainly analysed whether USP43 could participate in the process of ALI by regulating the ferroptosis process, and clarified its molecular mechanism. To investigate the functional role of USP43 in ALI, Usp43 knockout mice, USP43 knockdown and overexpressed human bronchial epithelial BEAS-2B cells and mouse alveolar type II epithelial MLE12 cells were treated with lipopolysaccharide (LPS) in vivo and in vitro. Subsequently, ferroptosis inhibitor and activator, Ferrostatin-1 and Erastin, were taken to explore the effect of ferroptosis on the regulation function of USP43 in ALI. Finally, co-immunoprecipitation (Co-IP), ubiquitination and rescue assays were conducted to determine the regulation mechanism of USP43. The expression of USP43 was up-regulated during ALI. Usp43-KO mice exhibited aggravated lung injury, inflammation and ferroptosis. Consistently, USP43 knockdown exacerbated LPS-stimulated cellular damage, inflammation and ferroptosis, while its overexpression exerted the opposite effect in vitro. Furthermore, the regulation effects of USP43 on ALI mainly depended on ferroptosis by administering a ferroptosis inducer and inhibitor, respectively. Mechanistically, USP43 was found to inhibit K48-linked polyubiquitination of solute carrier family 7 member 11 (SLC7A11), thereby stabilising SLC7A11. Overexpression of SLC7A11 rescued the ferroptosis, cellular and lung tissue injury and inflammation aggravated by USP43 knockdown or deficiency. USP43 prevents the progression of ALI by mediating K48-linked deubiquitination of SLC7A11, thereby inhibiting ferroptosis. Targeting USP43 may represent a potential therapeutic strategy for ALI treatment by enhancing SLC7A11 stability and inhibiting ferroptosis. USP43 has been proven to be upregulated during LPS-induced ALI. This study is the first to demonstrate that USP43 can inhibit the progression of LPS-induced ALI by suppressing ferroptosis. This study proved that USP43 can interects with SLC7A11 and removes the K48-linked ubiquitinaiton of SLC7A11, thereby enhances the stability of it and subsequently inhibiting ferroptosis during the LPS-induced ALI process. The regulation of USP43 on LPS-induced ALI mainly depends on SLC7A11, and USP43 is expected to become a new target for the treatment of ALI/ADRS.

Effects of inflammatory phenotypes in acute respiratory distress syndrome on mortality and partitioning of lung and chest wall mechanics in patients in the USA and Canada: a retrospective cohort study.

Protective effects of the ethyl acetate fraction from Madeng'ai on lipopolysaccharide-induced acute lung injury in mice: Insights from integrated multi-omics analysis.

Predictive value of early blood glucose trajectory for poor prognosis in ARDS patients.

H3K18 lactylation-regulated ATG10 is involved in the acute respiratory distress syndrome induced by acute exposure to hydrogen sulfide through activation of autophagy in lung epithelial cells.

Ventilatory ratio as a predictor of mortality in acute respiratory distress syndrome: a systematic review and Bayesian meta-analysis of observational studies.

Superimposed pressure (SP) is the hydrostatic pressure compressing dependent lung regions and is a major determinant of dorsal collapse in adult patients with acute respiratory distress syndrome (ARDS). CT studies clarify its role in determining the need for positive end-expiratory pressure (PEEP) in ARDS. We therefore aimed to describe SP in pediatric ARDS (pARDS) and assess its associations with anthropometric, clinical, and quantitative CT parameters. Retrospective cohort study. Urban academic tertiary care children's hospital in Italy. All children with pARDS undergoing noncontrast chest CT between 2014 and 2024 compared with age-matched control patients with normal lung findings undergoing chest CT. We included 12 pARDS patients and 24 controls. Quantitative CT analysis was used to measure lung aeration and the SP in 10 ventral-to-dorsal regions. The median (interquartile range [IQR]) SP increased from ventral to dorsal in both groups but was higher in pARDS patients: (dorsal SP, 5.9 cm H2O [IQR, 4.4-7.5 cm H2O] vs. 3.0 cm H2O [IQR, 2.4-4.0 cm H2O]; p < 0.001). Compared with controls, we found that pARDS patients had higher lung weight, lower gas/tissue ratio, and less normally aerated tissue. In pARDS patients, SP correlated with chest circumference (ρ = 0.60; p = 0.043), lung weight (ρ = 0.76; p = 0.006) and inversely with normally aerated tissue (ρ = -0.72; p = 0.011). We failed to identify a relationship between SP and oxygenation indices. None. SP in pARDS is lower and more variable compared with descriptions in adult patients with ARDS and is both affected by disease severity and chest size. We failed to identify an association between oxygenation indices and SP, which raises concerns about titrating PEEP based on oxygenation targets alone. Further studies are needed to confirm and integrate these in pARDS.

Endogenous oxidized phospholipid POVPC triggers pulmonary epithelial ferroptosis in acute lung injury and is restrained by RCN3.

Sanhuang Xiexin decoction ameliorates acute lung injury by disrupting NEK7-NLRP3 inflammasome activation.

Static thresholds for mechanical power (MP) may not prevent ventilator-induced lung injury because risk depends on exposure duration and the underlying respiratory compliance. We aimed to quantify how MP intensity and exposure duration interact with respiratory compliance to predict oxygenation changes consistent with acute respiratory distress syndrome worsening or 14-day mortality. A retrospective analysis of 2 large intensive care datasets. ICUs in the Netherlands and the United States from 2003 to 2016 and 2008 to 2019, respectively. Mechanically ventilated adults with oxygenation levels consistent with moderate to severe acute respiratory distress syndrome. None. Time-dependent Cox proportional hazards models stratified by respiratory compliance estimated the hour-specific associations of immediate exceedance and cumulative time above MP thresholds with the primary outcome. Estimated effects were integrated into a risk-adjusted mechanical-power score. Among 2150 mechanically ventilated acute respiratory distress syndrome patients risk from MP exposure was dictated by respiratory compliance: in higher-compliance lungs, risk followed a dose-response pattern, with immediate hazard beginning at 10 J/min (hazard ratio = 1.04) and cumulative harm amplifying significantly over time. Conversely, for low-compliance patients, risk was confined to a narrow power band (11-20 J/min) without evidence of cumulative harm. With risk-adjusted MP score as a predictor of outcome eXtreme Gradient Boosting yielded an area under the receiver operating characteristic curve of 0.863. A single "safe" MP threshold is insufficient for guiding ventilation; the risk of lung injury is governed by a dynamic interplay of power intensity, duration, and the patient's respiratory compliance. The risk-adjusted MP score unifies these factors into a time-varying, clinically interpretable metric that warrants prospective validation for personalized ventilator management.

Role of uridine triggering M2 macrophage polarization to alleviate LPS-induced acute lung injury through the STAT6 signaling pathway.

Tubuloside A attenuates sepsis-induced acute lung injury by modulating the NF-κB p50-Nrf2/GPX4 axis to suppress inflammation, oxidative stress and ferroptosis.

METTL3-mediated m6A modification of Smad3 affects ferroptosis in septic acute lung injury by mediating GRSF1/GPX4.