Traumatic brain injury (TBI) is a common cause of disability and mortality, affecting millions of people every year. The neuroinflammation and immune response post-TBI initially have neuroprotective and reparative effects, but prolonged neuroinflammation leads to secondary injury and increases the risk of chronic neurodegenerative diseases. Persistent microglial activation plays a critical role in chronic neuroinflammation post-TBI. Given the bidirectional communication along the brain–gut axis, it is plausible to suppose that gut microbiota dysbiosis post-TBI influences microglial activation. In the present study, hippocampal microglial activation was observed at 7 days and 28 days post-TBI. However, in TBI mice with a depletion of gut microbiota, microglia were activated at 7 days post-TBI, but not at 28 days post-TBI, indicating that gut microbiota contributes to the long-term activation of microglia post-TBI. In addition, in conventional mice colonized by the gut microbiota of TBI mice using fecal microbiota transplant (FMT), microglial activation was observed at 28 days post-TBI, but not at 7 days post-TBI, supporting the role of gut microbiota dysbiosis in persistent microglial activation post-TBI. The RNA sequencing of the hippocampus identified a microglial activation gene, Lyz2, which kept upregulation post-TBI. This persistent upregulation was inhibited by oral antibiotics and partly induced by FMT. 16s rRNA gene sequencing showed that the composition and function of gut microbiota shifted over time post-TBI with progressive dysbiosis, and untargeted metabolomics profiling revealed that the tryptophan metabolic phenotype was differently reshaped at 7 days and 28 days post-TBI, which may play a role in the persistent upregulation of Lyz2 and the activation of microglia. This study implicates that gut microbiota and Lyz2 are potential targets for the development of novel strategies to address persistent microglial activation and chronic neuroinflammation post-TBI, and further investigations are warranted to elucidate the specific mechanism.

Parkinson’s disease, a common neurodegenerative disorder in the elderly, is characterized by motor symptoms and non-motor symptoms such as anxiety, depression, sleep disturbances, and gastrointestinal dysfunction, highlighting its nature as a multisystem disease. The critical role of the microbiota-gut-brain axis in maintaining human homeostasis is well established, and growing evidence links its dysfunction and gut microbiota dysbiosis to Parkinson’s disease. Communication between the microbiota and the brain occurs through various pathways, including the vagus nerve, intestinal hormonal signals, the immune system, tryptophan metabolism, and microbial metabolites. Among these, tryptophan metabolism is a key metabolic pathway. As an essential amino acid that animal cells cannot synthesize, tryptophan and its metabolites in the intestine depend entirely on dietary intake and gut microbiota production. In the gastrointestinal tract, tryptophan metabolism occurs via three main pathways-the indole pathway, the kynurenine pathway, and the serotonin pathway-all directly or indirectly regulated by gut microbiota. These metabolites are vital in mediating the ‘microbiota-gut-brain’ dialogue and regulating gastrointestinal functions. Additionally, some metabolites mediate central nervous system inflammation and contribute to neurodegenerative disease processes as aromatic hydrocarbon receptor ligands. This review examines recent research on gut microbiota and host tryptophan co-metabolism and their roles in the development of Parkinson’s disease. Furthermore, it explores how targeting gut microbiota and modulating tryptophan metabolism could offer potential therapeutic approaches for Parkinson’s disease.

Traumatic brain injury refers to the damage caused to intracranial tissues by an external force acting on the head, leading to both immediate and prolonged harmful effects. Neuroinflammatory responses play a critical role in exacerbating the primary injury during the acute and chronic phases of TBI. Research has demonstrated that numerous neuroinflammatory responses are mediated through the “microbiota–gut–brain axis,” which signifies the functional connection between the gut microbiota and the brain. The aryl hydrocarbon receptor (AhR) plays a vital role in facilitating communication between the host and microbiota through recognizing specific ligands produced directly or indirectly by the microbiota. Tryptophan (trp), an indispensable amino acid in animals and humans, represents one of the key endogenous ligands for AhR. The metabolites of trp have significant effects on the functioning of the central nervous system (CNS) through activating AHR signalling, thereby establishing bidirectional communication between the gut microbiota and the brain. These interactions are mediated through immune, metabolic, and neural signalling mechanisms. In this review, we emphasize the co-metabolism of tryptophan in the gut microbiota and the signalling pathway mediated by AHR following TBI. Furthermore, we discuss the impact of these mechanisms on the underlying processes involved in traumatic brain injury, while also addressing potential future targets for intervention.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a critical life support technology for severely ill patients. Despite its benefits, patients face high costs and significant mortality risks. To improve clinical decision-making, this study aims to develop a non-invasive, efficient artificial intelligence (AI)-enabled model to predict the risk of mortality within 28 days post-weaning from VA-ECMO. A multicenter, retrospective cohort study was conducted across five hospitals in China, including all the patients who received VA-ECMO support between January 2020 and January 2024. Based on the innovatively selected 25 easily obtainable patient examination features as potentially relevant, this study involved developing ten predictive models using both classical and advanced machine learning techniques. The model’s performance is evaluated using various statistical metrics and the optimal predictive model are identified. Feature correlations are analyzed using Pearson correlation coefficients, and SHapley Additive exPlanations (SHAP) are employed to interpret feature importance. Decision curve analysis is used to evaluate the clinical utility of the predictive models. The study included 225 patients, with 66 patients from one hospital forming the training cohort. Three validation cohorts were used: internal validation with 16 patients from the training hospital and external validation with 30 and 60 patients from the other 4 hospitals. The random forest model emerged as the best predictor of 28-day mortality, achieving an AUROC of 1.00 in the training cohort and 1.00, 0.97, and 0.93 in the three validation cohorts, respectively. Despite the limited training data, the developed model, eCMoML, demonstrated high accuracy, generalizability and reliability. The model will be available online for immediate use by clinicians. The eCMoML model, validated in a multicenter cohort study, offers a rapid, stable, and accurate tool for predicting 28-day mortality post-VA-ECMO weaning. It has the potential to significantly enhance clinical decision-making, helping doctors better assess patient prognosis, optimize treatment plans, and improve survival rates.

Background: Pregnant women with ARDS are rare in themselves, and the rare complication of an abdominal wall hematoma during VV-ECMO is extremely aggressive. We report this rare case with the aim of informing clinicians to be alert to this serious complication and to share our treatment experience.Case presentation: A 42-year-old Chinese woman was infected with viral pneumonia at 26 weeks of gestation, which progressed to severe ARDS. After emergency termination of pregnancy, she was placed on VV-ECMO support and ventilated in the prone position. During this period, an unexplained drop in hemoglobin occurred, so she was withdrawn from the VV-ECMO support, and was diagnosed with an abdominal wall hematoma on CT examination, which was later cured with conservative treatment.Conclusion: Maternal prone abdominal wall hematoma found during VV-ECMO is rare and prone to adverse outcomes. We remind clinicians to be aware of this rare complication and prevent it.