Yong Yang

Chronic obstructive pulmonary disease (COPD) is a heterogeneous respiratory disorder characterized by a complex pathogenesis involving chronic inflammation, protease–antiprotease imbalance, oxidative stress, and epigenetic regulation. Experimental models, including cigarette smoke exposure, air pollution, and acute exacerbation models, provide essential platforms for investigating immune cell dynamics during disease initiation and progression. Macrophages contribute to inflammatory amplification and tissue destruction through polarization imbalance and metabolic reprogramming. Neutrophils exacerbate persistent lung injury via recruitment, protease release, NET formation, and delayed apoptosis, while also promoting airway remodeling during the repair phase. T cells—particularly CD8 ⁺ , Th1/Th17, and tissue-resident memory T cells—sustain chronic inflammation through cytotoxicity and cytokine networks, whereas impaired Treg function hinders inflammation resolution. Additional immune populations, such as NK cells, eosinophils, and fibrocytes, further drive inflammatory amplification and fibrotic remodeling. Therapeutic explorations targeting distinct inflammatory phenotypes indicate that conventional glucocorticoids and PDE4 inhibitors remain beneficial in eosinophil-driven inflammation, whereas biologics targeting IL-5, IL-13/IL-4, TSLP, and IL-33 have produced variable outcomes in COPD clinical trials. These findings highlight the importance of precision phenotyping and personalized immunomodulatory strategies. Overall, systematic elucidation of immune cell dynamics in COPD experimental models provides new insights into mechanisms of inflammation persistence and therapeutic responses, offering a theoretical basis for developing targeted interventions.

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic respiratory disease characterized by high prevalence, mortality, and disease burden. Current understanding of COPD pathogenesis primarily focuses on airway inflammation, immune dysfunction, oxidative stress, and protease-antiprotease imbalance. Notably, recent studies have increasingly highlighted the role of metabolic reprogramming in COPD. Metabolic reprogramming refers to cellular adaptation through metabolic pathway alterations in response to environmental stress, enabling physiological or pathological state transitions. This review systematically summarizes COPD pathogenesis, with particular focus on metabolic reprogramming features (glucose, lipid, and amino acid metabolism) in immune cells from COPD experimental models. Furthermore, we analyze the interactions between these metabolic alterations and chronic inflammatory responses, providing new insights into COPD pathogenesis.

Dysregulation of the homeostasis between regulatory T cell (Treg) and T helper 17 cell (Th17) is increasingly recognized as a pivotal mechanism in the pathogenesis of autoimmune diseases. Emerging evidence indicates that gut microbiota-derived metabolites, including short-chain fatty acids, secondary bile acids, and aromatic metabolites, modulate Treg/Th17 balance by shaping immune cell differentiation and function, thereby revealing novel therapeutic opportunities. This Review synthesizes recent clinical and preclinical findings on the influence of microbial communities and their metabolites on Treg/Th17 dynamics and examines the underlying mechanisms in representative autoimmune disorders, such as rheumatoid arthritis, systemic lupus erythematosus, Graves’ disease, autoimmune hepatitis, and myasthenia gravis. We critically evaluate current microbiome-targeted interventions and discuss their translational potential, highlighting both promises and challenges. Finally, we outline priorities for future research, focusing on multi-omic integration, the development of individualized therapeutic strategies, and rigorous clinical evaluation, to facilitate the development of safe and effective microbiota-based therapies for autoimmune diseases.

Pregnant women and infants are more vulnerable to infectious diseases than the general population. Vaccination during pregnancy can protect not only mothers and fetuses from diseases but also safeguard infants through maternal antibodies transferred via the placenta. It stands as one of the most effective strategies to reduce the incidence and mortality of infectious diseases among pregnant women and infants. Globally, pregnancy vaccination strategies are increasingly diversified. This review discusses the effectiveness and safety of various vaccines for preventing infectious diseases during pregnancy, as well as vaccination recommendations for pregnant women across different countries.

Purpose: As an important antibiotic for treating infections caused by drug-resistant Gram-negative bacteria, colistin’s clinical efficacy and safety might be influenced by multiple factors. This meta-analysis aimed to identify the key factors affecting the effectiveness and safety of colistin in treating these infections. The results of this study provide a reference for clinicians to choose treatment methods. At the same time, the rational use of colistin can prevent the occurrence of adverse drug reactions (AKI), improve the cure rate of patients, and delay the development of bacterial resistance. Methods: The overall mortality rate was designated as the primary effectiveness outcome, with clinical response rate and bacterial eradication rate serving as the secondary outcomes. The incidence of acute kidney injury (AKI) was evaluated as a safety endpoint. Key analytical variables included colistin dose (high-dose≥4.2 mg/kg/day and low-dose< 4.2 mg/kg/day), ACCI (low 6), co-therapy (carbapenems/tigecycline/fosfomycin, etc.), microbial species ( Acinetobacter baumannii/Pseudomonas aeruginosa/ Enterobacteriaceae, etc.), and administration methods (aerosolized plus intravenous colistin vs. intravenous colistin alone). Results: A total of 74 studies (N = 8,889 participants) were included in our analysis. Mortality was lower in the high-dose group compared to the low-dose group (34.09% vs. 41.08%, p = 0.09). In ACCI score subgroups (low, moderate, high), mortality rates were 27.11% vs. 44.69% vs. 47.11% (p < 0.01). Monotherapy was associated with a higher mortality rate compared to co-therapy (42.97% vs. 33.10%, p < 0.01). Although no statistical differences were observed among different pathogenic bacteria species, infection caused by A . baumannii exhibited the highest mortality rate at 43.75%. Mortality rates for aerosolized plus intravenous colistin versus intravenous colistin alone were 40.81% vs. 32.84% (p = 0.09). The incidence of AKI was significantly higher in the loading dose group, high-ACCI group, and group receiving concomitant nephrotoxic drugs while being notably lower in the Pseudomonas aeruginosa infection group. Conclusion: Loading dose, co-therapy (carbapenems or quinolones), microbial factors, and ACCI are the main factors associated with the effectiveness of colistin. Additionally, loading dose, microbial factors, ACCI, and co-therapy are associated with an increased risk of colistin-associated AKI. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/search , identifier CRD420250655507.

Background: The placental barrier is a critical interface that regulates drug transport between maternal and fetal circulation and is an important component in assessing fetal drug-exposure risk. Since pregnant women are often excluded from clinical trials, pharmacokinetic (PK) analysis data on placental drug transport remain limited. Currently, in vitro experiments and in silico simulation strategies are the primary and effective means for understanding drug transport across the placenta. Method: Various in vitro experimental methods, including cell monolayer models, ex vivo placental perfusion, and organ-on-a-chip platforms, along with model-based computational simulations, were systematically reviewed. The advantages, limitations, and potential future applications of these methods were evaluated. Result: A total of seven studies using cell models, 28 employing ex vivo perfusion, six utilizing placenta-on-a-chip technology, and 39 focusing on in silico simulations, were identified, involving 8, 34, 5, and 42 drugs, respectively. Antiviral agents, antibiotics, and opioids were the most frequently investigated drug types. Overall, in silico simulations informed by in vitro data as baseline parameters and constraints demonstrated higher predictive accuracy. Integrating multi-model data was shown to be a reliable strategy for improving the precision of placental PK studies. Conclusion: This review highlights the current strategies in placental PK research and supports safer drug use during pregnancy. Multi-model data integration is essential for developing reliable and quantitative fetal drug-exposure assessment frameworks, thus addressing data gaps caused by the exclusion of pregnant women from clinical trials.

In clinical practice, cases of drug-induced liver injury (DILI) often occur in renal transplant recipients treated with tacrolimus (Tac) as an immunosuppressive therapy. Numerous studies have confirmed the close relationship between gut microbiota (GM) and DILI. However, systematic studies on the GM and metabolomic characteristics of Tac-associated DILI are lacking, and the role of GM and its metabolites in DILI remains incompletely understood. Renal transplant recipients receiving Tac at the Organ Transplantation Center of Sichuan Provincial People’s Hospital were enrolled. Patients with DILI were assigned to the DILI group, and those with stable liver function to the control group. Stool samples were analyzed by 16 S rRNA gene sequencing and LC-MS non-targeted metabolomics, and blood samples were collected to measure Tac trough concentrations. Seventy-two renal transplant recipients were included, comprising 32 DILI patients and 40 controls. Oscillibacter and Ruminococcus gnavus group were significantly enriched in the DILI group, whereas Bacteroides, Lachnospiraceae NK4A136 group, Anaerostipes, Subdoligranulum, Eubacterium coprostanoligenes group, and Megamonas were significantly decreased in the DILI group. Metabolites such as icosadienoic acid and 1-acyl-sn-glycerol-3-phosphate were significantly elevated in the DILI group, while glycyrrhetinate, S-adenosylmethionine, and other related metabolites were significantly reduced. In renal transplant recipients, distinct GM and enteric metabolic profiles differentiate patients with DILI from those with stable liver function. Key microbial taxa—including Oscillibacter, Bacteroides, Ruminococcus gnavus group, and Lachnospiraceae NK4A136 group—potentially contribute to DILI pathogenesis through modulation of bile acid metabolism and inflammatory signaling pathways.

Digestive cancers are a significant global public health challenge due to their high incidence and mortality rates. Emerging research highlights the pivotal role of circular RNA (circRNA) and autophagy in the progression of digestive cancers. This review provides a summary of recent findings, showing that circRNA-mediated autophagy could either promote or suppress tumor development in esophageal, gastric, liver, pancreatic, and colorectal cancers. CircRNAs could regulate autophagy in digestive cancers by acting as competitive endogenous RNAs, influencing downstream target genes and signaling pathways. Dysregulated circRNAs contribute to tumor onset, progression, and chemoresistance by altering autophagy levels. Targeting specific circRNAs to modulate autophagy may offer potential as a diagnostic, prognostic biomarker, or therapeutic strategy for digestive cancers.

Lung cancer is the most prevalent malignant tumor worldwide and remains the leading cause of cancer-related mortality. Despite advances in treatment development, lung cancer patients often face poor quality of life and low survival rates. Increasing evidence highlights the significant roles of autophagy and non-coding RNAs (ncRNAs) in the initiation, progression, and therapeutic response of lung cancer. Autophagy and ncRNAs can function as both tumor-promoting and tumor-suppressing factors in lung cancer. Therefore, investigating the roles of autophagy and ncRNAs in lung cancer provides valuable insights into its pathophysiology. At the same time, non-coding RNA also plays an important role in regulating autophagy. This study reveals that autophagy affects the occurrence and development of lung cancer through multiple pathways. Then, we also studied that in lung cancer, ncRNAs (e.g., lncRNAs, miRNAs, circRNAs and piRNAs) can regulate autophagy to promote or inhibit tumorigenesis, metastasis and drug resistance in lung cancer. Finally, the problems and solutions of autophagy and ncRNAs in the treatment of lung cancer were explored. These findings suggest that autophagy and ncRNAs can be potential targets for the treatment of lung cancer.