ObjectiveBlood eosinophil (EOS) guides corticosteroid therapy in stable chronic obstructive pulmonary disease (COPD), but its prognostic value in COPD exacerbation (ECOPD) remains controversial. This study characterized clinical features and assessed the impact of EOS levels on clinical outcomes in hospitalized ECOPD patients.MethodsWe retrospectively reviewed hospitalized patients with ECOPD between 2018 and 2023. Patients were categorized according to percentage of peripheral blood eosinophil: the eosinophilic group (EOS ≥ 2%) and the non-EOS group (EOS < 2%). The primary outcome was in-hospital mortality, while the secondary outcomes included ICU admission, mechanical ventilation, and length of hospital stay.ResultsAmong 511 patients (EOS group, n = 139; non-EOS group, n = 372), the EOS group had lower levels of inflammatory markers (C-reactive protein and procalcitonin) and a lower detection rate of Gram-negative bacilli, especially Acinetobacter baumannii. The EOS group exhibited significantly lower rates of ICU admission (25.18% vs. 50.27%; P < 0.001) and in-hospital mortality (1.44% vs. 6.72%; p = 0.018). In the multivariable analyses, EOS% ≥ 2% remained associated with lower odds of in-hospital mortality after adjustment for age and heart failure (adjusted OR, 0.225; 95% CI, 0.052–0.971; p = 0.046) and with lower odds of ICU admission after adjustment for age, sex, and heart failure (adjusted OR, 0.357; 95% CI, 0.229–0.556; p < 0.001).ConclusionAmong hospitalized patients with ECOPD, elevated peripheral blood eosinophils were associated with favorable clinical outcomes, especially a reduced risk of ICU admission, as well as a lower systemic inflammation burden.

Background:The beneficial effects of omega-3 fatty acids for patients with chronic obstructive pulmonary disease (COPD) had been observed, including attenuating lung function decline and reducing their respiratory symptom burdens. However, the impact of omega-3 fatty acids on COPD exacerbation-related outcomes remains unclear. This study aimed to evaluate whether reduced serum omega-3 fatty acid levels are associated with a higher risk of future hospital readmission due to COPD exacerbation (ECOPD). Methods:This retrospective cohort study included 88 patients hospitalized for ECOPD between April 2017 and March 2018. Clinical data were collected, and serum omega-3 fatty acid levels were analyzed using liquid chromatography-mass spectrometry (LC-MS). All patients were followed up for a median period of 53.5 months and categorized into two groups based on whether they experienced ECOPD-related readmission during the follow-up period. The clinical characteristics and serum levels of omega-3 fatty acid levels, including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), between the two groups were compared. Additionally, patients were categorized into low and high DHA groups based on the median DHA level, and the association between DHA level and ECOPD-related readmission rate was analyzed using a Cox regression model. Result:Patients who experienced ECOPD-related readmission during the follow-up period (n = 36) had lower serum levels of DHA than those who did not experience readmission. The serum levels of EPA did not significantly differ between groups. Kaplan-Meier curve showed that patients in the low-DHA group exhibited a significantly higher ECOPD-related readmission rate compared to those in the high-DHA group (log-rank p = 0.023). Multivariable Cox regression analysis identified low DHA level as an independent risk factor for ECOPD-related readmission. A nomogram based on DHA levels demonstrated good predictive performance. Conclusion:A low DHA level serves as an independent risk factor for ECOPD-related readmission, suggesting DHA may have a potential protective effect to reduce the risk of exacerbation in patients with COPD.

Resectoscopic myomectomy (RM) is a standard minimally invasive procedure but carries risks of distinct complications. We report a rare case of a 36-year-old woman who simultaneously developed a triad of life-threatening complications during HM: carbon monoxide poisoning, gas embolism, and fluid overload. The patient presented with precipitous drops in end-tidal carbon dioxide and bispectral index silence. Arterial blood gas analysis revealed severe metabolic acidosis, electrolyte disturbances, and a carboxyhemoglobin level of 27.1%. Definitive diagnosis via arterial blood gas analysis and subsequent multimodal management, bolstered by the patient’s excellent physiological reserve, led to a full recovery. This case highlights the critical need for strict fluid management during RM and CO-oximetry's indispensable role in detecting concurrent carbon monoxide toxicity.

Normal weight obesity (NWO) is a subtype of obesity characterized by a normal weight but a high body fat percentage. However, its research in terms of metabolic health, particularly its relationship with mental health remains understudied. This study aims to explore the relationship between NWO and mental health status to provide more reliable information for future scientific research and clinical practice. This study recruited healthy people who received health checkups at a tertiary hospital in Beijing. General information of the participants was collected through a self-administered questionnaire. The mental health status of participants were assessed using the Symptom Checklist-90 (SCL-90) and the Stress Self-Assessment Questionnaire-53 (SSQ-53). False Discovery Rate (FDR) correction was applied using the Benjamini–Hochberg procedure implemented in R software. Pearson or Spearman correlation coefficients were used for correlation analysis. The A-test validation method is also employed for correlation calculations. The physiological status was assessed by collecting hematological indices. Binary logistic regression analysis assessed influencing factors associated with psychiatric symptoms. 1181 healthy participants were included, with 824 (69.8

Background:The current status of nutritional support for patients in Respiratory ICU across mainland China remains inadequately characterized. This multi-center study, conducted in RICUs, was designed to investigate nutritional practices in this specific patient population, focusing on initiation timing, energy/protein adequacy, and associations with clinical outcomes. Methods:A prospective, observational study enrolled 1,026 patients (ICU stay >48 h) across 68 Chinese RICUs. We analyzed EN initiation rates (24 h/48 h), caloric/protein intake adequacy during the first 7 days, and outcomes via multivariable Cox regression. Results:EN initiation occurred in 36.8% (24 h) and 43.4% (48 h) of patients. Excluding patients who could take oral food, the proportion of patients who started EN within 24 and 48 h increased to 86.9 and 95.3%. Among 499 EN-fed patients, 26.1% developed EN complications. Caloric analysis (n = 317) identified three trajectories: underfeeding (<70% targets, 32.5%), adequate feeding (70-110, 43.2%), and overfeeding (>110, 24.3%). Overfeeding independently predicted higher non-social infections and significantly increased mortality risk in patients >50 years (HR = 1.83, 95% CI 1.02-3.28; p = 0.04). Mean protein intake was 0.9 g/kg/day, with no 28-day mortality benefit at higher thresholds (≥1.2 g/kg: p = 0.31; ≥1.3 g/kg: p = 0.42). Conclusion:This multicenter study demonstrates optimal early EN initiation rates in Chinese RICUs. Energy overfeeding was associated with increased mortality risk only in patients >50 years and non-social infections risk, whereas protein adequacy showed no outcome associations. Protocolized EN delivery balancing adequacy and overfeeding risks is urgently needed in RICUs. Clinical trial registration:Identifier, NCT04958447.

Background According to World Health Organization data, the global obesity rate has nearly tripled since 1975, becoming a major public health concern. Obesity is closely associated not only with cardiovascular diseases and diabetes but also with mental health disorders such as depression and anxiety, though the underlying mechanisms remain incompletely understood. This study aimed to retrospectively investigate the relationship between obesity and mental health, as well as potential physiological mechanisms, within a health examination population. Methods We conducted a retrospective cross-sectional analysis using data from individuals who underwent routine health check-ups at a tertiary hospital in Beijing. Archived questionnaire data, including the Symptom Checklist-90 (SCL-90) and the Stress Self-Assessment Questionnaire-53 (SSQ-53), were used to assess mental health status. Archived hematological biomarkers were analyzed to evaluate physiological status. Statistical analyses included the Benjamini-Hochberg procedure for False Discovery Rate (FDR) correction, multiple linear regression, and binary logistic regression to identify factors associated with psychological symptoms. Results The analysis included 11,272 participants (6,041 normal weight, 3,797 overweight, 1,434 obese). The somatization subscale score increased significantly with BMI. The obesity group had a significantly higher positive rate for somatization (factor score ≥ 2) compared to the other groups (P = 0.011). Interestingly, the obese group reported lower levels of psychological and cognitive stress (FDR-adjusted P < 0.001) and more stable mood scores than the normal-weight group. Multivariable analysis confirmed that higher BMI, female gender, older age, and specific biochemical markers reflecting inflammation and metabolic dysregulation (e.g., total bilirubin, absolute lymphocyte count, all P < 0.001) were independently associated with more severe somatization symptoms. Conclusion In this retrospective health examination cohort, higher BMI was independently associated with increased somatization symptoms, linked to inflammatory and metabolic markers. Contrary to common assumption, the obese subgroup exhibited lower perceived stress and anxiety levels, which suggests a complex relationship between obesity and mental health. Further longitudinal research is needed to clarify causality.

Background According to World Health Organization data, the global obesity rate has nearly tripled since 1975, becoming a major public health concern. Obesity is closely associated not only with cardiovascular diseases and diabetes but also with mental health disorders such as depression and anxiety, though the underlying mechanisms remain incompletely understood. This study aimed to retrospectively investigate the relationship between obesity and mental health, as well as potential physiological mechanisms, within a health examination population. Methods We conducted a retrospective cross-sectional analysis using data from individuals who underwent routine health check-ups at a tertiary hospital in Beijing. Archived questionnaire data, including the Symptom Checklist-90 (SCL-90) and the Stress Self-Assessment Questionnaire-53 (SSQ-53), were used to assess mental health status. Archived hematological biomarkers were analyzed to evaluate physiological status. Statistical analyses included the Benjamini-Hochberg procedure for False Discovery Rate (FDR) correction, multiple linear regression, and binary logistic regression to identify factors associated with psychological symptoms. Results The analysis included 10,751 participants (5,520 normal weight, 3,797 overweight, 1,434 obese). The somatization subscale score increased significantly with BMI. The obesity group had a significantly higher positive rate for somatization (factor score ≥ 2) compared to the other groups (P for trend = 0.026). Interestingly, the obese group reported significantly lower levels of emotional stress (FDR-adjusted P = 0.002) than the normal-weight group. Multivariable analysis confirmed that higher BMI, female gender, older age, and specific biochemical markers reflecting inflammation and metabolic dysregulation (e.g., elevated white blood cell count, decreased absolute lymphocyte count, all P < 0.05) were independently associated with more severe somatization symptoms. Conclusion In this retrospective health examination cohort, higher BMI was independently associated with increased somatization symptoms, with the association partly explained by related inflammatory and metabolic disturbances. Contrary to the common assumption of uniform psychological distress, the obese subgroup reported lower perceived emotional stress. This pattern hints at a complex and non-linear relationship between obesity and mental health. Further longitudinal research is needed to clarify the underlying causal pathways.

BACKGROUND:Cupriavidus is an aerobic Gram-negative bacterium and a rare conditional pathogen that mainly infects immunocompromised patients or those undergoing invasive procedures. METHODS:We present the case of a 70-year-old male with diabetes mellitus who developed septic shock following influenza A virus (IAV) pneumonia. Cupriavidus gilardii (C. gilardii) was identified in his blood and sputum samples. Through a literature review, we identified 31 reported cases of Cupriavidus infections. Clinical data, including demographic information, clinical characteristics, comorbidities, laboratory results, Cupriavidus species, treatment, and clinical outcomes, were collected. RESULTS:Among these 32 patients (including our patient), 23 were male (71.9%) and 9 were female (28.1%). The median patient age was 32.5 (2.12-70) years. Most patients had relevant risk factors or comorbidities before Cupriavidus infection, including exposure to polluted environments and recent invasive procedures (68.9%). Among these cases, Cupriavidus pauculus was the most common strain, accounting for 56.3% of cases. The mortality rate was the highest for Cupriavidus pauculus infections. CONCLUSIONS:Cupriavidus is a rare opportunistic pathogen in patients with compromised immune function. Early identification of pathogen and timely treatment are crucial. When traditional microbiological detection methods encounter difficulties, gene sequencing can be used as an auxiliary diagnostic tool and can further predict drug resistance. Targeted anti-infection treatment is effective in most cases, but some severe infection cases may lead to death due to serious complications.

Background: Chronic obstructive pulmonary disease is associated with excess cardiovascular morbidity, but the circulating molecular signatures linking chronic obstructive pulmonary disease-related systemic biology with cardiovascular prognosis remain incompletely characterised. Methods: We analysed UK Biobank participants with baseline spirometry, Olink plasma proteomic profiling, and linked health records. Proteins associated with chronic obstructive pulmonary disease were identified using proteome-wide logistic regression. Among participants with chronic obstructive pulmonary disease, these proteins were evaluated for associations with incident cardiovascular and mortality outcomes using Cox models. Pathway enrichment, mediation-consistent analyses, and elastic-net prognostic modelling were performed. Findings: Among 36,728 participants, 6089 had chronic obstructive pulmonary disease. Chronic obstructive pulmonary disease was associated with higher risks of major adverse cardiovascular events, heart failure, atrial fibrillation, and stroke after multivariable adjustment. Proteome-wide analyses identified 1409 chronic obstructive pulmonary disease-associated proteins. Among participants with chronic obstructive pulmonary disease, recurrent prognostic proteins included cardiopulmonary stress, inflammatory, tissue-remodelling, and vascular markers. Protein-enhanced models improved prediction of major adverse cardiovascular events, heart failure, and atrial fibrillation beyond clinical predictors. Interpretation: Chronic obstructive pulmonary disease is characterised by systemic proteomic perturbations that are linked to cardiovascular prognosis. These proteins may help prioritise biological pathways and candidate markers for cardiovascular risk stratification in chronic obstructive pulmonary disease, pending external validation.

Chronic obstructive pulmonary disease (COPD) frequently coexists with extrapulmonary comorbidities, most notably cardiovascular diseases (CVD). However, the mechanisms linking COPD to CVD, particularly atherosclerotic CVD, remain poorly understood. Extracellular vesicles (EVs), as key mediators of inter-organ communication, may participate in this pathological connection. This study aims to determine whether EVs derived from airway epithelial cells (AECs) of individuals with COPD contribute to endothelial dysfunction and atherosclerosis. EVs were isolated from primary airway epithelial cells of COPD patients and matched controls. Their effects on endothelial cell function were assessed in vitro by evaluating inflammation, apoptosis, and monocyte adhesion. ApoE-/- mice were intravenously injected with these EVs to examine their impact on atherosclerotic lesion development. Differentially expressed microRNAs were identified, and the regulatory relationship between miR-141-3p and PDCD4 was validated through molecular assays. Additionally, miR-141-3p supplementation was performed to determine its therapeutic potential in mitigating endothelial injury and atherosclerosis. COPD AECs-derived EVs markedly increased endothelial inflammation, apoptosis, and monocyte adhesion compared with control EVs. In ApoE-/- mice, COPD-derived EVs accelerated the formation of atherosclerotic plaques. Mechanistic analyses revealed that miR-141-3p was significantly downregulated in COPD EVs and directly targeted the 3’ untranslated region of PDCD4 to regulate its transcription, leading to dysregulation of PDCD4/NF-κB signaling in endothelial cells. Restoration of miR-141-3p levels in COPD-derived EVs alleviated endothelial injury and reduced atherosclerotic lesion progression both in vitro and in vivo. This study identifies a previously unrecognized mechanism by which COPD AECs-derived EVs may promote atherosclerotic CVD via miR-141-3p–mediated regulation of PDCD4 and subsequent activation of NF-κB signaling. These findings highlight miR-141-3p as a promising therapeutic target to reduce vascular complications in COPD.

Sepsis is a severe and life-threatening medical syndrome that can lead to organ failure and death. Despite advances in medical treatment, current therapies are often inadequate, with high septic mortality rates. Therefore, there is a critical need for reliable prognostic markers to be used in clinical settings to improve the management and outcomes of patients with sepsis. Recent studies have suggested that mitochondrial dynamics, including the processes of mitochondrial fission and fusion, are closely related to the severity of sepsis and the status of inflammation. By monitoring transcriptomic signals related to mitochondrial dynamics, new and reliable biomarkers can be engineered to more accurately predict sepsis survival risk. Such biomarkers would be invaluable in clinical settings, aiding healthcare providers in the early identification of high-risk patients and improving treatment strategies. To achieve this goal, we utilized the major mitochondrial fission regulatory protein dynamin-related protein 1 (Drp1, gene code DNM1L) and identified Drp1-associated genes that are enriched with sepsis survival genes. A 12-gene signature (GS) was established as a differentially expressed gene (DEG)-based GS. Next, we compared genes of proteins that interact with Drp1 to sepsis survival genes and identified 7 common genes, establishing a GS we term as protein-protein interaction (PPI)-based GS. To evaluate if these GSs can predict sepsis survival, we used publicly available human blood transcriptomic datasets from sepsis patients. We confirmed that both GSs can successfully predict sepsis survival in both discovery and validation cohorts with high sensitivity and specificity, with the PPI-based GS showing enhanced prognostic performance. Together, this study successfully engineers a new and validated blood-borne biomarker (PPI-based 7-gene GS) for sepsis survival risk prediction. This biomarker holds the potential for improving the early identification of high-risk sepsis patients and optimizing personalized treatment strategies to reduce sepsis mortality.

BACKGROUND:Sarcopenia is a prevalent comorbidity in patients with chronic obstructive pulmonary disease (COPD). We aimed to investigate the impact of sarcopenia diagnosed by chest CT on mortality in critically ill patients with exacerbation of COPD (ECOPD). METHODS:This retrospective study enrolled 148 patients hospitalized in the intensive care unit due to ECOPD from 2018 to 2023. Sarcopenia was defined by the skeletal muscle index measured at the 12th thoracic vertebra (T12) level on chest CT. Patients were categorized into the sarcopenia and non-sarcopenia groups. Hospitalization duration, short-term (30 and 90-day) and long-term (1-year and overall) COPD-related mortality and all-cause mortality were compared between the two groups. Cox regression analyses were conducted to recognize the risk factors for mortality, and a sarcopenia-based nomogram was developed. RESULTS:Eighty-four patients (56.76 %) with sarcopenia were identified through chest CT measurements. The 1-year COPD-related and all-cause mortality, as well as overall COPD-related and all-cause mortality, were significantly higher in the sarcopenia group than the non-sarcopenia group (19.05 % vs. 4.69 %, p = 0.010; 28.57 % vs. 6.25 %, p = 0.001; 33.33 % vs. 15.63 %, p = 0.015; 47.62 % vs. 29.69 %, p = 0.027, respectively). Multivariate Cox regression analyses revealed sarcopenia as a risk factor for 1-year (HR = 3.981 [1.137-13.938], p = 0.031) and overall (HR = 2.308 [1.310-4.065], p = 0.004) mortality. The sarcopenia-based nomogram demonstrated favorable prognostic performance. CONCLUSIONS:Sarcopenia evaluated at the T12 level on chest CT may serve as a prognostic factor for predicting long-term mortality among critically ill patients with ECOPD.

With the rapid development of artificial intelligence (AI) technology, major changes have taken place in the field of medical education in China. In recent years, in order to respond to the training requirements of “new medicine” for compound talents, the demand for systematic evaluation of critical thinking ability of medical students in China is increasing. Based on SOAP clinical reasoning framework and integrating existing critical thinking theory, this study established a medical critical thinking assessment gauge covering six dimensions of “interpretation-analysis-evaluation-inference-self-adjustment-clinical adaptation”, each dimension has five levels, presenting a path from information processing to clinical decision-making ability, and introducing evidence-based medicine tools (such as AGREE II), cognitive bias and other professional concepts enhance the professionalism and consistency of evaluation, which can be used as the core quantitative basis of the generative AI-driven critical thinking education system. Meanwhile, the gauge realizes the paradigm transformation from static evaluation to dynamic diagnosis and from general scoring to personalized intervention, providing a reliable path for the cultivation of medical high-order thinking ability.

BACKGROUND:Emerging evidence indicated an association between preserved ratio impaired spirometry (PRISm) and cardiovascular disease (CVD) outcomes. However, the relationship between baseline characteristics, transitional trajectories of PRISm phenotypes, and CVD outcomes remains underexplored. METHODS:This study included 285,049 participants with spirometry measurements between 2006 and 2010, excluding those with preexisting CVD, including heart failure (HF), coronary heart disease (CHD), stroke, and those with airway obstruction (AO). Among them, 23,650 participants with follow-up spirometry (2014-2020) were analyzed for further pulmonary function transitions study. RESULTS:At baseline, restrictive (vs. non-restrictive) PRISm showed higher multivariate adjusted hazard ratios (HRs) of 1.20 (95 % confidence interval [CI], 1.03-1.46) for HF, 1.05 (95 % CI, 1.01-1.10) for stroke, and overall CVD events (HR = 1.10, 95 % CI = 1.00-1.23). For spirometry transition trajectory, restrictive PRISm tended to remain stable, while non-restrictive PRISm often transitioned to other status over time. Moreover, normal to restrictive PRISm (HR = 1.71; 95 % CI, 1.21-2.43), and normal to AO (HR = 1.45; 95 % CI, 1.05-2.00) were associated with higher CVD risk compared to consistently normal spirometry. CONCLUSIONS:Restrictive PRISm is more strongly associated with the development of CVD compared to non-restrictive PRISm and follows a distinct spirometry trajectory. Early intervention aimed at improving PRISm lung function may help mitigate the incidence of cardiovascular events.

Background: Bronchial asthma is a heterogeneous inflammatory airway disease with complex etiology. While the respiratory microbiome and host metabolism are implicated, their integrated roles in defining asthma subtypes remain underexplored. Methods: This multi-omics study utilized 16S rRNA sequencing and untargeted metabolomics on sputum samples from asthma patients and healthy controls. We characterized airway microbial and metabolic profiles, identified asthma subgroups through unsupervised clustering, and investigated microbe-metabolite interactions. Results: Asthma patients exhibited typical clinical hallmarks including elevated IgE and impaired lung function. Microbiome analysis revealed significant enrichment of Streptococcus, Veillonella, and Prevotella as key asthma-associated taxa, alongside dysregulation of crucial lipid metabolic pathways (eg, alpha-linolenic and arachidonic acid). Four highly discriminative diagnostic biomarkers (AUC >0.9), including cis-aconitic acid and LPE 20:1, were identified, indicating specific metabolic perturbations. Unsupervised clustering stratified asthma patients into 2 distinct endotypes: a severe Streptococcus-dominant cluster (Cluster 1) with profound systemic and local metabolic disturbances, and a milder cluster (Cluster 2) with microbial and metabolic profiles resembling healthy controls. These endotypes displayed differential lipid and amino acid metabolism, suggesting unique underlying mechanisms. Conclusion: Our findings precisely delineate asthma endotypes driven by distinct microbiome-metabolome interactions, providing novel diagnostic biomarkers and pathway-specific therapeutic targets. This study critically advances our understanding of asthma heterogeneity, highlighting the importance of integrated multi-omics for personalized precision medicine strategies. Clinical trial number: Not applicable.

With the hypothesis that Nardostachys jatamansi polysaccharides (NJPs) could be the functional constituent contributing to the pharmacological effects of N. jatamansi, this study comprehensively examined the extraction approach, chemical characteristics, and antioxidant activities of the polysaccharide from N. jatamansi. An ultrasonic-assisted extraction method was developed, with the critical optimum parameters determined as follows: ultrasonic temperature at 64 °C, solid-liquid ratio of 1:45, and ultrasonic time of 52 min. Through purification, a pure N. jatamansi polysaccharide (NJPW) was obtained, and its structure was characterized. The monosaccharides of NJPW mainly included glucose, arabinose, and galactose, with a molar weight of 21.907 kDa. NJPW exhibited irregular sheet-like structures, demonstrating the characteristic FTIR and NMR spectra of polysaccharides. NJPW mainly contained the α-d-glucan structure, which was primarily composed of an →4-glcp-(1→ linkage. NJPW exhibited practical activity to scavenge DPPH•, OH•, and ABTS•+ radicals as well as a protective effect against oxidative damage in human cells by decreasing MDA content and enhancing SOD activity. Collectively, the findings of this study expanded the phytochemical understanding of the therapeutic application of N. jatamansi and provided a natural antioxidant for further medicinal research and potentially drug development under various oxidative damage conditions.

Bacterial pneumonia is a significant public health burden, contributing to substantial morbidity, mortality, and healthcare costs. Current therapeutic strategies beyond antibiotics and adjuvant therapies are limited, highlighting the need for a deeper understanding of the disease pathogenesis. Here, we employed single-cell RNA sequencing of 444,146 bronchoalveolar lavage fluid cells (BALFs) from a large cohort of 74 individuals, including 58 patients with mild (n = 22) and severe (n = 36) diseases as well as 16 healthy donors. Enzyme‐linked immunosorbent and histological assays were applied for validation within this cohort. The heterogeneity of immune responses in bacterial pneumonia was observed, with distinct immune cell profiles related to disease severity. Severe bacterial pneumonia was marked by an inflammatory cytokine storm resulting from systemic upregulation of S100A8/A9 and CXCL8, primarily due to specific macrophage and neutrophil subsets. In contrast, mild bacterial pneumonia exhibits an effective humoral immune response characterized by the expansion of T follicular helper and T helper 2 cells, facilitating B cell activation and antibody production. Although both disease groups display T cell exhaustion, mild cases maintained robust cytotoxic CD8+T cell function, potentially reflecting a compensatory mechanism. Dysregulated neutrophil and macrophage responses contributed significantly to the pathogenesis of severe disease. Immature neutrophils promote excessive inflammation and suppress T cell activation, while a specific macrophage subset (Macro_03_M1) displaying features akin to myeloid-derived suppressor cells (M-MDSCs) suppress T cells and promote inflammation. Together, these findings highlight potential therapeutic targets for modulating immune responses and improving clinical outcomes in bacterial pneumonia.

The specific role of lysophospholipids (LysoPLs) in the pathogenesis of chronic obstructive pulmonary disease (COPD) is not yet fully understood. We determined serum LysoPLs in 20 patients with stable COPD and 20 healthy smokers using liquid chromatography-mass spectrometry (LC-MS) and matching with the lipidIMMS library, and integrated these data with spirometry, systemic inflammation markers, and quantitative chest CT generated by an automated 3D-U-Net artificial intelligence algorithm model. Our findings identified three differential LysoPLs, lysophosphatidylcholine (LPC) (18:0), LPC (18:1), and LPC (18:2), which were significantly lower in the COPD group than in healthy smokers. Significant negative correlations were observed between these LPCs and the inflammatory markers C-reactive protein and Interleukin-6. LPC (18:0) and (18:2) correlated with higher post-bronchodilator FEV1, and the latter also correlated with FEV1% predicted, forced vital capacity (FVC), and FEV1/FVC ratio. Additionally, these three LPCs were negatively correlated with the volume and percentage of low attenuation areas (LAA), high-attenuation areas (HAA), honeycombing, reticular patterns, ground-glass opacities (GGO), and consolidation on CT imaging. In the patients with COPD, the three LPCs were most significantly associated with HAA and GGO. In conclusion, patients with stable COPD exhibited a unique LysoPL metabolism profile, with LPC (18:0), LPC (18:1), and LPC (18:2) being the most significantly altered lipid molecules. The reduction in these three LPCs was associated with impaired pulmonary function and were also linked to a greater extent of emphysema and interstitial lung abnormalities.

AbstractA 65‐year‐old man presented with intermittent fever and progressive shortness of breath. He responded poorly to antibiotics and corticosteroids (methylprednisolone 40 mg/d). Chest computed tomography scans showed diffuse consolidations and ground glass density patchy opacities in both lungs and these lesions progressed rapidly. The diagnosis of acute fibrinous and organizing pneumonia (AFOP) was confirmed through transbronchial cryobiopsy. This patient had prostate cancer with bone metastasis for 4 months and took the anti‐prostate cancer medications including apalutamide and leuprorelin acetate. Considering his medication history, the patient was diagnosed with AFOP induced by anti‐prostate cancer medications through panel discussion of multidisciplinary teams. Intravenous methylprednisolone of 500 mg/day was administered for 3 days and then slowly tapered. The patient's shortness of breath gradually subsided. In addition, the lesions in the lungs improved significantly on follow up imaging. AFOP induced by anti‐prostate cancer medications is rare. To our knowledge, this is the first reported case and high‐dose glucocorticoid treatment may be required in some of these cases.

(1) Background: The implication of type 2 (T2) inflammatory response in COVID-19 remains controversial. This study aimed to evaluate the association of eosinophils, neutrophils expressing eosinophilic surface markers and T2 cytokines with the severity and outcome of COVID-19. (2) Methods: Patients who were admitted to hospital due to COVID-19 from 18 December 2022 to 31 January 2023 were enrolled. Peripheral blood WBC and differentials, T2 cellular markers (subsets of eosinophils and neutrophils expressing eosinophilic surface markers) and cytokines at admission were measured and compared between subjects with different disease severities and outcomes. (3) Results: Ten mild-to-moderate and 22 severe-to-very severe cases were enrolled for analysis. Of these patients, seven died of severe-to-very severe disease. The severe-to-very severe patients showed a higher number of neutrophils, but lower numbers of eosinophils, lymphocytes cells and neutrophils expressing eosinophilic surface markers. Similarly, deceased cases were also characterized by increased neutrophils, but decreased eosinophils and neutrophils expressing eosinophilic surface markers. The levels of T2 cytokines failed to demonstrate a significant correlation with the severity or outcome of COVID-19. (4) Conclusions: Eosinophils and neutrophils expressing eosinophilic surface markers were associated with milder disease and better outcomes of COVID-19, suggesting that a T2 inflammatory response may confer a potential protective effect against the disease.