ALKBH5 Modulates Asthma Progression by Downregulating N6-methyladenosine Methylation.

Asthma is a chronic respiratory disease that is characterized by airway inflammation, excessive mucus production, and airway remodeling. Prevention and treatment for asthma is an urgent issue in clinical studies. In recent years, N6-methyladenosine methylation (m6A) has emerged as a promising regulatory approach involved in multiple diseases. ALKBH5 (alkB homolog 5) is a demethylase widely studied in disease pathologies. This work aimed to explore the regulatory mechanisms underlying the ALKBH5-regulated asthma. We established an interleukin-13 (IL-13)-stimulated cell model to mimic the in vitro inflammatory environment of asthma. ALKBH5 knockdown in bronchial epithelial cells was performed using siRNAs, and the knockdown efficacy was analyzed by quantitative PCR (qPCR). Cell viability and proliferation were measured by cell counting kit 8 (CCK-8) and colony formation assay. The ferroptosis was assessed by measuring the total iron, Fe2+, lipid reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. The enrichment of N6-methyladenosine methylation (m6A) modification was detected by the MeRIP assay. Knockdown of ALKBH5 significantly elevated the survival and colony formation ability of bronchial epithelial cells in the IL-13 induction model. The levels of total iron, Fe2+, lipid ROS, and MDA were remarkedly elevated, and the SOD level was reduced in IL-13-induced bronchial epithelial cells, and depletion of ALKBH5 reversed these effects. Knockdown of ALKBH5 elevated the enrichment of m6A modification and expression of glutathione peroxidase 4 (GPX4). Knockdown of GPX4 abolished the pro-proliferation and anti-ferroptosis effects of siALKBH5. Knockdown of ALKBH5 improved the proliferation of bronchial epithelial cells and alleviated cell ferroptosis.

Bronchial Valves for Persistent Air Leak: A Systematic Review and Meta-analysis.

BACKGROUND: Patients with persistent air leak (PAL) pose a therapeutic challenge to physicians, with prolonged hospital stays and high morbidity. There is little evidence on the efficacy and safety of bronchial valves (BV) for PAL. METHODS: We systematically searched the PubMed and Embase databases to identify studies evaluating the efficacy and safety of BV for PAL. We calculated the success rate (complete resolution of air leak or removal of intercostal chest drain after bronchial valve placement and requiring no further procedures) of BV for PAL in individual studies. We pooled the data using a random-effects model and examined the factors influencing the success rate using multivariable meta-regression. RESULTS: We analyzed 28 observational studies (2472 participants). The pooled success rate of bronchial valves in PAL was 82% (95% confidence intervals, 75 to 88; 95% prediction intervals, 64 to 92). We found a higher success rate in studies using intrabronchial valves versus endobronchial valves (84% vs. 72%) and in studies with more than 50 subjects (93% vs. 77%). However, none of the factors influenced the success rate of multivariable meta-regression. The overall complication rate was 9.1% (48/527). Granulation tissue was the most common complication reported followed by valve migration or expectoration and hypoxemia. CONCLUSION: Bronchial valves are an effective and safe option for treating PAL. However, the analysis is limited by the availability of only observational data.

In situ pulmonary mucus hydration assay using rotational and translational diffusion of gold nanorods with polarization-sensitive optical coherence tomography.

Significance: Assessing the nanostructure of polymer solutions and biofluids is broadly useful for understanding drug delivery and disease progression and for monitoring therapy. Aim: Our objective is to quantify bronchial mucus solids concentration (wt. %) during hypertonic saline (HTS) treatment in vitro via nanostructurally constrained diffusion of gold nanorods (GNRs) monitored by polarization-sensitive optical coherence tomography (PS-OCT). Approach: Using PS-OCT, we quantified GNR translational (DT) and rotational (DR) diffusion coefficients within polyethylene oxide solutions (0 to 3 wt. %) and human bronchial epithelial cell (hBEC) mucus (0 to 6.4 wt. %). Interpolation of DT and DR data is used to develop an assay to quantify mucus concentration. The assay is demonstrated on the mucus layer of an air-liquid interface hBEC culture during HTS treatment. Results: In polymer solutions and mucus, DT and DR monotonically decrease with increasing concentration. DR is more sensitive than DT to changes above 1.5 wt. % of mucus and exhibits less intrasample variability. Mucus on HTS-treated hBEC cultures exhibits dynamic mixing from cilia. A region of hard-packed mucus is revealed by DR measurements. Conclusions: The extended dynamic range afforded by simultaneous measurement of DT and DR of GNRs using PS-OCT enables resolving concentration of the bronchial mucus layer over a range from healthy to disease in depth and time during HTS treatment in vitro.

Airway epithelial CD47 plays a critical role in inducing influenza virus-mediated bacterial super-infection.

Respiratory viral infection increases host susceptibility to secondary bacterial infections, yet the precise dynamics within airway epithelia remain elusive. Here, we elucidate the pivotal role of CD47 in the airway epithelium during bacterial super-infection. We demonstrated that upon influenza virus infection, CD47 expression was upregulated and localized on the apical surface of ciliated cells within primary human nasal or bronchial epithelial cells. This induced CD47 exposure provided attachment sites for Staphylococcus aureus, thereby compromising the epithelial barrier integrity. Through bacterial adhesion assays and in vitro pull-down assays, we identified fibronectin-binding proteins (FnBP) of S. aureus as a key component that binds to CD47. Furthermore, we found that ciliated cell-specific CD47 deficiency or neutralizing antibody-mediated CD47 inactivation enhanced in vivo survival rates. These findings suggest that interfering with the interaction between airway epithelial CD47 and pathogenic bacterial FnBP holds promise for alleviating the adverse effects of super-infection.

Coinfection with respiratory syncytial virus and rhinovirus increases IFN-λ1 and CXCL10 expression in human primary bronchial epithelial cells.

Acute respiratory tract infection (ARTI) is common in all age groups, especially in children and the elderly. About 85% of children who present with bronchiolitis are infected with respiratory syncytial virus (RSV); however, nearly one-third are coinfected with another respiratory virus, such as human rhinovirus (HRV). Therefore, it is necessary to explore the immune response to coinfection to better understand the molecular and cellular pathways involving virus-virus interactions that might be modulated by innate immunity and additional host cell response mechanisms. This study aims to investigate the host innate immune response against RSV-HRV coinfection compared with monoinfection. Human primary bronchial/tracheal epithelial cells (HPECs) were infected with RSV, HRV, or coinfected with both viruses, and the infected cells were collected at 48 and 72 hours. Gene expression profiles of IL-6, CCL5, TNF-α, IFN-ß, IFN-λ1, CXCL10, IL-10, IL-13, IRF3, and IRF7 were investigated using real-time quantitative PCR, which revealed that RSV-infected cells exhibited increased expression of IL-10, whereas HRV infection increased the expression of CXCL10, IL-10, and CCL5. IFN-λ1 and CXCL10 expression was significantly different between the coinfection and monoinfection groups. In conclusion, our study revealed that two important cytokines, IFN-λ1 and CXCL10, exhibited increased expression during coinfection.

Assessment of a randomized controlled trial on the safety of pre-placing bronchial balloons in transbronchial lung cryobiopsy for diagnosing interstitial lung disease.

RATIONALE AND OBJECTIVES: Bleeding is a major complication of transbronchial lung cryobiopsy (TBLC), and pre-placing a bronchial balloon is one of the clinical practices used to prevent it, but with very weak evidence, which should be confirmed. This study aimed to conduct whether pre-placing a bronchial balloon in TBLC for diagnosing interstitial lung disease (ILD) is more safety. MATERIALS AND METHODS: In this prospective, single-center, randomized controlled trial, patients with suspected ILD were enrolled and randomly assigned to pre-placed balloon and none-pre-placed balloon groups. The primary outcome was incidence of moderate bleeding in each group. The secondary endpoints were the incidence of severe bleeding, pneumothorax, and other procedural complications. RESULTS: Exactly 250 patients were enrolled between August 2019 and March 2022, with 125 in each group. There were no significant differences in severe bleeding between the none-pre-placed balloon group and pre-placed balloon group (1.6% vs. 0.8%; adjusted p = 0.520), while more moderate bleeding occurred in the none-pre-placed balloon group (26.4% vs. 6.4%, adjusted p = 0.001), as well as more use of hemostatic drug (28.0% vs. 6.4%, adjusted p = 0.001). Three patients in the none-pre-placed balloon group used the bronchial balloon. More samples could be acquired in the pre-placed balloon group than in the none-pre-placed balloon group (3.8 ± 0.9 vs. 3.1 ± 0.9, p < 0.001). There were no significant differences in multidisciplinary discussion (MDD) between the two groups (89.6% vs. 91.2%, adjusted p = 0.182). CONCLUSION: A pre-placed bronchial balloon can reduce the incidence of moderate bleeding and increase the confidence of the bronchoscopists. However, it had no effect on increasing the diagnostic rate of MDD and reducing severe bleeding. REGISTRATION NUMBER: NCT04047667 ( www. CLINICALTRIALS: gov identifier).

[Aloperine suppresses TLR4/NF-κB/NLRP3 signaling to ameliorate cigarette smoke-induced injury to human bronchial epithelial cells].

Objective To explore the effects of aloperine (Alo) on cigarette smoke-induced injury in human bronchial epithelial cells and its potential mechanism. Methods After human bronchial epithelial 16HBE cells were co-treated by 100 mL/L cigarette smoke extract (CSE) and various concentrations (50,100 and 200 µmol/L) of Alo, cell viability was assessed using CCK-8 assay. Lactate dehydrogenase (LDH) activity was measured with a related kit. Cell apoptosis was evaluated using the terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) and Western blot analysis. The levels of inflammatory factors were detected by ELISA. Oxidative stress levels were assessed using 2'7'-dichlorofluorescin diacetate (DCFH-DA) staining. The expression of Toll-like receptor 4 (TLR4)/nuclear factor-kappaB (NF-κB)/NLR family pyrin domain containing 3 (NLRP3) signaling-associated proteins was measured by Western blot analysis. After cells were co-treated with 100 mL/L CSE and 200 µmol/L Alo, the aforementioned assays were applied to evaluate the effects of TLR4 overexpression on the TLR4/NF-κB/NLRP3 signaling, LDH activity, apoptosis, inflammatory response and oxidative stress in cells. Results CSE exposure might inhibit 16HBE cell viability, increase LDH activity, apoptosis, inflammatory response and oxidative stress levels and activate TLR4/NF-κB/NLRP3 signaling. Treatment with Alo promoted cell viability, decreased LDH activity, cell apoptosis, inflammation and oxidative stress levels, and inactivated TLR4/NF-κB/NLRP3 signaling. Furthermore, TLR4 overexpression might reverse the protective role of Alo treatment in CSE-induced injury in 16HBE cells. Conclusion Alo may ameliorate CSE-induced injury in human bronchial epithelial cells via inhibiting TLR4/NF-κB/NLRP3 signaling.

Expression of glucocorticoid receptor and HDACs in airway smooth muscle cells is associated with response to steroids in COPD.

BACKGROUND: Steroid insensitivity in Chronic Obstructive Pulmonary Disease (COPD) presents a problem for controlling the chronic inflammation of the airways. The glucocorticoid receptor (GR) mediates the intracellular signaling of inhaled corticosteroids (ICS) by interacting with transcription factors and histone deacetylases (HDACs). The aim of this study was to assess if COPD patients' response to ICS in vivo, may be associated with the expression of GR, the complex of GR with transcription factors, and the expression of various HDACs in vitro. METHODS: Primary airway smooth muscle cells (ASMC) were established from endobronchial biopsies obtained from patients with asthma (n = 10), patients with COPD (n = 10) and subjects that underwent diagnostic bronchoscopy without pathological findings and served as controls (n = 6). ASMC were also established from 18 COPD patients, 10 responders and 8 non-responders to ICS, who participated in the HISTORIC study, an investigator-initiated and driven clinical trial that proved the hypothesis that COPD patients with high ASMC in their endobronchial biopsies respond better to ICS than patients with low ASMC. Expression of GR and its isoforms GRα and GRß and HDACs was investigated in primary ASMC in the absence or in the presence of dexamethasone (10- 8M) by western blotting. The complex formation of GR with transcription factors was assessed by co-immunoprecipitation. RESULTS: Expression of GR and its isoform GRα but not GRß was significantly reduced in ASMC from COPD patients as compared to controls. There were no significant differences in the expression of GR, GRα and GRß between responders and non-responders to ICS. However, treatment with dexamethasone upregulated the expression of total GR (p = 0.004) and GRα (p = 0.005) after 30 min in responders but not in non-responders. Τhe formation of the complex GR-c-Jun was increased 60 min after treatment with dexamethasone only in responders who exhibited significantly lower expression of HDAC3 (p = 0.005) and HDAC5 (p < 0.0001) as compared to non-responders. CONCLUSIONS: These data suggest that ASMC from COPD patients who do not respond to treatment with ICS, are characterized by reduced GR-c-Jun complex formation and increased expression of HDAC3 and HDAC5. TRIAL REGISTRATION: ISRCTN11017699 (Registration date: 15/11/2016).

Slide tracheoplasty for congenital tracheal stenosis with involvement of the carina and bronchi: a case report.

A female newborn presented with respiratory distress at birth and was diagnosed with congenital tracheal stenosis. The stenosis was positioned at the distal trachea and compromised the carina and the right and left bronchi. She underwent surgical treatment using circulatory life support with veno-arterial peripheral extracorporeal membrane oxygenation, and the airway was reconstructed using the slide tracheoplasty technique to build a neocarina. The patient had an excellent postoperative course, was successfully weaned from extracorporeal membrane oxygenation and invasive ventilation, and was discharged.

Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism.

Micro- and nanoplastic particles, including common forms like polyethylene and polystyrene, have been identified as relevant pollutants, potentially causing health problems in living organisms. The mechanisms at the cellular level largely remain to be elucidated. This study aims to visualize nanoplastics in bronchial smooth muscle (BSMC) and small airway epithelial cells (SAEC), and to assess the impact on mitochondrial metabolism. Healthy and asthmatic human BSMC and SAEC in vitro cultures were stimulated with polystyrene nanoplastics (PS-NPs) of 25 or 50 nm size, for 1 or 24 h. Live cell, label-free imaging by holotomography microscopy and mitochondrial respiration and glycolysis assessment were performed. Furthermore, 25 and 50 nm NPs were shown to penetrate SAEC, along with healthy and diseased BSMC, and they impaired bioenergetics and induce mitochondrial dysfunction compared to cells not treated with NPs, including changes in oxygen consumption rate and extracellular acidification rate. NPs pose a serious threat to human health by penetrating airway tissues and cells, and affecting both oxidative and glycolytic metabolism.

Mitigation of acute lung injury by human bronchial epithelial cell-derived extracellular vesicles via ANXA1-mediated FPR signaling.

Acute lung injury (ALI) is characterized by respiratory failure resulting from the disruption of the epithelial and endothelial barriers as well as immune system. In this study, we evaluated the therapeutic potential of airway epithelial cell-derived extracellular vesicles (EVs) in maintaining lung homeostasis. We isolated human bronchial epithelial cell-derived EVs (HBEC-EVs), which endogenously express various immune-related surface markers and investigated their immunomodulatory potential in ALI. In ALI cellular models, HBEC-EVs demonstrated immunosuppressive effects by reducing the secretion of proinflammatory cytokines in both THP-1 macrophages and HBECs. Mechanistically, these effects were partially ascribed to nine of the top 10 miRNAs enriched in HBEC-EVs, governing toll-like receptor-NF-κB signaling pathways. Proteomic analysis revealed the presence of proteins in HBEC-EVs involved in WNT and NF-κB signaling pathways, pivotal in inflammation regulation. ANXA1, a constituent of HBEC-EVs, interacts with formyl peptide receptor (FPR)2, eliciting anti-inflammatory responses by suppressing NF-κB signaling in inflamed epithelium, including type II alveolar epithelial cells. In a mouse model of ALI, intratracheal administration of HBEC-EVs reduced lung injury, inflammatory cell infiltration, and cytokine levels. Collectively, these findings suggest the therapeutic potential of HBEC-EVs, through their miRNAs and ANXA1 cargo, in mitigating lung injury and inflammation in ALI patients.

Pulmonary Function in People Living With Human Immunodeficiency Virus: A Meta-Analysis

Background: HIV can infect bronchial epithelial cells rendering individuals susceptible to lung damage. Our objective was to determine the effects of human immunodeficiency virus (HIV) infection on pulmonary function tests. Methods: We performed a meta-analysis after conducting a literature search in PubMed, Embase, Cochrane Library and Virtual Health Library databases from inception to December 31st, 2022. We employed the inverse variance method with a random effects model to calculate the effect estimate as the mean difference (MD) and 95% confidence interval (CI). We calculated the heterogeneity with the I2 statistic and performed a meta-regression analysis by age, sex, smoking, CD4 T-cells count and antiretroviral therapy. We also conducted a sensitivity analysis according to the studies’ publication date, and excluding the study with the greatest weight in the effect. The PROSPERO registry number was CRD42023401105. Results: The meta-analysis included 20 studies, with 7621 living with HIV and 7410 control participants. The pooled MD (95%CI) for the predicted percentage of FEV1, FVC and DLCO were −3.12 (−5.17, −1.06); p=0.003, −1.51 (−3.04, 0.02); p=0.05, and −5.26 (−6.64, −3.87); p<0.001, respectively. The pooled MD for FEV1/FVC was −0.01 (−0.02, −0.01); p=0.002. In all cases, there was a considerable heterogeneity. The meta-regression analysis showed that among studies heterogeneity was not explained by patient age, smoking, CD4 T-cells count or antiretroviral therapy. Conclusion: Pulmonary function tests are impaired in people living with HIV, independently of age, smoking, CD4 T-cells count, and geographical region. (AU)

Is it in their eyes? Correlation between microorganisms isolated from bronchial aspirates and conjunctival swabs in a Pediatric Intensive Care Unit / ¿Está en sus ojos? Correlación entre microorganismos aislados de aspirados bronquiales e hisopos conjuntivales en una Unidad de Cuidados Intensivos Pediátricos

Objectives. Our observational, retrospective study aimed to determine the correlation between bacteria isolated from bronchial aspirates of pediatric ICU patients (PICU) with respiratory infections and those obtained from conjunctival swabs of the same patients exhibiting clinical conjunctivitis. Material and methods. Throughout the period from 2015 to 2022, we reviewed all clinically significant bronchial aspirates (≥105 CFU/mL) and positive conjunctival swabs obtained from PICU patients. These records were retrieved from the microbiology database, cross-referencing the data to identify patients who tested positive for both during the same clinical episode. Results. The median age of the patients was 5 months (interquartile range: 1-7). Among the cohort, twenty-one patients exhibited positivity in both bronchial aspirate and conjunctival swab samples, showcasing a microbial match in 85.71% of cases (18 out of 21). The most frequently isolated microorganisms were Haemophilus influenzae (55.6%), followed by Pseudomonas aeruginosa (14.3%), Klebsiella aerogenes (9.5%), and Escherichia coli, Stenotrophomonas maltophilia, and Enterobacter cloacae, each accounting for 4.8% of the isolates. Conclusions. Our study demonstrates a strong concordance between the isolated microorganisms from both samples in patients presenting clear symptoms of clinical conjunctivitis. These findings provide a basis for future prospective studies that may leverage conjunctival swabs as a predictive tool for identifying microorganisms involved in respiratory infections. (AU)

Objetivos. Nuestro estudio observacional y retrospectivo tuvo como objetivo determinar la correlación entre las bacterias aisladas de aspirados bronquiales de pacientes de UCI pediátrica (UCIP) con infecciones respiratorias y las obtenidas de hisopos conjuntivales de los mismos pacientes que presentaban conjuntivitis clínica. Material y métodos. A lo largo del periodo comprendido entre 2015 y 2022, se revisaron todos los aspirados bronquiales clínicamente significativos (≥105 UFC/mL) y los hisopos conjuntivalespositivos obtenidos de pacientes de UCIP. Estos registros se recuperaron de la base de datos de microbiología, cruzando los datos para identificar a los pacientes que dieron positivo en ambos durante el mismo episodio clínico. Resultados. La mediana de edad de los pacientes fue de 5 meses (rango intercuartílico: 1-7). Entre la cohorte, veintiún pacientes presentaron positividad tanto en las muestras de aspirado bronquial como en las de hisopo conjuntival, mostrando una coincidencia microbiana en el 85,71% de los casos (18 de 21). Los microorganismos más frecuentemente aislados fueron Haemophilus influenzae (55,6%), seguido de Pseudomonas aeruginosa (14,3%), Klebsiella aerogenes (9,5%) y Escherichia coli, Stenotrophomonas maltophiliay Enterobacter cloacae, cada uno de los cuales representó el 4,8% de los aislamientos. Conclusiones. Nuestro estudio demuestra una fuerte concordancia entre los microorganismos aislados de ambas muestras en pacientes que presentan síntomas claros de conjuntivitis clínica. Estos hallazgos proporcionan una base para futuros estudios prospectivos que podrían aprovechar los hisopos conjuntivales como herramienta predictiva para identificar microorganismos implicados en infecciones respiratorias. (AU)

Misdiagnosed Asthma Turned Out to Be Bronchial Fibroepithelial Polyp: Case Report and Review of Literature.

Bronchial fibroepithelial polyps are exceedingly rare with few cases have been reported. They can manifest with a wide array of symptoms; ranging from being totally asymptomatic, cough, refractory dyspnea, and hemoptysis. In our case, our patient's condition was diagnosed and was managed as asthma. It is one of the rare benign conditions to be encountered, shares similar morphology with other tumors such as angiomyofibroblastoma, aggressive angiomyxoma, and cellular angiofibroma. These lesions have a slow growth pattern which may end up with obstruction. According to the tumor size and symptoms caused by it, treatment varies from observation to complete resection. This case describes an incidental finding of fibroepithelial polyp in the main bronchus for a patient with long-term refractory cough for 5 years, was misdiagnosed to have asthma. Diagnosis typically involves imaging and bronchoscopy, followed by appropriate therapeutic measures and careful monitoring to assess the prognosis.

Eosinophil peroxidase promotes bronchial epithelial cells to secrete asthma-related factors and induces the early stage of airway remodeling.

Asthma is a heterogeneous disease characterized by chronic airway inflammation, reversible airflow limitation, and airway remodeling. Eosinophil peroxidase (EPX) is the most abundant secondary granule protein unique to activated eosinophils. In this study, we aimed to illustrate the effect of EPX on the epithelial-mesenchymal transition (EMT) in BEAS-2B cells. Our research found that both EPX and ADAM33 were negatively correlated with FEV1/FVC and FEV1%pred, and positively correlated with IL-5 levels. Asthma patients had relatively higher levels of ADAM33 and EPX compared to the healthy control group. The expression of TSLP, TGF-ß1 and ADAM33 in the EPX intervention group was significantly higher. Moreover, EPX could promote the proliferation, migration and EMT of BEAS-2B cells, and the effect of EPX on various factors was significantly improved by the PI3K inhibitor LY294002. The findings from this study could potentially offer a novel therapeutic target for addressing airway remodeling in bronchial asthma, particularly focusing on EMT.

[Complete Disruption of the Left Main Bronchus Treated with Extracorporeal Membrane Oxygenation Support and Pneumonectomy].

A 60-year old woman, sandwiched between two boats was brought to our hospital with severe respiratory failure. She was in pre-shock and there was extensive cutaneous emphysema from the face to abdomen. She required respirator support and bilateral chest tubes for hemopneumothorax. On the patient's 3rd hospital day, she received venovenous extracorporeal membrance oxgenation( ECMO) due to sudden ventilatory failure. The bronchofiberscopy revealed complete disruption of the left main bronchus and occlusion of the right one owing to blood clot and sputum. Because of significant destruction of the left main bronchus, we didn't attempt bronchoplasty, and performed left pneumonectomy under veno-venous (VV)-ECMO. The postoperative course was uneventful, and she was discharged after 30 days with satisfactory outcome.

[Management of Tracheobronchial Injuries due to Brunt Trauma].

BACKGROUND: Tracheobronchial injuries resulting from blunt trauma are relatively rare among chest injuries. However, if these injuries are not managed properly, they can be fatal. The prognosis is intricately linked to the precise diagnosis and treatment. We herein report three cases of tracheobronchial trauma that required surgical intervention. Case 1:A 17-year-old male sustained injuries when his torso became entangled in heavy machinery. The diagnosis revealed a tear in the right main bronchus, which required transportation with left single- lung ventilation. The patient was treated by tracheobronchial reconstruction. Case 2:A 71-year-old male experienced trauma when his car collided with a utility pole. He was transported to the hospital after tracheal intubation due to a laceration of the tracheal membranous area. The site of the injury was closed with sutures. Case 3:A 17-year-old female who had been struck by a train suffered acute respiratory failure and was transported to the hospital after intubation. Veno-venous extracorporeal membrane oxgenation (VV-ECMO) was initiated in response to poor oxygenation. Complete rupture of the right middle bronchial trunk and laceration of the right main bronchial membrane were observed, and bronchoplasty was performed. CONCLUSION: A swift and accurate diagnosis, coupled with timely and judicious therapeutic interventions, play a pivotal role in managing tracheal and bronchial injuries.

Different anatomical variations in the anterior segment of the right upper lung.

During a routine physical examination three years ago, a 47-year-old woman received a diagnosis of a nodule in her right upper lung. Since then, she has been regularly attending outpatient clinic appointments for follow-up. Over time, the nodule has shown gradual growth, leading to a suspicion of lung cancer. Through the use of enhanced CT imaging, a three-dimensional reconstruction was performed to examine the bronchi and blood vessels in the patient's chest. This reconstruction revealed several variations in the anatomy of the anterior segment of the right upper lobe. Specifically, the anterior segmental bronchus (B3) was found to have originated from the right middle lung bronchus. Additionally, the medial subsegmental artery of the anterior segmental artery (A3b) and the medial segmental artery (A5) were observed to share a common trunk. As for the lateral subsegmental artery of the anterior segmental artery (A3a), it was found to have originated from the right inferior pulmonary trunk. Furthermore, the apical subsegmental artery of the apical segmental artery (A1a) and the posterior segmental artery (A2) were found to have a shared trunk.

Bronchoconstriction damages airway epithelia by crowding-induced excess cell extrusion.

Asthma is deemed an inflammatory disease, yet the defining diagnostic feature is mechanical bronchoconstriction. We previously discovered a conserved process called cell extrusion that drives homeostatic epithelial cell death when cells become too crowded. In this work, we show that the pathological crowding of a bronchoconstrictive attack causes so much epithelial cell extrusion that it damages the airways, resulting in inflammation and mucus secretion in both mice and humans. Although relaxing the airways with the rescue treatment albuterol did not affect these responses, inhibiting live cell extrusion signaling during bronchoconstriction prevented all these features. Our findings show that bronchoconstriction causes epithelial damage and inflammation by excess crowding-induced cell extrusion and suggest that blocking epithelial extrusion, instead of the ensuing downstream inflammation, could prevent the feed-forward asthma inflammatory cycle.