Bronchial Damage Research Articles

Modern problems of bronchial tuberculosis in the world and the Russian Federation: A review

In the Russian Federation there is a positive trend in reducing the incidence of tuberculosis. However, there is a tendency to increase the prevalence of tuberculosis in the bronchi. According to foreign authors, the prevalence of bronchial tuberculosis ranges from 10% to 40%. There are no official statistics on the incidence of bronchial tuberculosis in the Russian Federation. The main contingent of bronchial tuberculosis lesions are young non-smoking women. At the same time, the most common target is the left main bronchus. Currently, no additional methods have been developed in the scheme of specific treatment of patients with pulmonary tuberculosis complicated by bronchial tuberculosis. It is important to understand that the eradication of MBT after an effective course of chemotherapy does not prevent the formation of cicatricial bronchial stenosis. It is also important to note that bacterial excretion in patients with bronchial tuberculosis is much more common than in patients with a comparable process in the lungs, but without bronchial damage. Consequently, tuberculosis of the trachea and bronchi has not only clinical, but also great epidemiological significance.

Common double-lumen tube selection methods overestimate adequate tube sizes in individual patients – a 3D reconstruction study

BackgroundAppropriate selection of double-lumen tube sizes for one-lung ventilation is crucial to prevent airway damage. Current selection methods rely on demographic factors or 2D radiography. Prediction of left bronchial diameter is indispensable for choosing the adequate tube size. This prospective observational study investigates if current selection methods sufficiently predict individuals’ left bronchial diameters for DLT selection compared to the 3D reconstruction.Methods100 patients necessitating thoracic surgery with one-lung ventilation and left-sided double-lumen tubes, ≥ 18 years of age, and a set of chest X-rays and 2D thorax CT scans for 3D reconstruction of the left main bronchus were included between 07/2021 and 06/2023. The cross-validated prediction error and the width of the 95%-prediction intervals of the 3D left main bronchial diameter utilizing linear prediction models were based on current selection methods.ResultsThe mean bronchial diameter in 3D reconstruction was 13.6 ± 2.1 mm. The ranges of the 95%-prediction intervals for the bronchial diameter were 6.4 mm for demographic variables, 8.3 mm for the tracheal diameter from the X-ray, and 5.9 mm for bronchial diameter from the 2D-CT scans. Current methods violated the suggested ‘≥1 mm’ safety criterion in up to 7% (men) and 42% (women). Particularly, 2D radiography overestimated women’s left bronchial diameter. Current methods even allowed the selection of double-lumen tubes with bronchial tube sections greater than the bronchial diameter in women.ConclusionsNeither demographic nor 2D-radiographic methods sufficiently account for the variability of the bronchial diameter. Wide 95%-prediction intervals for the bronchial diameter hamper accurate individual double-lumen tube selection. This increases women’s risk of bronchial damage, particularly if they have other predisposing factors. These patients may benefit from 3D reconstruction of the left main bronchus.Trial registrationNot applicable.

Polylactic acid nanoplastics (PLA-NPLs) induce adverse effects on an in vitro model of the human lung epithelium: The Calu-3 air-liquid interface (ALI) barrier

The expected increments in the production/use of bioplastics, as an alternative to petroleum-based plastics, require a deep understanding of their potential environmental and health hazards, mainly as nanoplastics (NPLs). Since one important exposure route to NPLs is through inhalation, this study aims to determine the fate and effects of true-to-life polylactic acid nanoplastics (PLA-NPLs), using the in vitro Calu-3 model of bronchial epithelium, under air-liquid interphase exposure conditions. To determine the harmful effects of PLA-NPLs in a more realistic scenario, both acute (24 h) and long-term (1 and 2 weeks) exposures were used. Flow cytometry results indicated that PLA-NPLs internalized easily in the barrier (∼10 % at 24 h and ∼40 % after 2 weeks), which affected the expression of tight-junctions formation (∼50 % less vs control) and the mucus secretion (∼50 % more vs control), both measured by immunostaining. Interestingly, significant genotoxic effects (DNA breaks) were detected by using the comet assay, with long-term effects being more marked than acute ones (7.01 vs 4.54 % of DNA damage). When an array of cellular proteins including cytokines, chemokines, and growth factors were used, a significant over-expression was mainly found in long-term exposures (∼20 proteins vs 5 proteins after acute exposure). Overall, these results described the potential hazards posed by PLA-NPLs, under relevant long-term exposure scenarios, highlighting the advantages of the model used to study bronchial epithelium tissue damage, and signaling endpoints related to inflammation.

Phenolic-rich fraction of green tea attenuates histamine-mediated cardiopulmonary toxicity by inhibiting Cox-2/NF-κB signaling pathway and regulating oxidant/antioxidant balance

BackgroundHistamine (HIS) has a substantial impact on the development of numerous allergic disorders including asthma. Antihistamines mostly target histamine receptor-1 alone, so it is not entirely effective in the treatment of allergic diseases. In the current investigation, we examine the growing evidence for novel therapeutic strategies that aim to treat histamine-mediated cardiopulmonary toxicity with the phenolic-rich fraction of green tea (PRFGT).ResultsOur findings demonstrated that weekly ingestion of HIS to rats induced oxidant/antioxidant imbalance in both lung and heart homogenates. The histopathological examination demonstrated extensive interstitial pneumonia with progressive alveolar and bronchial damage in HIS receiving groups. Heart sections showed severe myocardial necrosis and hemorrhage. All lesions were confirmed by the immunohistochemical staining that demonstrated strong caspase-3, cyclooxygenase-2 (Cox-2), and tumor necrosis factor-α (TNF-α) protein expressions along with upregulation of the pulmonary m-RNA expression of TNF-α, nuclear factor kappa-B (NF-κB), and interleukin-1β (IL-1β) genes and cardiac levels of many apoptotic genes. Otherwise, the pretreatment of rats with PRFGT had the ability to alleviate all the aforementioned toxicological parameters and return the microscopic picture of both lung and heart sections to normal histology.ConclusionsWe concluded that PRFGT’s powerful antioxidant, anti-inflammatory, and anti-apoptotic properties can reduce cardiopulmonary toxicity caused by HIS. We recommended daily intake of green tea as a beverage or adding it to foods containing elevated levels of HIS to prevent its possible toxicity.

SARS-CoV-2-induced disruption of a vascular bed in a microphysiological system caused by type-I interferon from bronchial organoids.

Blood vessels show various COVID-19-related conditions including thrombosis and cytokine propagation. Existing in vitro blood vessel models cannot represent the consequent changes in the vascular structure or determine the initial infection site, making it difficult to evaluate how epithelial and endothelial tissues are damaged. Here, we developed a microphysiological system (MPS) that co-culture the bronchial organoids and the vascular bed to analyze infection site and interactions. In this system, virus-infected organoids caused damage in vascular structure. However, vasculature was not damaged or infected when the virus was directly introduced to vascular bed. The knockout of interferon-related genes and inhibition of the JAK/STAT pathway reduced the vascular damage, indicating the protective effect of interferon response suppression. The results demonstrate selective infection of bronchial epithelial cells and vascular damage by cytokines and also indicate the applicability of MPS to investigate how the infection influences vascular structure and functions.

Mechanistic Approach on the Pulmonary Oxido-Inflammatory Stress Induced by Cobalt Ferrite Nanoparticles in Rats

Cobalt ferrite nanoparticles (CFN) are employed in data storage, imaging, medication administration, and catalysis due to their superparamagnetic characteristics. The widespread use of CFN led to significantly increased exposure to people and the environment to these nanoparticles. Until now, there is not any published paper describing the adverse effect of repeated oral intake of this nanoformulation on rats’ lungs. So, the current research aims to elucidate the pulmonary toxicity prompted by different concentrations of CFN in rats as well as to explore the mechanistic way of such toxicity. We used 28 rats that were divided equally into 4 groups. The control group received normal saline, and the experimental groups received CFN at dosage levels 0.05, 0.5, and 5 mg/kg bwt. Our findings revealed that CFN enhanced dose-dependent oxidative stress manifested by raising in the MDA levels and declining in the GSH content. The histopathological examination revealed interstitial pulmonary inflammation along with bronchial and alveolar damage in both 0.5 and 5 mg CFN given groups. All these lesions were confirmed by the immunohistochemical staining that demonstrated strong iNOS and Cox-2 protein expression. There was also a significant upregulation of TNFα, Cox-2, and IL-1β genes with downregulation of IL-10 and TGF-β genes. Additionally, the group receiving 0.05 mg CFN did not exhibit any considerable toxicity in all measurable parameters. We concluded that the daily oral intake of either 0.5 or 5 mg CFN, but not 0.05 mg, could induce pulmonary toxicity via NPs and/or its leached components (cobalt and iron)-mediated oxido-inflammatory stress. Our findings may help to clarify the mechanisms of pulmonary toxicity generated by these nanoparticles through outlining the standards for risk assessment in rats as a human model.

Bronchial Safety After Pulsed Field Ablation for Paroxysmal Atrial Fibrillation.

Thermal left atrial ablation can cause bronchial damage. Pulsed field ablation (PFA) is a novel, nonthermal ablation modality for paroxysmal atrial fibrillation. We report on bronchial effects after pulmonary vein isolation using PFA for paroxysmal atrial fibrillation. A computed tomography scan showing the respiratory tract adjacent to the left atrial was obtained. Oral anticoagulation was interrupted on procedure day. Peri-procedurally, patients received heparin with an activated clotting time goal of >350 seconds. All pulmonary veins were individually isolated with a 13F steerable sheath and a pentaspline PFA catheter using either a straight-tip or J-tip guide wire. The J-tip guide wire patients were added to test the hypothesis that the straight-tip guidewire was associated with bleeding complications. One day afterward, bronchoscopy was performed. Serial hemoglobin levels were measured during 30-day follow-up. In 2 series of 30 patients, PFA was performed, with all pulmonary veins acutely isolated. Clinical course was uneventful, no patient had chest discomfort, coughing, or hemoptysis. All patients underwent uncomplicated bronchoscopy, without thermal lesions or ulcers. In 12 out of 30 (40%) straight-tip guide wire patients, small amounts of old blood without active bleeding were seen in multiple segments. All hemoglobin levels remained clinically stable. At 30-day follow-up, all patients were asymptomatic. Pulmonary vein isolation using PFA for paroxysmal atrial fibrillation does not cause thermal lesions in the bronchial system. Use of a straight-tip, extrastiff guide wire for the over-the-wire PFA catheter can lead to asymptomatic bleeding in the bronchial system without clinical relevance at 30-day follow-up, opposite to use of a J-tip guide wire.

Effect of TLR3/dsRNA complex inhibitor on Poly(I:C)-induced airway inflammation in Swiss albino mice.

Rhinovirus infection frequently causes COPD and asthma exacerbations. Impaired anti-viral signaling and reduced viral clearance have both been seen in sick bronchial epithelium, potentially increasing exacerbations. Polyinosinic:polycytidylic acid (Poly(I:C)), a Toll-like receptor-3 (TLR3) ligand, has been shown to cause a viral exacerbation of severe asthma by detecting double-stranded RNA (dsRNA). The purpose of this work was to determine the effect of a TLR3/dsRNA complex inhibitor-Calbiochem drug in the prevention of Poly(I:C)-induced airway inflammation following TLR3 activation and to uncover a potential pathway for the cure of asthma through TLR3 inhibition. Mice were sensitized with Poly(I:C) as an asthma model before being challenged by PBS and ovalbumin (OVA) chemicals. The mice were administered a TLR3/dsRNA complex inhibitor. Throughout the trial, the mice's body weight was measured after each dosage. Biochemical methods are used to analyze the protein as well as enzyme composition in airway tissues. BALF specimens are stained using Giemsa to identify inflammatory cells and lung histopathology to determine morphological abnormalities in lung tissues. By using the ELISA approach, cytokine levels such as TNF-α, IL-13, IL-6, IL-5, and IgE antibody expression in lung tissue and blood serum were assessed. TLR3/dsRNA complex inhibitor drug significantly lowered the number of cells in BALF and also on Giemsa staining slides. It also downregulated the level of TNF-α and IL-6 in contrast to OVA and Poly(I:C) administered in animals. A TLR3/dsRNA complex inhibitor decreased the fraction of oxidative stress markers (MDA, GSH, GPx, and CAT) in lung tissues while keeping the mice's body weight constant during the treatment period. By decreasing alveoli, bronchial narrowing, smooth muscle hypertrophy, and granulocyte levels, the TLR3/dsRNA complex blocker significantly reduced the histopathological damage caused by OVA and Poly(I:C) compounds. In an animal model utilizing ovalbumin, TLR3/dsRNA complex inhibitors similarly reduced the bronchial damage produced by Poly(I:C). A novel TLR3/dsRNA complex inhibitor is expected to be employed in clinical studies since it suppresses airway inflammation without inducing antiviral approach resistance.

SWYER JAMES: A SHIFT IN THE DIAGNOSIS

SWYER JAMES: A SHIFT IN THE DIAGNOSIS

Cigarette smoke extract-mediated FABP4 upregulation suppresses viability and induces apoptosis, inflammation and oxidative stress of bronchial epithelial cells by activating p38 MAPK/MK2 signaling pathway

BackgroundLong-term inhalation of cigarette smoke is considered to be one of the main causes of bronchial epithelioid cell damage, but its underlying mechanism has to be further clarified.MethodsGene expression at mRNA level and protein levels were detected by qRT-PCR and western blot analysis respectively. CCK-8, TUNEL assays, ELISA, western blot analysis and commercial kits were utilized to test cell viability, apoptosis inflammatory response and oxidative stress. The correlation between fatty acid binding protein 4 (FABP4) and the p38 mitogen-activated protein kinase (MAPK)/MAPK activated kinase 2 (MK2) signaling pathway was verified by western blot analysis and rescue assays.ResultsCigarette smoke extract (CSE) exposure decreased viability, induced apoptosis and inflammatory response in 16HBE cells. Moreover, the expression of FABP4 in CSE-treated 16HBE cells was up-regulated in a time and dose-dependent manner. Ablation of FABP4 in 16HBE cells significantly protected against CSE-mediated cell viability decline and apoptosis. Further, FABP4 knockdown suppressed inflammatory response by down-regulating the elevated levels of cellular inflammatory factors including TNF-α, IL-1β, IL-6, Cyclooxygenase-2 (Cox-2) and inducible nitric oxide synthase (iNOS) in CSE-treated 16HBE cells. The oxidative stress induced by CSE in 16HBE cells was also inhibited by FABP4 silence as evidence by reduced ROS and MDA level but increased SOD activity caused by FABP4 silence. Finally, all the above effects of FABP4 silence on CSE-treated 16HBE cells were reversed by asiatic acid, an agonist of p38 mitogen-activated protein kinase (MAPK).ConclusionsThe up-regulation of FABP4 expression mediated by CSE exerted pro-inflammatory, pro-oxidative stress and pro-apoptotic effects on bronchial epithelial cells by activating the p38 MAPK/MK2 signaling pathway. Our findings help to further understand the underlying mechanism of cigarette smoke-induced bronchial inflammation.

The cytotoxicity of PM2.5 and its effect on the secretome of normal human bronchial epithelial cells.

Exposure to airborne fine particulate matter (PM2.5) induced various adverse health effects, such as metabolic syndrome, systemic inflammation, and respiratory disease. Many works have studied the effects of PM2.5 exposure on cells through intracellular proteomics analyses. However, changes of the extracellular proteome under PM2.5 exposure and its correlation with PM2.5-induced cytotoxicity still remain unclear. Herein, the cytotoxicity of PM2.5 on normal human bronchial epithelia cells (BEAS-2B cells) was evaluated, and the secretome profile of BEAS-2B cells before and after PM2.5 exposure was investigated. A total of 83 proteins (58 upregulated and 25 downregulated) were differentially expressed in extracellular space after PM2.5 treatment. Notably, we found that PM2.5 promoted the release of several pro-apoptotic factors and induced dysregulated secretion of extracellular matrix (ECM) constituents, showing that the abnormal extracellular environment attributed to PM2.5-induced cell damage. This study provided a secretome data for the deep understanding of the molecular mechanism underlying PM2.5-caused human bronchial epithelia cell damage.

Pulsed field ablation for paroxysmal atrial fibrillation is safe for the bronchial system

Abstract Funding Acknowledgements Type of funding sources: None. Background Thermal LA ablation, like cryo can cause bronchial damage, like hemorrhagic lesions, atrio-bronchial fistula and severe bleedings. Pulsed field ablation (PFA) is a novel, non-thermal ablation modality. Objective We report on possible bronchial injury after PVI using PFA for paroxysmal AF. Methods A LA bipolar voltage 3D map was created. All PVs were individually isolated using a 13F steerable sheath and a pentaspline over-the-wire PFA catheter. After ablation, mapping was repeated to assess lesion formation. One day after PVI, bronchoscopy without biopsies was performed. Serial hemoglobin levels were measured during 30-day follow-up. Results In 30 patients (mean 63 years; 47% male), uncomplicated PFA was performed, with all PVs acutely isolated. Post ablation, all voltage maps consistently showed extensive antral PV lesions. ACT was >325 seconds in all patients. Clinical course was uneventful, no patient had chest discomfort, coughing or hemoptysis. All patients underwent uncomplicated bronchoscopy, without thermal lesions or ulcers. In 12 patients (40%), small amounts of blood clots without active bleeding were seen in multiple segments. All hemoglobin levels remained stable. At 30-day follow-up, all patients were asymptomatic. Conclusion PVI using PFA for paroxysmal AF is safe for the bronchial system. PFA using a straight tip, extra-sti! wire can lead to asymptomatic blood oozing in the bronchial system without clinical relevance at 30-day follow-up. Figures: Postero-anterior LA view before (above) and after (below) ablation with the trachea and main bronchi (dark grey) projected over the roof and posterior wall. The right bipolar voltage 3D map shows extensive, non-magenta antral ablation lesions.

PO-634-07 PULSED FIELD ABLATION FOR PAROXYSMAL ATRIAL FIBRILLATION IS SAFE FOR THE BRONCHIAL SYSTEM

Thermal LA ablation, like cryo can cause bronchial damage, like hemorrhagic lesions, atrio-bronchial fistula and severe bleedings. Pulsed field ablation (PFA) is a novel, non-thermal ablation modality.

Baicalin inhibits inflammation of lipopolysaccharide-induced acute lung injury toll like receptor-4/myeloid differentiation primary response 88/nuclear factor-kappa B signaling pathway.

To explore the effect and mechanism of baicalin in the treatment of acute lung injury (ALI) by and experiments. ALI was induced by instilling 10 mg/mL lipopolysaccharide (LPS) into the airway of rats. Different doses of baicalin (50 and 100 mg·kg ·d) were administered by gavage one day before modeling. Baicalin significantly reduced the permeability of the alveolocapillary membrane, alleviated tissue injury and inflammatory infiltration, and inhibited the secretion of inflammatory factors and the infiltration of neutrophils. The decline in these inflammations was related to the inhibition of the toll like receptor-4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB)/nod-like receptor pyrin containing 3 (NLRP3) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathway. Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-MyD88-NF-κB/NLRP3 pathway and the MAPK signaling pathway. Thus, it reduces lung bronchial epithelial layer, alveolar damage, and pulmonary edema as detected in the and experiments. Therefore, baicalin may be a potential preventive and therapeutic drug for ALI.

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training.

Ambient particulate matter (PM2.5), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM2.5 exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM2.5 exposure, exercise+PM2.5 exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek−1, 1hday−1). PM-exposed rats were exposed to ambient PM2.5 (6h day−1) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM2.5 exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM2.5 in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E2 (PGE2). Thus, pre-exercise training may be an effective way to protect against PM2.5-induced lung inflammatory injury in rats.

Clinical and Diagnostic Implications of the Bronchiectasis - COPD Association

Abstract The aim of this study is to provide partially updated data on observational, non-interventional research that aims to determine the potential clinical and diagnostic implications of the association of bronchiectasis in patients with COPD. Both COPD and bronchiectasis are two chronic lung diseases with a high prevalence in the general population and can coexist in a large number of cases. Their coexistence is increasingly diagnosed in clinical practice, but this association has not yet been well studied. The overlap of these two pathological entities has been established as a unique phenotype, because patients are prone to more severe and frequent exacerbations. It is therefore important to identify and study the presence of bronchiectasis in patients with COPD, as the clinical, prognostic, and therapeutic implications are different. Materials and methods. The study was based on a cohort of 100 patients (n) with a positive diagnosis of COPD, following the establishment of the 2 study groups as follows: patients who were identified to also associate the diagnosis of bronchiectasis (x), these being the second study group, the first group including the remaining COPD patients without bronchiectasis (n-x). Therefore, the study, conducted between 2018-2020, contains 100 patients who addressed the Marius Nasta Institute of Pneumoftiziology, Bucharest, managed and followed for 12 months after inclusion, according to the developed scientific research protocol. Patients were included in the study after an anamnesis as complete as possible and subsequent completion of the informed consent form. The ethical aspects were respected by the existence of the agreement of the Ethics Commission of the Institute of Pneumoftiziology “Marius Nasta”, Bucharest, for the study and by the presence of the informed consent of the patient (attached to each medical record / per hospitalized patient). The comparative evaluation of the 2 groups of patients, group I (COPD) and group II (COPD and Bronchiectasis), consisted of periodic clinical-paraclinical monitoring (T0, T3, T6, T12), highlighting the negative impact of the presence of bronchiectasis in patients with COPD. Results. The study cohort includes 100 patients: group I - 38 patients (diagnosis of COPD) and group II - 62 patients (diagnosis of COPD + BE), 20% being female patients. The mean age of the patients was 65.26 years. The occurrence of “de novo” bronchiectasis was identified in 4.84% of patients. Lung lobes involvement was identified in patients in group II, COPD + BE confirmed, while patients in group I had no bronchial damage. The number of exacerbations was higher in patients with BCOS. The presence of infections with potentially pathogenic microorganisms and, in particular, with Pseudomonas aeruginosa, is a variable frequently associated with the presence of bronchiectasis in patients with COPD, being considered a predictor of mortality in these patients. Discussions. BCOS syndrome is a time and resources consumer, so early diagnosis is essential to improve patients’ quality of life and increase survival. Conclusions. COPD and Bronchiectasis are two conditions commonly encountered in current practice, with relatively similar clinical, pathophysiological and molecular consequences, and overlap syndrome has a higher risk of morbidity and mortality compared to each of the conditions taken separately. This study highlighted the negative impact of bronchiectasis in patients with COPD, clinically by increasing the number of exacerbations, affecting the quality of life, and reducing survival. Early identification of this phenotype, entitled BCOS in the literature, is necessary because therapeutic management is influenced by the particular clinical-paraclinical evidence of this new clinical syndrome. Although the data obtained in this paperwork were in absolute agreement with the data of other existing studies in the literature, the number of patients included in the study was not high enough, and the pandemic context of the COVID-19 that broke out in Romania in March 2020 had quite obvious negative repercussions on the course of the study.

Endothelium-derived Cdk5 deficit aggravates air pollution-induced peripheral vasoconstriction through AT1R upregulation

PM2.5 infiltrates into circulation and increases the risk of systemic vascular dysfunction. As the first-line barrier against external stimuli, the molecular mechanism of the biological response of vascular endothelial cells to PM2.5 exposure remains unclear. In this study, 4-week-old mice were exposed to Hangzhou ‘real’ airborne PM2.5 for 2 months and were found to display bronchial and alveolar damage. Importantly, in the present study, we have demonstrated that Cdk5 deficit induced peripheral vasoconstriction through angiotensin II type 1 receptor under angiotensin II stimulation in Cdh5-cre;Cdk5f/n mice. In the brain, Cdk5 deficit increased the myogenic activity in the medullary arterioles under external pressure. On the other hand, no changes in cerebral blood flow and behavior patterns were observed in the Cdh5-cre;Cdk5f/n mice exposed to PM2.5. Therefore, our current findings indicate that CDK5 plays an important role in endothelium cell growth, migration, and molecular transduction, which is also a sensor for the response of vascular endothelial cells to PM2.5.

A clinical case of successful treatment of complete abruption of the trachea from the larynx

Tracheobronchial injuries as a consequence of chest blunt trauma are rare. Blunt traumas of the cervical part of the trachea are a rarer pathology presenting a serious diagnostic problem for a clinician. Traumas of the larynx and the trachea account for 40 to 80% of lethality. The tracheas cervical part is vulnerable despite that it is covered with the neck muscles, spine, clavicles, and mandible. In cut/stab wounds, the tracheas cervical part is often damaged together with the adjacent structures. In blunt trauma, under a direct action of a traumatizing agent, the mobile trachea displaces toward the spine, accompanied by damage to the tracheal cartilages, its membranous part, and the soft surrounding tissues with preservation of the integrity of the skin.
 Tracheal ruptures along the distance up to 1 cm from the cricoid cartilage account for not more than 4% of all tracheal ruptures. A complete tracheal rupture and its abruption from the larynx are extremely rare pathology. Because of severe respiratory disorders, most victims die at the site where their injury occurred.
 This article presents a clinical case of the successful treatment of patient Z., 41 years of age, with complete tracheal abruption from the larynx. The cause of tracheal damage was blunt neck trauma in a traffic accident. A peculiarity of this clinical case was that the victim arrived at a specialized thoracic surgery unit with a functioning tracheostomy two days after the trauma.
 Conclusion. Tracheal trauma is a potentially fatal condition. Therefore, early diagnosis of tracheobronchial damage is essential since it permits timely surgical intervention and diminished risk of lethal outcome. When dealing with patients with trauma of the head, neck, and chest with non-corresponding clinical data and the absence of effective recommended standard therapeutic measures, a clinician should become alert and exclude the tracheal and bronchial damage.
 X-ray computed tomography and fibrotracheobronchoscopy are strongly recommended as reliable methods to diagnose tracheobronchial damages. In a surgical intervention, it is necessary to perform the primary suture on the trachea, avoid preventive tracheostomy, and delay interventions associated with poorer prognosis and a high complication rate.

Clinical characteristics and treatment outcome of Candida tracheobronchitis.

Although Candida species can cause invasive fungal diseases, such as disseminated infection and pneumonia, they rarely cause tracheobronchitis, which is often fatal.To identify the clinical characteristics of Candida tracheobronchitis, we retrospectively evaluated 8 patients who had pathologically proven Candida tracheobronchitis.Their median age was 64 (range: 51–70) years and 5 were females. Three patients had solid cancers and 5 had hematological malignancies. We classified tracheobronchitis into localized and diffuse types. Of the 8 patients, 5 had localized and 3 had diffuse tracheobronchitis. While all patients with diffuse tracheobronchitis had predisposing risk factors for invasive fungal disease, such as prolonged corticosteroid use, recent use of nucleoside analogues, or recent neutropenia (<500/m3), only 2 of the 5 with localized tracheobronchitis had predisposing risk factors. Four of the 5 patients with localized tracheobronchitis had loco-regional bronchial mucosal damage (e.g., radiation or photodynamic therapy). Although all 8 patients ultimately died, some improved with or without antifungal treatment. Two of the 5 patients (1 with localized and the other with diffuse tracheobronchitis) who received antifungal agents improved after treatment, and 1 patient with localized tracheobronchitis who did not receive antifungal treatment improved spontaneously. Two of the 3 patients with diffuse tracheobronchitis did not respond to antifungal treatment.Candida tracheobronchitis can present as both localized and diffuse types. While the former was influenced more by loco-regional mucosal damage, the latter was influenced more by the patient's immune status. The treatment outcomes were especially poor in patients with diffuse tracheobronchitis.

Application of green tea catechins, polysaccharides, and flavonol prevent fine dust induced bronchial damage by modulating inflammation and airway cilia

Airborne fine dust particles (FDPs) have been identified as major toxins in air pollution that threaten human respiratory health. While searching for an anti-FDP reagent, we found that green tea extract (GTE) and fractions rich in flavonol glycosides (FLGs) and crude tea polysaccharides (CTPs) had protective effects against FDP-stimulated cellular damage in the BEAS-2B airway epithelial cell line. The GTE, FLGs, and CTPs significantly increased viability and lowered oxidative stress levels in FDP-treated cells. Combined treatment with GTE, FLGs, and CTPs also exerted synergistic protective effects on cells and attenuated FDP-induced elevations in inflammatory gene expression. Moreover, the green tea components increased the proportion of ciliated cells and upregulated ciliogenesis in the airway in FDP-stimulated BEAS-2B cells. Our findings provide insights into how natural phytochemicals protect the airway and suggest that green tea could be used to reduce FDP-induced airway damage as an ingredient in pharmaceutical, nutraceutical, and also cosmeceutical products.