Chronic Airway Inflammation Research Articles

Network pharmacology prediction, molecular docking, and molecular dynamics simulation-based strategy to explore the potential mechanism of Huashanshen dripping pill against asthma.

Asthma is a heterogeneous disease characterized by chronic airway inflammation. Huashanshen dripping pills (HSS) are commonly utilized for relieving asthma, relieving cough, and expelling phlegm. At present, the molecular mechanism against airway inflammation remains unclear. In this study, network pharmacology, molecular docking technology, and molecular dynamic simulation were used to predict the therapeutic pathways of HSS for asthma. The ovalbumin-induced mouse model was used to further validate the prediction by RT-qPCR, western blot, immunofluorescence, and related methods. The findings indicate that HSS improves lung function and relieves lung inflammation by reducing inflammatory cell infiltration around the bronchus and reducing eosinophilic counts in bronchoalveolar lavage fluid (BALF). In addition, it lowers the levels of inflammatory cytokines and the expression levels of interleukin-4, interleukin-5, and interleukin-13 mRNA. HSS also inhibits the phosphorylation and nuclear translocation of NF-κB p65 protein. All results suggested that HSS can decrease airway inflammation in asthmatic mice by inhibiting NF-κB signaling pathway. This finding will shed light on how it can be used to treat asthma.

Neutrophil serine proteases in cystic fibrosis: role in disease pathogenesis and rationale as a therapeutic target.

Chronic airway inflammation is a central feature in the pathogenesis of bronchiectasis (BE), which can be caused by cystic fibrosis (CFBE; hereafter referred to as CF lung disease) and non-CF-related conditions (NCFBE). Inflammation in both CF lung disease and NCFBE is predominantly driven by neutrophils, which release proinflammatory cytokines and granule proteins, including neutrophil serine proteases (NSPs). NSPs include neutrophil elastase, proteinase 3 and cathepsin G. An imbalance between NSPs and their antiproteases has been observed in people with CF lung disease and people with NCFBE. While the role of the protease/antiprotease imbalance is well established in both CF lung disease and NCFBE, effective therapies targeting NSPs are lacking. In recent years, the introduction of CF transmembrane conductance regulator (CFTR) modulator therapy has immensely improved outcomes in many people with CF (pwCF). Despite this, evidence suggests that airway inflammation persists, even in pwCF treated with CFTR modulator therapy. In this review, we summarise current data on neutrophilic inflammation in CF lung disease to assess whether neutrophilic inflammation and high, uncontrolled NSP levels play similar roles in CF lung disease and in NCFBE. We discuss similarities between the neutrophilic inflammatory profiles of people with CF lung disease and NCFBE, potentially supporting a similar therapeutic approach. Additionally, we present evidence suggesting that neutrophilic inflammation persists in pwCF treated with CFTR modulator therapy, at levels similar to those in people with NCFBE. Collectively, these findings highlight the ongoing need for new treatment strategies targeting neutrophilic inflammation in CF lung disease.

Comparative safety of monoclonal antibodies in chronic inflammatory airway diseases (chronic sinusitis with nasal polyposis and asthma): A network meta-analysis

ObjectiveSeveral monoclonal antibodies (MoAbs) targeting specific type 2 immune reactions have been developed as innovative therapeutic approaches for chronic inflammatory airway diseases, such as chronic sinusitis with nasal polyps (CRSwNP) and asthma. However, the clinical safety of these MoAbs and how to choose them are not clear. Therefore, we aimed to assess the systemic drug- and dose-based safety of MoAbs in chronic airway inflammation using network meta-analysis (NMA). MethodsElectronic databases were systematically searched for relevant studies published in English between January 2009 and December 2022. Eligible studies must have clearly reported adverse events (AEs) among the MoAbs’ safety data. Results1). Regarding serious AEs, mepolizumab was significantly safer than placebo; in terms of permanent treatment discontinuation, reslizumab and dupilumab were significantly safer than benralizumab. 2). Regarding asthma worsening, dupilumab was associated with the best safety profile; was safer than dupilumab/300 mg/q2-4w. 3). In terms of injection-site reactions, dupilumab posed a higher risk than placebo; dupilumab/300 mg/qw posed a higher risk than dupilumab/300 mg/q2w and dupilumab/300 mg/q2-4w; lebrikizumab/250 mg/q4w posed a higher risk than lebrikizumab/37.5 mg/q4w; mepolizumab/100 mg/q4w posed a higher risk than mepolizumab/75 mg/q4w; benralizumab/30 mg/q4-8w posed a higher risk than benralizumab/20 mg/q4-8w. 4) In CRSwNP patients combined with asthma, the risks of experiencing AEs were not increased. ConclusionOverall, biologics are safe and well tolerated in chronic inflammatory airway disease. This drug- and dose-based NMA provides further evidence on the different safety profiles of different emerging MoAbs. This information may help guide rational drug use and provide clinical recommendations for choosing MoAbs.Trial Registration: SYSTEMATIC REVIEW REGISTRATION (PROSPERO #CRD42023387610).

FGF receptors mediate cellular senescence in the cystic fibrosis airway epithelium.

The number of adults living with cystic fibrosis (CF) has already increased significantly because of drastic improvements in life expectancy attributable to advances in treatment, including the development of highly effective modulator therapy. Chronic airway inflammation in CF contributes to morbidity and mortality, and aging processes like inflammaging and cell senescence influence CF pathology. Our results show that single-cell RNA sequencing data, human primary bronchial epithelial cells from non-CF and CF donors, a CF bronchial epithelial cell line, and Cftr-knockout (Cftr-/-) rats all demonstrated increased cell senescence markers in the CF bronchial epithelium. This was associated with upregulation of fibroblast growth factor receptors (FGFRs) and mitogen-activated protein kinase (MAPK) p38. Inhibition of FGFRs, specifically FGFR4 and to some extent FGFR1, attenuated cell senescence and improved mucociliary clearance, which was associated with MAPK p38 signaling. Mucociliary dysfunction could also be improved using a combination of senolytics in a CF ex vivo model. In summary, FGFR/MAPK p38 signaling contributes to cell senescence in CF airways, which is associated with impaired mucociliary clearance. Therefore, attenuation of cell senescence in the CF airways might be a future therapeutic strategy improving mucociliary dysfunction and lung disease in an aging population with CF.

The amount of hyaluronic acid and airway remodelling increase with the severity of inflammation in neutrophilic equine asthma

BackgroundEquine asthma (EA) is a chronic lower airway inflammation that leads to structural and functional changes. Hyaluronic acid (HA) has crucial functions in the extracellular matrix homeostasis and inflammatory mediator activity. HA concentration in the lungs increases in several human airway diseases. However, its associations with naturally occurring EA and airway remodelling have not been previously studied. Our aim was to investigate the association of equine neutrophilic airway inflammation (NAI) severity, airway remodelling, and HA concentration in horses with naturally occurring EA. We hypothesised that HA concentration and airway remodelling would increase with the severity of NAI. HA concentrations of bronchoalveolar lavage fluid supernatant (SUP) and plasma of 27 neutrophilic EA horses, and 28 control horses were measured. Additionally, remodelling and HA staining intensity were assessed from endobronchial biopsies from 10 moderate NAI horses, 5 severe NAI horses, and 15 control horses.ResultsThe HA concentration in SUP was higher in EA horses compared to controls (p = 0.007). Plasma HA concentrations were not different between the groups. In the endobronchial biopsies, moderate NAI horses showed epithelial hyperplasia and inflammatory cell infiltrate, while severe NAI horses also showed fibrosis and desquamation of the epithelium. The degree of remodelling was higher in severe NAI compared to moderate NAI (p = 0.048) and controls (p = 0.016). Intense HA staining was observed in bronchial cell membranes, basement membranes, and connective tissue without significant differences between the groups.ConclusionThe release of HA to the airway lumen increases in naturally occurring neutrophilic EA without clear changes in its tissue distribution, and significant airway remodelling only develops in severe NAI.

An interpretable cluster-based logistic regression model, with application to the characterization of response to therapy in severe eosinophilic asthma.

Asthma is a disease characterized by chronic airway hyperresponsiveness and inflammation, with signs of variable airflow limitation and impaired lung function leading to respiratory symptoms such as shortness of breath, chest tightness and cough. Eosinophilic asthma is a distinct phenotype that affects more than half of patients diagnosed with severe asthma. It can be effectively treated with monoclonal antibodies targeting specific immunological signaling pathways that fuel the inflammation underlying the disease, particularly Interleukin-5 (IL-5), a cytokine that plays a crucial role in asthma. In this study, we propose a data analysis pipeline aimed at identifying subphenotypes of severe eosinophilic asthma in relation to response to therapy at follow-up, which could have great potential for use in routine clinical practice. Once an optimal partition of patients into subphenotypes has been determined, the labels indicating the group to which each patient has been assigned are used in a novel way. For each input variable in a specialized logistic regression model, a clusterwise effect on response to therapy is determined by an appropriate interaction term between the input variable under consideration and the cluster label. We show that the clusterwise odds ratios can be meaningfully interpreted conditional on the cluster label. In this way, we can define an effect measure for the response variable for each input variable in each of the groups identified by the clustering algorithm, which is not possible in standard logistic regression because the effect of the reference class is aliased with the overall intercept. The interpretability of the model is enforced by promoting sparsity, a goal achieved by learning interactions in a hierarchical manner using a special group-Lasso technique. In addition, valid expressions are provided for computing odds ratios in the unusual parameterization used by the sparsity-promoting algorithm. We show how to apply the proposed data analysis pipeline to the problem of sub-phenotyping asthma patients also in terms of quality of response to therapy with monoclonal antibodies.

Recurrent Bronchopneumonia in Bronchiectasis, Despite Antibiotic Treatment: A Case Report on Combined Treatment with Korean and Western Medicine

Background: Bronchiectasis is a chronic respiratory condition leading to recurrent respiratory infections. Despite the use of antibiotics and other standard treatments, managing bronchiectasis remains challenging due to the frequent recurrence of airway infections and concerns about antimicrobial resistance. Given these challenges, traditional Korean medicine (TKM) has gained attention due to its potential to reduce the frequency of respiratory infections, possibly minimizing the need for antibiotics.Case report: A 59-year-old female with bronchiectasis experienced recurrent pneumonia and was treated with antibiotics for over 2 weeks without any significant improvement in clinical symptoms. She received comprehensive Korean medicine treatment, including herbal medicine (Sikyungbanha-tang combined with Bigwabojungikki-tang-gami), acupuncture, and Chuna manual therapy, for pulmonary rehabilitation. Post-treatment, clinically meaningful improvements were observed in symptoms, serum C-reactive protein (CRP) levels, and bronchopneumonic lesions on chest X-rays.Conclusion: This case suggests that complex traditional Korean medicine treatments for recurrent chronic airway inflammation due to bronchiectasis can lead to clinically significant improvements in symptoms and help to prevent recurrence.

Elastin-derived peptides favor type 2 innate lymphoid cells in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a condition characterized by chronic airway inflammation and obstruction, primarily caused by tobacco smoking. Although the involvement of immune cells in COPD pathogenesis is well established, the contribution of innate lymphoid cells (ILCs) remains poorly understood. ILCs are a type of innate immune cells that participate in tissue remodeling processes, but their specific role in COPD has not been fully elucidated. During COPD, the breakdown of pulmonary elastin generates elastin peptides that elicit biological activities on immune cells. This study aimed to investigate the presence of ILC in patients with COPD and examine the impact of elastin peptides on their functionality. Our findings revealed an elevated proportion of ILC2 in the peripheral blood of patients with COPD, and a general activation of ILC as indicated by an increase in their cytokine secretion capacity. Notably, our study demonstrated that serum from patients with COPD promotes ILC2 phenotype, likely due to the elevated concentration of IL-5, a cytokine known to favor ILC2 activation. Furthermore, we uncovered that this increase in IL-5 secretion is partially attributed to its secretion by macrophages upon stimulation by elastin peptides, suggesting an indirect role of elastin peptides on ILC in COPD. These findings shed light on the involvement of ILC in COPD and provide insights into the potential interplay between elastin breakdown, immune cells, and disease progression. Further understanding of the mechanisms underlying ILC activation and their interaction with elastin peptides could contribute to the development of novel therapeutic strategies for COPD management.NEW & NOTEWORTHY Elastin-derived peptides, generated following alveolar degradation during emphysema in patients with COPD, are able to influence the response of type 2 innate lymphoid cells. We show that the orientation of innate lymphoid cells in patients with COPD is shifted toward a type 2 profile and that elastin peptides are indirectly participating in that shift through their influence of macrophages, which in turn impact innate lymphoid cells.

A Japanese herbal medicine (kampo), hochuekkito (TJ-41), has anti-inflammatory effects on the chronic obstructive pulmonary disease mouse model

Chronic obstructive pulmonary disease (COPD) is a progressive disease that is characterized by chronic airway inflammation. A Japanese herbal medicine, hochuekkito (TJ-41), is prominently used for chronic inflammatory diseases in Japan. This study aimed to analyze the anti-inflammatory effect of TJ-41 in vivo and its underlying mechanisms. We created a COPD mouse model using intratracheal administration of porcine pancreatic elastase and lipopolysaccharide (LPS) and analyzed them with and without TJ-41 administration. A TJ-41-containing diet reduced inflammatory cell infiltration of the lungs in the acute and chronic phases and body weight loss in the acute phase. In vitro experiments revealed that TJ-41 treatment suppressed the LPS-induced inflammatory cytokines in BEAS-2B cells. Furthermore, TJ-41 administration activated the AMP-activated protein kinase (AMPK) pathway and inhibited the mechanistic target of the rapamycin (mTOR) pathway, both in cellular and mouse experiments. We concluded that TJ-41 administration reduced airway inflammation in the COPD mouse model, which might be regulated by the activated AMPK pathway, and inhibited the mTOR pathway.

A bronchiole-on-a-chip and a stretching system for studying human disease model of asthma attack

Asthma is an important public health issue in developed and developing countries, with a prevalence of 300 million worldwide. It is a heterogeneous disease characterized by chronic airway inflammation and hyperresponsiveness. A bronchiole-on-a-chip with a compact stretching system, which is comparable to the small-size incubator and can provide continuous cyclical scratches, is reported here for emulating the physiology of asthma and other types of lung diseases with various breathing rates. In this study, bronchial smooth muscle cells (BSMCs) are cultured on the bronchiole-on-a-chip under cyclic stretching, mimicking the respiratory rates for healthy adults and asthma patients under bronchospasm. With the cyclical cell stretching, the physiology of BSMCs is affected. In an asthma-conditioned bronchial chip, secretions of pro-inflammatory cytokines IL-6 and IL-8 increase significantly from BSMCs compared with the static or healthy condition. In on-chip treatment studies, BSMCs are treated with various concentrations of indacaterol, a long-acting bronchodilator for asthma. The secretion of IL-6 is suppressed for the indacaterol-treated group under asthma conditions. The alignment of stretched BSMCs is also affected by mechanical stretching. Bronchiole-on-a-chip demonstrates the possibility of mimicking the physiological condition of asthma in vitro and a potential drug screening system for lung diseases.

Uncovering the Cellular Microenvironment in Chronic Rhinosinusitis via Single-Cell RNA Sequencing: Application and Future Directions.

Chronic rhinosinusitis (CRS) is a heterogenic disease characterized by persistent mucosal inflammation of the upper airway. Researches of CRS have progressed from phenotype-based to endotype-based, looking more deeply into molecular biomarkers, signaling pathways, and immune microenvironment. Single-cell RNA sequencing is an effective tool in analyzing composition, function, and interaction of cells in disease microenvironment at transcriptome level, showing great advantage in analyzing potential biomarkers, pathogenesis, and heterogeneity of chronic airway inflammation in an unbiased manner. In this article, we will review the latest advances in scRNA-seq studies of CRS to provide new perspectives for the diagnosis and treatment of this heterogeneous disease.

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-β1 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.

The Fractional exhaled Nitric Oxide (FeNO)- test as add-on test in the diagnostic work-up of asthma: a study protocol.

Asthma is a common disease characterized by chronic inflammation of the lower airways, bronchial hyperactivity, and (reversible) airway obstruction. The Global Initiative of Asthma Guideline recommends a flowchart to diagnose asthma with first-step spirometry with reversibility and a bronchial challenge test (BPT) with histamine or methacholine as a second step [1]. The BPT is considered burdensome, time-consuming for patients and staff, can cause side effects, and is expensive. In addition, this test strongly encumbers lung function capacity. Elevated Nitric Oxide (NO) is associated with airway eosinophilic inflammation in asthma patients and can be measured in exhaled air with the Fractional exhaled (Fe) NO-test. This low-burden FeNO-test could be used as an 'add-on' test in asthma diagnostics [2, 3]. This multi-center prospective study (Trial number: NCT06230458) compares the 'standard asthma diagnostic work-up' (spirometry with reversibility and BPT) to the 'new asthma diagnostics work-up' (FeNO-test as an intermediate step between the spirometry with reversibility and the BPT), intending to determine the impact of the FeNO-based strategy, in terms of the number of avoided BPTs, cost-effectiveness and reduced burden to the patient and health care. The cost reduction of incorporating the FeNO-test in the new diagnostic algorithm will be established by the number of theoretically avoided BPT. The decrease in burden will be studied by calculating differences in the Visual Analogue Scale (VAS) -score and Asthma Quality of Life Questionnaire (AQLQ) -score after the BPT and FeNO-test with an independent T-test. The accuracy of the FeNO-test will be calculated by comparing the FeNO-test outcomes to the (gold standard) BPTs outcomes in terms of sensitivity and specificity. The intention is to include 171 patients. The local medical ethics committee approved the proposed study and is considered a low-burden and risk-low study. The local medical ethics committee registration number: R23.005. Strengths: This is the first study that investigates the value of the FeNO-test (cut off ≥ 50 ppb) as an add-on test, to determine the impact of the FeNO-based strategy, in terms of the number of avoided BPTs, cost-effectiveness, and reduced burden on the patient and health care. High FeNO levels may also be observed in other diseases such as eosinophilic chronic bronchitis and allergic rhinitis. The FeNO-test can be used to rule in a diagnosis of asthma with confidence, however, due to the poor sensitivity it is not suitable to rule out asthma.

The Determinants of Eosinophilia in Patients With Severe Asthma.

Asthma is defined by the Global Initiative for Asthma (GINA) as a heterogeneous disease characterized by chronic airway inflammation. The pathogenesis of the disease is better understood with the comprehension of immunological pathways. These pathways differ by the type of recruited cells and released interleukin (IL). Thus, asthma can be classified into subtypes based on the underlying immune mechanism: eosinophilic asthma (EA) and non-eosinophilic asthma (NEA). Patients with EA tend to respond better to inhaled corticosteroid as compared to those with NEA. The distinction of EA is very important in the light of emergent type 2 inflammation targeted therapies. We performed a 1-year (2018) retrospective cohort analysis of the Nationwide Inpatient Database (NIS). We included all adult patients presenting with severe asthma. Patients were stratified into two groups: eosinophilic severe asthma and non-eosinophilic severe asthma. The primary outcomes measures were the prevalence of chronic steroid use, status asthmaticus, family history of asthma, food, drug and environmental allergies, presence of nasal polyps, allergic rhinitis, allergic dermatitis, need for mechanical ventilation, need for oxygen supplementation, gastroesophageal reflux disease, in-hospital mortality, and length of stay. We performed descriptive statistics. Continuous parametric variables were reported using a mean and standard deviation. Continuous nonparametric variables were reported using a median and interquartile range. To compare the characteristics of the two groups, we used the independent t-test for continuous parametric variables and the Mann-Whitney U test for continuous nonparametric variables. The Chi-square test was used to assess differences in categorical variables. A total of 2,646 patients were included, out of which 882 belonged to the eosinophilic group and 1,764 were in the non-eosinophilic group. Comparing EA versus NEA, we have found that eosinophilic group was characterized by higher percentage of steroid use (18.3% vs. 9.5%, P < 0.001). This group also had higher rates of status asthmaticus and positive family history (P = 0.009 and 0.004, respectively). The presence of allergies, allergic rhinitis, nasal polyps, and allergic dermatitis was higher among patients with eosinophilia. The need for mechanical ventilation and supplemental oxygen was also higher among this group (P < 0.001 for both); however, there was no significant difference in mortality rate (P = 0.347) and the length of hospital stay was similar in both groups (P < 0.001). We showed herein that the eosinophilic subtype of asthma differs widely from the non-eosinophilic phenotype. Clinically, patients with eosinophilia might exhibit different symptomatology, more atopy, and concomitant comorbidities. However, this group might have better response to steroid therapy and might benefit from the new emergent T2 immune targeted therapy. The identification of EA is crucial for better disease control.

&lt;i&gt;Avena sativa’s&lt;/i&gt; Therapeutic Potential: Exploring Antiasthmatic Effects in Guinea Pig Asthma Model

Avena sativa (oat) has emerged as a potential therapeutic candidate for asthma, a global health challenge characterized by chronic airway inflammation. This research investigates the anti-asthmatic potential of the Hydro-Alcoholic Extract of Avena sativa (HAEAS) in a guinea pig asthma model induced by histamine and ovalbumin. The study explores the influence of HAEAS on oxidative stress markers, leucocytes, eosinophils, and histopathological changes in lung tissues. Results reveal that HAEAS, particularly at 400 mg/kg, significantly increases the latent period and percentage protection in histamine induced bronchospasm. In ovalbumin-sensitized guinea pigs, HAEAS demonstrates a notable reduction in total leucocyte count, eosinophils, neutrophils, and macrophages in bronchoalveolar lavage fluid. Moreover, HAEAS exhibits antioxidative effects by increasing superoxide dismutase levels and decreasing malondialdehyde levels. Histopathological analysis demonstrates a decrease in inflammatory cell infiltration, hyperplasia, and bronchoconstriction. This study highlights the potential of Avena sativa as a novel therapeutic avenue for asthma, offering anti-inflammatory and antioxidant benefits.

Sustained control of recalcitrant chronic spontaneous urticaria after initiation of inflammatory airway diseases treatment: two case reports

BackgroundCurrent classification of chronic urticaria is primarily based on clinical presentation of skin manifestations. Hence, therapeutic treatment is primarily aimed locally for immediate symptom relief. We reason that limiting therapeutic strategies to the skin pathology might be inadequate since cellular activation and inflammation might be triggered remotely.Case presentationIn this series two patients had exhausted all current treatments for recalcitrant urticaria but remained symptomatic. The first case was 26-year-old Caucasian female and the second was 63-year-old African American female. Both cases had frequent breakthrough urticaria requiring frequent pulsating courses of prednisone to control urticaria despite treatment with omalizumab and antihistamines. When inflammatory airway disease was discovered and managed with inhaled corticosteroid, urticaria is controlled much faster without the need of high dose immunosuppression over several years of observation. Coincidentally, autoimmune thyroiditis and anti-immunogobulin-E immunoglobulin-G titers dropped significantly in one case with sustained inhaled corticosteroid therapy.ConclusionsWe suggest a novel approach of controlling remote epithelial site inflammation in these two cases that resulted in sustained-control of urticaria symptoms without the need for systemic corticosteroids or immunosuppressant. The changes of autoimmune antibodies might be the consequences of tolerance breaking from chronic lower airway inflammation as observed in other epithelial inflammatory condition like in celiac disease and rheumatoid arthritis.

Effect of fractional exhaled carbon monoxide on patients with sleep apnea-hypopnea syndrome and its mechanism.

Sleep-disordered breathing (SDB) is a common sleep disorder as-sociated with chronic airway inflammation and lung function impairment. This article aimed to investigate the fractional exhaled carbon monoxide (FeCO) expression level in obstructive sleep apnea-hypopnea syndrome (OSAHS) and its correlation with disease indicators. Subjects with OSAHS, asthma, chronic obstructive pulmonary disease (COPD), and healthy subjects were selected to collect clinical data. FeCO concentration, eosinophil (Eos), erythrocyte sed-imentation rate (ESR), C-reactive protein (CRP), FEV1, and FEV1/FVC were measured. The Pearson correlation coefficient and receiver operating charac-teristic (ROC) curve were used for statistical analysis. The FeCO concentra-tion, Eos count, ESR and CRP levels, and lung function in the OSAHS group were higher than the healthy and COPD groups (p&lt;0.05) and slightly lower than the asthma group. FeCO was positively correlated with Eos, ESR, and CRP (p&lt;0.05), but there was no apparent correlation between FeCO and lung func-tion. FeCO has a high sensitivity and specificity in the diagnosis of OSAHS. There is chronic airway inflammation and systemic inflammation in patients with OSAHS. Lung function impairment in patients with OSAHS is mild, but some limitations remain. FeCO may be an auxiliary diagnostic index particu-larly valuable in diagnosing OSAHS.

Atomized inhalation of Icaritin reduces airway inflammation and remodeling in asthmatic mice

Background Asthma is a disease characterized by airway hyperresponsiveness and airway inflammation. Icaritin (ICT) is a plant hormone with various pharmacological activities such as anti-inflammatory, immune regulation, and anti-tumor. This study mainly explored the effects of nebulized inhalation of ICT on airway inflammation and airway remodeling in asthmatic mice. Method Different groups of ovalbumin (OVA)-induced asthma mice with acute and chronic airway inflammation received ICT. Asthmatic mice received budesonide (BDND) aerosol inhalation as a positive control, while normal control and asthma model mice received the same volume of saline. Following finishing of the study, analyses were conducted on behavioral tests, biochemical indices, and histological structures of lung tissues. Results Aerosol inhalation of ICT can notably reduce inflammatory cells infiltration around the airways and pulmonary vessels, and suppressed goblet cell hyperplasia in asthmatic mice. Long-term inhalation of ICT can decrease airway collagen deposition and airway smooth muscle hyperplasia, and alleviate airway hyperresponsiveness, mirroring the effects observed with hormone employed in clinical practice. Conclusion Nebulized inhalation of ICT can effectively inhibit airway inflammation in asthmatic mice, improve airway remodeling, and reduce airway hyperresponsiveness, with effects similar to those of hormones. It may serve as a potential candidate used as a hormone replacement asthma treatment.

Exercise-Induced Asthma: Managing Respiratory Issues in Athletes.

Asthma is a complex respiratory condition characterized by chronic airway inflammation and variable expiratory airflow limitation, affecting millions globally. Among athletes, particularly those competing at elite levels, the prevalence of respiratory conditions is notably heightened, varying between 20% and 70% across specific sports. Exercise-induced bronchoconstriction (EIB) is a common issue among athletes, impacting their performance and well-being. The prevalence rates vary based on the sport, training environment, and genetics. Exercise is a known trigger for asthma, but paradoxically, it can also improve pulmonary function and alleviate EIB severity. However, athletes' asthma phenotypes differ, leading to varied responses to medications and challenges in management. The unique aspects in athletes include heightened airway sensitivity, allergen, pollutant exposure, and temperature variations. This review addresses EIB in athletes, focusing on pathogenesis, diagnosis, and treatment. The pathogenesis of EIB involves complex interactions between physiological and environmental factors. Airway dehydration and cooling are key mechanisms, leading to osmotic and thermal theories. Airway inflammation and hyper-responsiveness are common factors. Elite athletes often exhibit distinct inflammatory responses and heightened airway sensitivity, influenced by sport type, training, and environment. Swimming and certain sports pose higher EIB risks, with chlorine exposure in pools being a notable factor. Immune responses, lung function changes, and individual variations contribute to EIB in athletes. Diagnosing EIB in athletes requires objective testing, as baseline lung function tests can yield normal results. Both EIB with asthma (EIBA) and without asthma (EIBwA) must be considered. Exercise and indirect bronchoprovocation tests provide reliable diagnoses. In athletes, exercise tests offer effectiveness in diagnosing EIB. Spirometry and bronchodilation tests are standard approaches, but the diagnostic emphasis is shifting toward provocation tests. Despite its challenges, achieving an optimal diagnosis of EIA constitutes the cornerstone for effective management, leading to improved performance, reduced risk of complications, and enhanced quality of life. The management of EIB in athletes aligns with the general principles for symptom control, prevention, and reducing complications. Non-pharmacological approaches, including trigger avoidance and warming up, are essential. Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. Leukotriene receptor antagonists (LTRA) and mast cell stabilizing agents (MCSA) are potential options. Optimal management improves the athletes' quality of life and allows them to pursue competitive sports effectively.

Serum proteomics identifies novel diagnostic biomarkers for asthma in preschool children.

Asthma is characterized by airway hyperresponsiveness, reversible airway obstruction, and chronic airway inflammation. It is the most common chronic disease in childhood. However, the diagnosis of childhood asthma remains challenging, and there is an urgent need to develop new diagnostic methods. To identify biomarkers of asthma in children, we adopted the Orbitrap-based data-independent acquisition (DIA) mass spectrometry proteomics method to analyze the serum proteomic signatures of children with acute asthma and convalescent children. We identified 747 proteins in 46 serum samples and 50 differentially expressed proteins (DEPs) that distinguished between asthmatic and healthy children. Next, functional enrichment analysis of the DEPs was conducted, it was indicated that the DEPs were significantly enriched in immune-related and function terms and pathways. Furthermore, we performed statistical analysis and identified MMP14, ABHD12B, PCYOX1, LTBP1, CFHR4, APOA1, IGHG4, ANG and IGFALS proteins as the diagnostic biomarker candidates. Ultimately, a promising asthma diagnostic model for preschool children based on IGFALS was built and evaluated. The area under the curve (AUC) of the IGFALS model was 0.959. In this study, the DIA proteome strategy was used and the largest number of proteins of asthmatic children serum proteomics was identified. The proteomics results showed that the DEPs play the central role of the inflammation-immune mechanism in asthma pathogenesis, suggesting that these proteins may be used in asthma diagnosis, prognosis, or therapy, and suggested biomarkers for asthma of preschool children. In conclusion, our results provide insight into the pathophysiology of asthma. We believe that the diagnostic model will facilitate clinical decision-making regarding asthma in preschool children.