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Lower respiratory tract infections are often treated with antibiotics without evidence of clinically relevant bacterial disease. Serum calcitonin precursor concentrations, including procalcitonin, are raised in bacterial infections. We aimed to assess a procalcitonin-based therapeutic strategy to reduce antibiotic use in lower respiratory tract infections with a new rapid and sensitive assay. 243 patients admitted with suspected lower respiratory tract infections were randomly assigned standard care (standard group; n=119) or procalcitonin-guided treatment (procalcitonin group; n=124). On the basis of serum procalcitonin concentrations, use of antibiotics was more or less discouraged (<0·1 μg/L or <0·25 μg/L) or encouraged (≥;0·5 μg/L or ≥0·25 μg/L), respectively. Reevaluation was possible after 6–24 h in both groups. Primary endpoint was use of antibiotics and analysis was by intention to treat. Final diagnoses were pneumonia (n=87; 36%), acute exacerbation of chronic obstructive pulmonary disease (60; 25%), acute bronchitis (59; 24%), asthma (13; 5%), and other respiratory affections (24; 10%). Serological evidence of viral infection was recorded in 141 of 175 tested patients (81%). Bacterial cultures were positive from sputum in 51 (21%) and from blood in 16 (7%). In the procalcitonin group, the adjusted relative risk of antibiotic exposure was 0·49 (95% CI 0·44–0·55; p<0·0001) compared with the standard group. Antibiotic use was significantly reduced in all diagnostic subgroups. Clinical and laboratory outcome was similar in both groups and favourable in 235 (97%). Procalcitonin guidance substantially reduced antibiotic use in lower respiratory tract infections. Withholding antimicrobial treatment did not compromise outcome. In view of the current overuse of antimicrobial therapy in often self-limiting acute respiratory tract infections, treatment based on procalcitonin measurement could have important clinical and financial implications. Published online Feb 10, 2004. http://image.thelancet.com/extras/04art1162web.pdf

Background Previous research has demonstrated a notable increase in neutrophil counts among pediatric patients with plastic bronchitis (PB) associated with Mycoplasma pneumoniae pneumonia (MPP). However, the role of neutrophils in MPP-associated PB remains largely elusive. Methods This is a nested case-control study that enrolled patients diagnosed with MPP who underwent bronchoscopy in our department during the MPP pandemic from September 2023 to January 2024. We conducted an analysis of clinical characteristics, blood samples, bronchoalveolar lavage fluid (BALF), and cast specimens, correlating these factors with the development and outcomes of PB. Results Among the 557 patients with MPP included in the study, 21 (3.8%) developed PB. The peripheral neutrophil count was identified as an independent risk factor for PB (OR = 3.113 [95%CI 1.050–9.224], P  = 0.04) and exhibited strong predictive value for the condition (AUC = 0.885 [95%CI 0.796–0.975], P  < 0.001). Notably, there was a marked presence of neutrophil infiltration and neutrophil extracellular traps (NETs) formation in the blood, BALF, and cast samples from patients with PB. Furthermore, the levels of neutrophils and NETs correlated significantly with clinical outcomes. Conclusion A high level of neutrophils poses a risk for PB and demonstrates strong predictive value for its diagnosis. Neutrophils and NETs are closely linked to the clinical outcomes of PB in patients with MPP.

Background Refractory Mycoplasma pneumoniae pneumonia (RMPP) frequently leads to complications, including plastic bronchitis (PB). This study aimed to identify clinical risk factors for PB development in pediatric RMPP. Methods A total of 361 pediatric patients with RMPP underwent bronchoscopy intervention were divided into a PB group and a non-PB group. Clinical characteristics, laboratory parameters, and chest CT findings were evaluated. Univariate analysis was initially performed to identify potential risk factors of PB, followed by multivariate logistic regression analysis to determine independent predictors, with receiver operating characteristic (ROC) analysis assessing their predictive value. A scoring system for PB risk assessment was developed based on odds ratio (OR) values. Results PB patients showed significantly higher rates of extrapulmonary lesions (48.98% vs. 18.59%, p  < 0.001), pleural effusion (59.18% vs. 25.64%, p  < 0.001), and treatment resistance. Furthermore, PB patients demonstrated significantly elevated levels of neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), procalcitonin (PCT), erythrocyte sedimentation rate (ESR), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), D-dimer (DD), and pulmonary lesion volume ratio. Conversely, platelet count (PLT), prealbumin (PA), albumin (ALB), complement 3 (C3), complement 4 (C4), activated partial thromboplastin time (APTT), and the proportion of neutrophils in bronchial alveolar lavage fluid (BALF) were significantly lower compared to non-PB group (all P -values < 0.05). Multivariate analysis identified five independent predictors: NLR ≥ 3.30 (OR 2.92), LDH ≥ 451.0 U/L (OR 4.91), ALT ≥ 21.75 U/L (OR 5.68), pulmonary lesion volume ratio ≥ 8.23% (OR 8.83), and APTT ≤ 35.95s (OR 4.20). The combination of these predictors demonstrated strong diagnostic performance, with a sensitivity of 85.70%, specificity of 84.90%, and an area under the curve (AUC) of 0.92 for identifying PB cases. Using a scoring system based on ORs, we stratified 361 RMPP patients into risk groups: the high-risk group had 32 (60.38%) PB out of 53, the middle-risk group had 13 (22.02%) PB out of 59, and the low-risk group had 4 (1.61%) PB out of 249. Conclusions Elevated NLR, increased LDH, higher ALT, greater pulmonary lesion volume ratio, and reduced APTT were identified as independent risk factors for PB. Pulmonary lesion volume ratio combined with key laboratory markers may facilitate early risk stratification and clinical intervention for PB in pediatric RMPP.

Background Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction and loss of lung tissue mainly consisting of extracellular matrix (ECM). Three of the main ECM components are type I collagen, the main constituent in the interstitial matrix, type VI collagen, and elastin, the signature protein of the lungs. During pathological remodeling driven by inflammatory cells and proteases, fragments of these proteins are released into the bloodstream, where they may serve as biomarkers for disease phenotypes. The aim of this study was to investigate the lung ECM remodeling in healthy controls and COPD patients in the COPDGene study. Methods The COPDGene study recruited 10,300 COPD patients in 21 centers. A subset of 89 patients from one site (National Jewish Health), including 52 COPD patients, 12 never-smoker controls and 25 smokers without COPD controls, were studied for serum ECM biomarkers reflecting inflammation-driven type I and VI collagen breakdown (C1M and C6M, respectively), type VI collagen formation (Pro-C6), as well as elastin breakdown mediated by neutrophil elastase (EL-NE). Correlation of biomarkers with lung function, the SF-36 quality of life questionnaire, and other clinical characteristics was also performed. Results The circulating concentrations of biomarkers C6M, Pro-C6, and EL-NE were significantly elevated in COPD patients compared to never-smoking control patients (all p  < 0.05). EL-NE was significantly elevated in emphysema patients compared to smoking controls ( p  < 0.05) and never-smoking controls ( p  < 0.005), by more than 250%. C1M was inversely associated with forced expiratory volume in 1 s (FEV 1 ) ( r  = −0.344, p  = 0.001), as was EL-NE ( r  = −0.302, p  = 0.004) and Pro-C6 ( r  = −0.259, p  = 0.015). In the patients with COPD, Pro-C6 was correlated with percent predicted Forced Vital Capacity (FVC) ( r  = 0.281, p  = 0.046) and quality of life using SF-36. C6M and Pro-C6, were positively correlated with blood eosinophil numbers in COPD patients ( r  = 0.382, p  = 0.006 and r  = 0.351, p  = 0.012, respectively). Conclusions These data suggest that type VI collagen turnover and elastin degradation by neutrophil elastase are associated with COPD-induced inflammation (eosinophil-bronchitis) and emphysema. Serological assessment of type VI collagen and elastin turnover may assist in identification of phenotypes likely to be associated with progression and amenable to precision medicine for clinical trials.

This study evaluated serum eosinophil cationic protein (ECP) as a biomarker for pediatric allergic airway diseases. A cross-sectional analysis was performed on children (1–17 years) with allergic asthma (AA, n = 124), allergic rhinitis (AR, n = 74), acute bronchitis (AB, n = 72), and healthy controls (HC, n = 58). Serum ECP, total IgE, eosinophil counts, allergen sensitization, and lung function were measured. Diagnostic performance was assessed using receiver operating characteristic (ROC) curves, and correlations among biomarkers were examined. Compared with HC, serum ECP levels were significantly elevated across all disease groups (AA, AR, and AB), with a particularly marked difference observed between AA and AR patients (p < 0.0001). The combination of ECP and IgE significantly improved the diagnostic accuracy for AA (AUC = 0.9494) and AR (AUC = 0.9501). Higher ECP levels were associated with increased sensitization to specific inhalant allergens and impaired pulmonary function, particularly in small airway indices. Serum ECP reflects eosinophil-mediated airway inflammation and enhances diagnostic performance for pediatric AA and AR, supporting its role as an auxiliary biomarker in evaluating pediatric allergic airway diseases.

Hypovitaminosis D has been linked to several non-bone diseases. Relation between 25-hydroxyvitamin D [25(OH)D] and lung function and lung diseases has received little attention at the global level. Cross-sectional data from three National Health and Nutrition Examination Surveys, 2007–2008, 2009–2010, and 2011–2012 were used to investigate the relationship between serum 25(OH)D concentrations and lung function makers [forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1)] and lung diseases (asthma, emphysema, and chronic bronchitis) with multivariate regression models (n = 11,983; men, 6,010; women, 5,973). Serum 25(OH)D concentrations were directly associated with FVC and FEV1 (P for trend < 0.01). Individuals in the 4th quartile serum 25(OH)D had significantly higher FVC and FEV1 compared to those in the 1st quartile (P < 0.01). When data were stratified based on gender and smoking status, we found similar associations between serum 25(OH)D concentrations and lung function markers. There was no relation between serum 25(OH)D and prevalence of asthma, chronic bronchitis, and emphysema in US adults. Serum 25(OH)D concentration is associated with improved lung function markers but not with the prevalence of asthma, emphysema, and chronic bronchitis. Controlled studies are needed to determine if the vitamin D supplementation improves lung function in adults and in smokers.

Lower respiratory tract infections (LRTIs) remain the leading cause of infant morbidity and mortality worldwide and affect long-term respiratory health. Identifying immunological determinants of LRTI susceptibility may help stratify disease risk and identify therapies. This study aimed to identify neonatal immunological factors predicting LRTI risk in infancy. Cord blood plasma from 191 neonates from the Boston Birth Cohort was analyzed for 28 soluble immune factors. LRTI was defined as bronchiolitis, bronchitis, or pneumonia during the first year of life. Welch’s t-test demonstrated significantly higher log10 transformed concentrations of IL-17 and IFNγ in the LRTI group compared to neonates without LRTI in the first year of life (p < 0.05). Risk associations were determined using multivariate survival models. There were 29 infants with LRTIs. High cord blood levels of IFNγ (aHR = 2.35, 95% CI 1.07–5.17), TNF-β (aHR = 2.86, 95% CI 1.27–6.47), MIP-1α (aHR = 2.82, 95% CI 1.22–6.51), and MIP-1β (aHR = 2.34, 95% CI 1.05–5.20) were associated with a higher risk of LRTIs. RANTES was associated with a lower risk (aHR = 0.43, 95% CI 0.19–0.97). Soluble immune factors linked to antiviral immunity (IFNγ) and cytokines mediating inflammatory responses (TNF-β), and cell homing (MIP-1α/b), at birth were associated with an increased risk of LRTIs during infancy.

The objective was to evaluate the association between serum carotenoid levels and respiratory morbidity and mortality in a nationally representative sample of US adults. We assessed the association of serum carotenoid levels with respiratory morbidity and mortality using logistic regression and proportional hazards regression models. Meanwhile, a series of confounders were controlled in regression models and restricted cubic spline, which included age, sex, race, marriage, education, income, drinking, smoking, regular exercise, BMI, daily energy intake, vitamin E, vitamin C, fruit intake, vegetable intake, diabetes, hypertension, asthma, emphysema and chronic bronchitis. Compared with participants in the lowest tertiles, participants in the highest tertiles of serum total carotenoids, β-cryptoxanthin and lutein/zeaxanthin levels had a significantly lower prevalence of emphysema (ORtotal carotenoids = 0·61, 95% CI: 0·41–0·89, OR β-cryptoxanthin = 0·67, 95% CI: 0·49–0·92), chronic bronchitis (OR β-cryptoxanthin = 0·66, 95% CI: 0·50–0·87) and asthma (Q2: ORlutein/zeaxanthin = 0·78, 95% CI: 0·62–0·97); participants in the highest tertiles of total carotenoids, α-carotene, lutein/zeaxanthin and lycopene had a lower risk of respiratory mortality (hazard ratio (HR)total carotenoids = 0·62, 95% CI: 0·42–0·90, HR α-carotene = 0·54, 95% CI: 0·36–0·82, HRlutein/zeaxanthin = 0·48, 95% CI: 0·33–0·71, HRlycopene = 0·66, 95% CI: 0·45–0·96) than those in the lowest tertiles. Higher serum total carotenoids and β-cryptoxanthin levels is associated with decreased prevalence of emphysema and chronic bronchitis, and higher serum total carotenoids, α-carotene, lutein/zeaxanthin and lycopene levels had a lower mortality of respiratory disease.

Introduction: The global burden of chronic airway diseases represents an important public health concern. The role of oxidative stress and inflammation in the pathogenesis of these diseases is well known. The aim of this study is to evaluate the behavior of both inflammatory and oxidative stress biomarkers in patients with chronic bronchitis, current asthma and past asthma in the frame of a population-based study. Methods: For this purpose, data collected from the Gene Environment Interactions in Respiratory Diseases (GEIRD) Study, an Italian multicentre, multicase-control study, was evaluated. Cases and controls were identified through a two-stage screening process of individuals aged 20-65 years from the general population. Out of 16,569 subjects selected from the general population in the first stage of the survey, 2259 participated in the clinical evaluation. Oxidative stress biomarkers such as 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), 8-isoprostane and glutathione and inflammatory biomarkers such as Fractional Exhaled Nitric Oxide (FENO) and white blood cells were evaluated in 1878 subjects. Results: Current asthmatics presented higher levels of FENO (23.05 ppm), leucocytes (6770 n/µL), basophils (30.75 n/µL) and eosinophils (177.80 n/µL), while subjects with chronic bronchitis showed higher levels of GSH (0.29 mg/mL) and lymphocytes (2101.6 n/µL). The multivariable multinomial logistic regression confirmed high levels of leucocytes (RRR = 1.33), basophils (RRR = 1.48), eosinophils (RRR = 2.39), lymphocytes (RRR = 1.26) and FENO (RRR = 1.42) in subjects with current asthma. Subjects with past asthma had a statistically significant higher level of eosinophils (RRR = 1.78) with respect to controls. Subjects with chronic bronchitis were characterized by increased levels of eosinophils (RRR = 2.15), lymphocytes (RRR = 1.58), GSH (RRR = 2.23) and 8-isoprostane (RRR = 1.23). Conclusion: In our study, current asthmatics show a greater expression of the inflammatory profile compared to subjects who have had asthma in the past and chronic bronchitis. On the other hand, chronic bronchitis subjects showed a higher rate of expression of oxidative stress biomarkers compared to asthmatic subjects. In particular, inflammatory markers such as circulating inflammatory cells and FENO seem to be more specific for current asthma, while oxidative stress biomarkers such as glutathione and 8-isoprostane appear to be more specific and applicable to patients with chronic bronchitis.

Background Chronic bronchitis (CB), as a core precursor of Chronic Obstructive Pulmonary Disease (COPD), is crucial for global disease burden prevention and control. Although the association between heavy metal exposure and respiratory damage has been preliminarily demonstrated, traditional linear models are difficult to resolve the nonlinear interactions and dose–response heterogeneity. The aim of this study was to construct the first heavy metal exposure-chronic bronchitis risk prediction model by integrating exposureomics data through machine learning (ML). Methods Weighted logistic regression was used to assess the association of 14 blood and urine heavy metals with CB based on nationally representative samples from the 2005–2015 National Health and Nutrition Examination Survey (NHANES). The Boruta algorithm was further applied to screen the characteristic variables and construct 10 ML models. The best model was selected by four evaluation metrics: accuracy, specificity, sensitivity, and area under the ROC curve (AUC), and the best model was visually interpreted using Shapley's additive interpretation (SHAP). Results The multifactorial logistic regression model showed that urinary cadmium (OR = 1.53, 95% CI = 1.17–1.98) versus blood cadmium (OR = 1.36, 1.13–1.65) was an independent risk factor for CB. The CatBoost model had the best predictive performance (AUC = 0.805), with smoking as the most significant predictor, followed by blood cadmium concentration and gender. Conclusion In this research, the first risk prediction diagnostic model for heavy metal-chronic bronchitis was developed, in which CatBoost model had the best performance, and it provides a referenceable prediction model for the screening of high-risk groups.