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Background: Ambient PM2.5 is associated with asthma exacerbation. The association between the concentration of PM2.5 and the severity of asthma exacerbation has yet to be thoroughly clarified. The study aims to explore the association between the piror 30 days average concentration of PM2.5 and the severity of acute asthma exacerbation in hospitalized children., Methods: A total of 269 children with acute exacerbation of asthma were enrolled and divided into three groups according to the PM2.5 exposure concentrations: group 1 (PM2.5: <37.5 μg/m 3 ), group 2 (PM2.5: 37.5-75 μg/m 3 ), group 3 (PM2.5: ≥75 μg/m 3 ), respectively. The ordered logistic regression modeling was conducted to explore the influence of daily PM2.5 concentration on the clinical severity of children's asthma exacerbation. Multiple linear regression was conducted to explore the association between the concentration of PM2.5 and the length of stay in the hospital (LOS). We also conducted a receiver operating characteristic (ROC) curve analysis to explore the cutoff value of PM2.5 to predict the children's asthma exacerbation., Results: There was no statistical difference among the three groups of children in gender, age, body mass index, ethnicity, the first diagnosis of asthma, allergic history, passive smoke exposure, or family history of asthma. There was a statistically significant difference in many hospitalization characteristics (p < 0.05) among the three groups of children. Significant differences were found in terms of accessory muscles of respiration (p = 0.005), respiratory failure (p = 0.012), low respiratory tract infectious (p = 0.020), and the severity of asthma exacerbation (p < 0.001) among the three groups. PM2.5 concentration was primarily positively correlated to neutrophile inflammation. The ordered multivariate logistic regression model showed that higher PM2.5 concentrations were significantly associated with greater odds of more severe asthma exacerbation in one and two-pollutant models. The adjusted odds ratio of severe asthma exacerbation was 1.029 (1.009, 1.049) in the one-pollutant model. The most significant odds ratio of severe asthma exacerbation was 1.050 (1.027, 1.073) when controlling NO 2 in the two-pollutant models. Multiple linear regression showed that PM2.5 concentration was significantly associated with longer LOS in both one-pollutant and two-pollutant models. By performing ROC analysis, the average daily concentration of 44.5 µg/m 3 of PM2.5 (AUC = 0.622, p = 0.002) provided the best performance to predict severe asthma of children exacerbation with a sensitivity of 59.2% and a specificity of 63.8%., Conclusion: The increased prior 30 days average concentration of PM2.5 was associated with greater asthma exacerbation severity and longer length of stay in the hospital of children with asthma exacerbation., (© 2023 Wiley Periodicals LLC.)

Background: Small airways are the major sites of inflammation and airway remodeling in all severities of asthma patients. However, whether small airway function parameters could reflect the airway dysfunction feature in preschool asthmatic children remain unclear. We aim to investigate the role of small airway function parameters in evaluating airway dysfunction, airflow limitation and airway hyperresponsiveness (AHR)., Methods: Eight hundred and fifty-one preschool children diagnosed with asthma were enrolled retrospectively to investigate the characteristics of small airway function parameters. Curve estimation analysis was applied to clarify the correlation between small and large airway dysfunction. Spearman's correlation and receiver-operating characteristic (ROC) curves were employed to evaluate the relationship between small airway dysfunction (SAD) and AHR., Results: The prevalence of SAD was 19.5% (166 of 851) in this cross-sectional cohort study. Small airway function parameters (FEF25-75%, FEF50%, FEF75%) showed strong correlations with FEV 1 % (r = 0.670, 0.658, 0.609, p<0.001, respectively), FEV 1 /FVC% (r = 0.812, 0.751, 0.871, p<0.001, respectively) and PEF% (r = 0.626, 0.635, 0.530, p<0.01, respectively). Moreover, small airway function parameters and large airway function parameters (FEV 1 %, FEV 1 /FVC%, PEF%) were curve-associated rather than linear-related (p<0.001). FEF25-75%, FEF50%, FEF75% and FEV 1 % demonstrated a positive correlation with PC 20 (r = 0.282, 0.291, 0.251, 0.224, p<0.001, respectively). Interestingly, FEF25-75% and FEF50% exhibited a higher correlation coefficient with PC 20 than FEV 1 % (0.282 vs. 0.224, p = 0.031 and 0.291 vs. 0.224, p = 0.014, respectively). ROC curve analysis for predicting moderate to severe AHR showed that the area under the curve (AUC) was 0.796, 0.783, 0.738, and 0.802 for FEF25-75%, FEF50%, FEF75%, and the combination of FEF25-75% and FEF75%, respectively. When Compared to children with normal lung function, patients with SAD were slightly older, more likely to have a family history of asthma and airflow obstruction with lower FEV 1 % and FEV 1 /FVC%, lower PEF% and more severe AHR with lower PC 20 ( all p<0.05)., Conclusion: Small airway dysfunction is highly correlated with large airway function impairment, severe airflow obstruction and AHR in preschool asthmatic children. Small airway function parameters should be utilized in the management of preschool asthma., (© 2023. The Author(s).)

Objective: To develop and validate a clinical prediction model to identify school-age asthma in preschool asthmatic children., Study Design: In this retrospective prognosis cohort study, asthmatic children aged 3-5 years were enrolled with at least 2 years of follow-up, and their potential variables at baseline and the prognosis of school-age asthma were collected from medical records. A clinical prediction model was developed using Logistic regression. The performance of prediction model was assessed and quantified by discrimination of the area under the receiver operating characteristic curve (AUC) and calibration of Brier score. The model was validated by the temporal-validation method., Results: In the development dataset, 2748 preschool asthmatic children were included for model development, and 883 (32.13%) children were translated to school-age asthma. The independent prognostic variables with an increased risk for school-age asthma were used to develop the prediction model, including: age, parental asthma, early frequent wheezing, allergic rhinitis, eczema, allergic conjunctivitis, obesity, and aeroallergen of dust mite. While assessing model performance, the discrimination power of AUC was moderate [0.788 (0.770-0.805)] with sensitivity (81.5%) and specificity (60.9%), and the calibration of Brier score was 0.169, supporting the calibration ability. In the temporal-validation dataset of 583 preschool asthmatic children, our model showed satisfactory discrimination (AUC 0.818) and calibration (Brier score 0.150). The prediction model was presented by the web-based calculator (https://casthma.shinyapps.io/dynnomapp/) and a nomogram for clinical application., Conclusion: In preschool asthmatic children, our prediction model could be used to predict the risk of school-age asthma., (© 2023 Wiley Periodicals LLC.)

Background: Predicting which preschool children with recurrent wheezing (RW) will develop school-age asthma (SA) is difficult, highlighting the critical need to clarify the pathogenesis of RW and the mechanistic relationship between RW and SA. Despite shared environmental exposures and genetic determinants, RW and SA are usually studied in isolation. Based on network analysis of nasal and tracheal transcriptomes, we aimed to identify convergent transcriptomic mechanisms in RW and SA., Methods: RNA-sequencing data from nasal and tracheal brushing samples were acquired from the Gene Expression Omnibus. Combined with single-cell transcriptome data, cell deconvolution was used to infer the composition of 18 cellular components within the airway. Consensus weighted gene co-expression network analysis was performed to identify consensus modules closely related to both RW and SA. Shared pathways underlying consensus modules between RW and SA were explored by enrichment analysis. Hub genes between RW and SA were identified using machine learning strategies and validated using external datasets and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Finally, the potential value of hub genes in defining RW subsets was determined using nasal and tracheal transcriptome data., Results: Co-expression network analysis revealed similarities in the transcriptional networks of RW and SA in the upper and lower airways. Cell deconvolution analysis revealed an increase in mast cell fraction but decrease in club cell fraction in both RW and SA airways compared to controls. Consensus network analysis identified two consensus modules highly associated with both RW and SA. Enrichment analysis of the two consensus modules indicated that fatty acid metabolism-related pathways were shared key signals between RW and SA. Furthermore, machine learning strategies identified five hub genes, i.e., CST1, CST2, CST4, POSTN, and NRTK2, with the up-regulated hub genes in RW and SA validated using three independent external datasets and qRT-PCR. The gene signatures of the five hub genes could potentially be used to determine type 2 (T2)-high and T2-low subsets in preschoolers with RW., Conclusions: These findings improve our understanding of the molecular pathogenesis of RW and provide a rationale for future exploration of the mechanistic relationship between RW and SA., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wang, He, Li, Zhao, Zhang and Luo.)

We performed a systematic review and meta-analysis to investigate the effects of vitamin D (VitD) supplementation on children with allergic diseases. MEDLINE, Embase, Web of Science, the Cochrane library, and three Chinese databases were searched up to 15 August 2022. Randomized controlled trials (RCTs) comparing a VitD supplementation versus a placebo for children with allergic diseases were included. Thirty-two RCTs with 2347 participants were included. VitD supplementation did not reduce the risk of asthma exacerbations in children compared with placebo overall (risk ratio (RR) = 0.84, 95% confidence interval (CI): 0.65 to 1.08, p = 0.18), but reduced the risk of asthma exacerbation in children with baseline serum 25(OH)D of <10 ng/mL compared with placebo (RR = 0.48, 95% CI: 0.28 to 0.83, p = 0.009). VitD supplementation significantly reduced Scoring Atopic Dermatitis or the Eczema Area and Severity Index scores in children with atopic dermatitis compared with placebo (standard mean difference = −0.5, 95% CI: −0.87 to −0.12, p = 0.009). VitD supplementation also reduced the symptom-medication score in children with allergic rhinitis compared with placebo (mean (standard deviation): 43.7 (3.3) vs. 57.8 (4.4), p = 0.001). In conclusion, VitD supplementation did not reduce asthma exacerbation risk in children overall but may reduce asthma exacerbation risk in children with serum 25(OH)D concentration < 10 ng/mL. VitD supplementation reduces the severity of atopic dermatitis and symptoms of allergic rhinitis in children.

Objective: The study aimed to determine if and how environmental factors correlated with asthma admission rates in geographically different parts of Guangxi province in China., Setting: Guangxi, China., Participants: This study was done among 7804 asthma patients., Primary and Secondary Outcome Measures: Spearman correlation coefficient was used to estimate correlation between environmental factors and asthma hospitalisation rates in multiple regions. Generalised additive model (GAM) with Poisson regression was used to estimate effects of environmental factors on asthma hospitalisation rates in 14 regions of Guangxi., Results: The strongest effect of carbon monoxide (CO) was found on lag1 in Hechi, and every 10 µg/m 3 increase of CO caused an increase of 25.6% in asthma hospitalisation rate (RR 1.26, 95% CI 1.02 to 1.55). According to the correlation analysis, asthma hospitalisations were related to the daily temperature, daily range of temperature, CO, nitrogen dioxide (NO 2 ) and particulate matter (PM 2.5 ) in multiple regions. According to the result of GAM, the adjusted R 2 was high in Beihai and Nanning, with values of 0.29 and 0.21, which means that environmental factors are powerful in explaining changes of asthma hospitalisation rates in Beihai and Nanning., Conclusion: Asthma hospitalisation rate was significantly and more strongly associated with CO than with NO 2 , SO 2 or PM 2.5 in Guangxi. The risk factors of asthma exacerbations were not consistent in different regions, indicating that targeted measures should differ between regions., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Asthma is a major public health concern throughout the world. Numerous researches have shown that the spatial-temporal patterns of asthma are inconsistent, leading to the suggestion that these patterns are determined by multiple factors. This study aims to detect spatial-temporal clusters of asthma and analyze socio-ecological factors associated with the asthma hospitalization rate in Guangxi, China., Methods: Asthma hospitalization and socio-ecological data for 88 counties/municipal districts in Guangxi, China in 2015 was collected. Space-time scan statistics were applied to identify the high-risk periods and areas of asthma hospital admissions. We further used GeoDetector and Spearman correlation coefficient to investigate the socio-ecological factors associated with the asthma hospitalization rates., Results: There were a total of 7804 asthma admissions in 2015. The high-risk period was from April to June. The age groups of 0-4 and ≥65 years were both at the highest risk, with hospital admission rates of 45.0/10 5 and 46.5/10 5 , respectively. High-risk areas were found in central and western Guangxi with relative risk (RR) values of asthma hospitalizations greater than 2.0. GDP per capita and altitude were positively associated with asthma hospitalizations, while air pressure and wind speed had a negative association. The explanatory powers of these factors (i.e., GDP per capita, altitude, air pressure, wind speed) were 22%, 20%, 14% and 10%, respectively., Conclusions: The GDP per capita appears to have the strongest correlation with asthma hospitalization rates. High-risk areas were identified in central and western Guangxi characterized by high GDP per capita. These findings may be helpful for authorities developing targeted asthma prevention policies for high-risk areas and vulnerable populations, especially during high-risk periods., Competing Interests: Declaration of competing interest Authors have no conflict of interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Studies demonstrated that pneumonia can decrease vitamin A productions and vitamin A reduction/deficiency may promote asthma development. Our previous study showed that neonatal Streptococcus pneumoniae (S. pneumoniae) infection promoted asthma development. Whether neonatal S. pneumoniae pneumonia induced asthma was associated with vitamin A levels remains unclear. The aim of this study was to investigate the effects of neonatal S. pneumoniae pneumonia on vitamin A expressions, to explore the effects of vitamin A supplement after neonatal S. pneumoniae pneumonia on adulthood asthma development. Non-lethal S. pneumoniae pneumonia was established by intranasal inoculation of neonatal (1-week-old) female BALB/c mice with D39. S. pneumoniae pneumonia mice were supplemented with or without all-trans retinoic acid 24 hours after infection. Vitamin A concentrations in lung, serum and liver were measured post pneumonia until early adulthood. Four weeks after pneumonia, mice were sensitized and challenged with OVA to induce allergic airway disease (AAD). Twenty-four hours after the final challenge, the lungs and bronchoalveolar lavage fluid (BALF) were collected to assess AAD. We stated that serum vitamin A levels in neonatal S. pneumoniae pneumonia mice were lower than 0.7µmol/L from day 2-7 post infection, while pulmonary vitamin A productions were significantly lower than those in the control mice from day 7-28 post infection. Vitamin A supplement after neonatal S. pneumoniae pneumonia significantly promoted Foxp3 + Treg and Th1 productions, decreased Th2 and Th17 cells expressions, alleviated airway hyperresponsiveness (AHR) and inflammatory cells infiltration during AAD. Our data suggest that neonatal S. pneumoniae pneumonia induce serum vitamin A deficiency and long-time lung vitamin A reduction, vitamin A supplement after neonatal S. pneumoniae pneumonia inhibit the progression of asthma by altering CD4 + T cell subsets.

Background: Air pollution is a major cause of asthma exacerbation. Most studies have shown that exposure to coarse and fine particulate matter is associated with asthma exacerbation. Ultrafine particles (UFPs, aerodynamic diameter ≤ 0.1 µm) are the smallest airborne particles, which are capable of penetrating deep into the lungs. Toxicological studies have suggested that exposure to UFPs may have serious effects on respiratory health. However, epidemiological evidence on the effects of UFPs exposure on asthma exacerbation in children remains unclear., Objective: We conducted a meta-analysis to quantitatively assess the effects of exposure to UFPs on childhood asthma exacerbation., Methods: We searched four databases for epidemiological studies published until March 20, 2018. Pooled Odds Ratios (OR) and 95% confidence intervals (95% CIs) per 10000 particles/cm3 were estimated using fixed-effect models. Subgroup analyses, sensitivity analyses, and Begg's and Egger's regression were also performed., Results: Eight moderate-high quality studies with 51542 events in total satisfied the inclusion criteria. Exposure to UFPs showed a positive association with childhood asthma exacerbation [OR (95% CI): 1.070 (1.037, 1.104)], increased asthma-associated emergency department visits [OR (95% CI): 1.111 (1.055, 1.170)], and asthma-associated hospital admissions [OR (95% CI): 1.045 (1.004, 1.088)] and had a stronger association with childhood asthma exacerbation at long lags [OR (95% CI):1.060 (1.039, 1.082)]. A low heterogeneity and no publication bias were detected., Conclusion: Exposure to UFPs may increase the risk of asthma exacerbation and may be strongly associated with childhood asthma exacerbation at long lags., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model. [ABSTRACT FROM AUTHOR]

Background: A growing body of evidence shows that childhood wheezing may lead to recurrent or persistent symptoms in adulthood, such that persistent wheezing associated with lung function deficits often have their roots in the first few years of life. Objectives: We summarized information from several prospective cohort studies following children with or without wheezing into adulthood, to estimate the effect of childhood wheezing on adulthood lung function. Methods: Medical literatures were searched in the Medline, PubMed, ScienceDirect, Web of Science and Embase databases up to October 31, 2016. The adulthood lung function was selected as primary outcome, and chronic obstructive pulmonary disease (COPD) prevalence was selected as secondary outcome. The meta-analysis was performed with the Stata Version 14.0. A random-effects model was applied to estimate standardized mean difference (SMD) of lung function, and relative risk (RR) of COPD. Results: Six articles enrolling 1141 and 1005 children with and without wheezing, respectively. Meta-analysis showed that childhood wheezing decreased adulthood lung function as compared with no-wheezing subjects (SMD = -0.365, 95% confidence interval (CI): -0.569~-0.161, P = 0.000). Subgroup analyses indicated that childhood atopic wheezing reduced adulthood FEV1/FVC and FEV1%pred when compared with no-wheezing subjects. In addition, childhood atopic wheezing was significantly associated with COPD prevalence (RR = 5.307, 95% CI:1.033~27.271, P = 0.046). Conclusions: Our meta-analysis suggests that childhood wheezing may induce ongoing declined lung function that extends into adult life, as well as an increased risk of COPD prevalence when accompanied with atopy. [ABSTRACT FROM AUTHOR]