Author Correction: S100A9 in adult asthmatic patients: a biomarker for neutrophilic asthma.
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ABSTRACT:
SUBMITTER: Quoc QL
PROVIDER: S-EPMC9440014 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
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Author Correction: S100A9 in adult asthmatic patients: a biomarker for neutrophilic asthma.
Quoc Quang Luu QL Choi Youngwoo Y Thi Bich Tra Cao TC Yang Eun-Mi EM Shin Yoo Seob YS Park Hae-Sim HS
Experimental & molecular medicine 20220801 8
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Project description:The biomarkers and therapeutic targets of neutrophilic asthma (NA) are poorly understood. Although S100 calcium-binding protein A9 (S100A9) has been shown to correlate with neutrophil activation, its role in asthma pathogenesis has not been clarified. This study investigated the mechanism by which S100A9 is involved in neutrophil activation, neutrophil extracellular trap (NET)-induced airway inflammation, and macrophage polarization in NA. The S100A9 levels (by ELISA) in sera/culture supernatant of peripheral blood neutrophils (PBNs) and M0 macrophages from asthmatic patients were measured and compared to those of healthy controls (HCs). The function of S100A9 was evaluated using airway epithelial cells (AECs) and PBNs/M0 macrophages from asthmatic patients, as well as a mouse asthma model. The serum levels of S100A9 were higher in NA patients than in non-NA patients, and there was a positive correlation between serum S100A9 levels and sputum neutrophil counts (r = 0.340, P = 0.005). Asthmatic patients with higher S100A9 levels had lower PC20 methacholine values and a higher prevalence of severe asthma (SA) (P < .050). PBNs/M0 macrophages from SA released more S100A9 than those from non-SA patients. PBNs from asthmatic patients induced S100A9 production by AECs, which further activated AECs via the extracellular signal-regulated kinase (ERK) pathway, stimulated NET formation, and induced M1 macrophage polarization. Higher S100A9 levels in sera, bronchoalveolar lavage fluid, and lung tissues were observed in the mouse model of NA but not in the other mouse models. These results suggest that S100A9 is a potential serum biomarker and therapeutic target for NA.
| S-EPMC8333352 | biostudies-literature
Project description:PurposeWe evaluated the role of serum amyloid A1 (SAA1) in the pathogenesis of airway inflammation according to the phenotype of asthma.MethodsOne hundred twenty-two asthmatic patients and 60 healthy control subjects (HCs) were enrolled to measure SAA1 levels. The production of SAA1 from airway epithelial cells (AECs) and its effects on macrophages and neutrophils were investigated in vitro and in vivo.ResultsThe SAA1 levels were significantly higher in sera of asthmatic patients than in those of HCs (P = 0.014); among asthmatics, patients with neutrophilic asthma (NA) showed significantly higher SAA1 levels than those with non-NA (P < 0.001). In vitro, polyinosinic:polycytidylic acid (Poly I-C) treatment markedly enhanced the production of SAA1 from AECs, which was further augmented by neutrophils; SAA1 could induce the production of interleukin (IL)-6, IL-8, and S100 calcium-binding protein A9 from AECs. Additionally, SAA1 activated neutrophils and macrophages isolated from peripheral blood of asthmatics, releasing neutrophil extracellular traps (NETs) and secreting proinflammatory cytokines presenting M1 phenotype, respectively. In ovalbumin-induced asthma mice, Poly I-C treatment significantly increased SAA1 levels as well as IL-17A/interferon-gamma/IL-33 levels in bronchoalveolar lavage fluid (BALF), leading to airway hyperresponsiveness and inflammation. The highest levels of SAA1 and neutrophilia were noted in the BALF and sera of the NA mouse model, followed by the mixed granulocytic asthma (MA) model. Especially, SAA1 induced IL-17/retinoic acid receptor-related orphan receptor γt expression from activated CD4+ T lymphocytes in asthmatic mice.ConclusionsThe results show that SAA1 could induce neutrophilic airway inflammation by activating neutrophils along with NET formation, M1 macrophages, and Th2/Th17 predominant cells, contributing to the phenotype of NA or MA.
| S-EPMC8724823 | biostudies-literature
Project description:ObjectiveAsthma is a major public health problem worldwide. Despite various attempts, it is still uncontrolled in most parts of the world. Moreover, it is contributing to the national and global burden of non-communicable diseases. Studying factors associated with uncontrolled asthma in different parts of Ethiopia is crucial to control the disease and improving the quality of life of asthmatic patients. Thus, this study aimed to determine the factors associated with uncontrolled asthma among adult asthmatic patients in Eastern Ethiopia.MethodsFacility-based cross-sectional study was employed from 1st October 2020 to 30th January 2021. A total of 416 adult asthmatic patients participated in the study from six hospitals follow-up clinics. Asthma control test was used to assess the participants level of asthma control and a score of ⩽19 were regarded to have uncontrolled asthma. Data were analyzed using SPSS version 24. Bivariable and multivariable analyses were carried out to identify factors associated with uncontrolled asthma and variables with a p value of less than 0.05 were considered statistically significant.ResultThe prevalence of uncontrolled asthma was 66.1 % (95% confidence interval: 61.5-70.4). Not attending scheduled medical follow-up (adjusted odds ratio: 2.54; 95% confidence interval: 1.28-4.99), poor knowledge about asthma (adjusted odds ratio = 4.59; 95% confidence interval: 2.01-10.51), negative attitude toward asthma (adjusted odds ratio = 3.72; 95% confidence interval: 1.83-7.59), and poor adherence to medications (adjusted odds ratio = 2.53; 95% confidence interval: 1.25-5.13) were significantly associated with uncontrolled asthma.ConclusionIn this study, the prevalence of uncontrolled asthma was considerably high. Not attending scheduled medical follow-up, poor knowledge about asthma, negative attitude toward asthma, and poor adherence to anti-asthma medications were associated with uncontrolled asthma. Therefore, it is crucial to focus on increasing the patients' level of awareness about asthma control, improving medication adherence, and avoiding triggering factors.
| S-EPMC9583198 | biostudies-literature
Project description:BackgroundThe evaluation of asthma symptoms is a core outcome measure in asthma clinical research. The Asthma Symptom Utility Index (ASUI) was developed to assess the frequency and severity of asthma symptoms. The psychometric properties of the ASUI are not well characterized, and a minimal important difference (MID) is not established.ObjectivesWe assessed the reliability, validity, and responsiveness to change of the ASUI in a population of adult asthmatic patients. We also sought to determine the MID for the ASUI.MethodsAdult asthmatic patients (n = 1648) from 2 previously completed multicenter randomized trials were included. Demographic information, spirometric results, ASUI scores, and other asthma questionnaire scores were obtained at baseline and during follow-up visits. Participants also kept a daily asthma diary.ResultsThe internal consistency reliability of the ASUI was 0.74 (Cronbach α). Test-retest reliability was 0.76 (intraclass correlation). Construct validity was demonstrated by significant correlations between ASUI scores and Asthma Control Questionnaire scores (Spearman correlation r = -0.79; 95% CI, -0.85 to -0.75; P < .001) and Mini Asthma Quality of Life Questionnaire scores (r = 0.59; 95% CI, 0.51-0.61; P < .001). Responsiveness to change was demonstrated, with significant differences between mean changes in ASUI scores across groups of participants differing by 10% in percent predicted FEV(1) (P < .001) and by 0.5 points in Asthma Control Questionnaire scores (P < .001). Anchor-based and statistical methods support an MID for the ASUI of 0.09 points.ConclusionsThe ASUI is reliable, valid, and responsive to changes in asthma control over time. The MID of the ASUI (range of scores, 0-1) is 0.09.
| S-EPMC3501248 | biostudies-literature
Project description:Long non-coding RNA (lncRNA) are known to be important in many diseases. There has been some reports that lncRNA take part in the pathogenesis of systemic inflammation of asthma. lncRNA regulates gene transcription, protein expression and epigenetic regulation. However, the lncRNAs associated with differently airway phenotype such as eosinophilic and neutrophilic asthma remains unknown. We aimed at identifying the differences in circulating lncRNA signature in Eos and Neu samples. lncRNA expression were studied between blood samples from Eos patients, Neu patients and healthy individuals (Control). Bioinformatic analysis was used to describe relevant biological pathways. Using quantitative real-time PCR, lncRNA expression was measured. Comparing with Control samples, Eos sample has 190 own lncRNA and Neu sample has 166 own lncRNA(difference ≥ 2-fold). KEGG pathway annotation data and GO terms revealed that several lncRNAs are possibly associated with respective phenotype. lncRNA was identifying to differ significantly between Eos and Neu samples by using qRT-PCR. The results show us that lncRNA may be involved in different phenotypes of asthma. Whether we can recognize different phenotypes of asthma through these lncRNA (as biomarkers) needs further study.
2019-04-09 | GSE117038 | GEO
Project description:Background/aimsRole of autophagy in neutrophil function and the association of autophagy and autophagy related (ATG) gene polymorphisms with asthma susceptibility were suggested. In this study, we investigated the genetic association of ATG5 and ATG7 polymorphisms with asthma risk, severity and neutrophilic airway inflammation.MethodsWe recruited 408 asthma patients and 201 healthy controls. Sputum neutrophil counts were determined by H&E staining. Serum interleukin 8 (IL-8) levels were measured by enzyme-linked immunosorbent assay (ELISA). Genetic polymorphisms of ATG5 (-769T>C, -335G>A, and 8830C>T) and ATG7 (-100A>G and 25108G>C) were genotyped. The functional activities of ATG5 -769T>C and -335G>A variants were investigated by luciferase reporter assays.ResultsNo associations of ATG5 and ATG7 polymorphisms with asthma susceptibility and severity were found. ATG5 -769T>C and -335G>A were in complete linkage disequilibrium. In the asthma group, GA/AA genotypes at ATG5 -335G>A were associated with higher neutrophil counts in sputum (p < 0.05); CC/TT genotype at ATG5 8830C>T associated with lower FEV1% predicted value (p < 0.05). DNA fragments containing ATG5 -769T and -335G alleles had higher promoter activities compared to those with -769C and -335A in both human airway epithelial cells (A549, p < 0.01) and human mast cell (HMC-1, p < 0.001). GG and CC genotype at ATG7 -100A>G and 25108G>C were significantly associated with high serum levels of IL-8 (p < 0.05 for both variants).ConclusionsGenetic polymorphisms of ATG5 and ATG7 could contribute to neutrophilic airway inflammation in the pathogenesis of adult asthma.
| S-EPMC4773719 | biostudies-literature
Project description:IntroductionAdherence to anti-asthmatic medications plays a vital role in enhancing an asthma patient's quality of life and prognosis. However, in Ethiopia, the level of adherence and contributing factors were rarely studied. Therefore, this study was conducted to determine the level of adherence to anti-asthma medications and associated factors among adult asthmatic patients in Eastern Ethiopia.MethodInstitutional based cross-sectional study was conducted at six governmental hospitals found in Eastern Ethiopia. A total of 320 asthma patients aged 18 years and above and using asthma medicines for at least 12 months were involved. An interviewer based structured questionnaires were used to collect the data. Bivariable and multivariable logistic regression analyses were carried out using IBM SPSS version 22 (SPSS, Chicago, IL). The Adjusted Odds Ratio (AOR) with 95% Confidence Interval (CI) was used to determine the strength of association between independent variables and outcome variable. Variables with a p-value of ≤ 0.05 were considered statistically significant.ResultOf the 320 asthma patients that participated in the study, 109(34.1%:28.8-39.1%) of them had good adherence to anti-asthmatic medications. Being a housewife (AOR = 4.265, 95%CI: 1.333, 13.653), having good knowledge about asthma (AOR = 2.921, 95%CI (1.472, 5.795), positive attitude towards asthma (AOR = 3.129, 95%CI: 1.555, 6.293), and use of oral corticosteroid drugs (AOR = 1.967, 95%CI: 1.008, 3.841) were factors positively associated with good adherence to anti-asthmatic medications. Participants on treatment for 2-3 years (AOR = .295, 95%CI: 0.099, 0.873), and those on medication for ≥ 4 years (AOR = 0.229, 95%CI: 0.079, 0.664) were 70.5% and 77.1% times less likely to adhere to anti-asthmatic medications respectively.ConclusionThe current study signified a low level of adherence to anti-asthmatic medications. Participant's characteristics and medication related factors were significantly associated with good adherence to anti-asthmatic medications. Health education and advice during follow-up for asthma patients is crucial for better adherence.
| S-EPMC9731407 | biostudies-literature
Project description:IntroductionAcute asthma attack is one of the most common causes of visits to hospital emergency departments in all age groups of the population and accounts for the greater part of healthcare burden from the disease. Despite, Acute asthma attack is an important public health problem that affects not only the patients, but also to the family, health professionals, health care institutions and development of the nation, little is known about the risk factors of acute asthma attack.Therefore, this study is aimed to investigate the determinants of acute asthma attack among.ObjectiveThe aim of this study was to assess the determinant factors of acute asthma attack among adult asthmatic patients visiting general hospitals of central zone, Tigray, Ethiopia, 2019.MethodHospital based unmatched case control study design was conducted in general hospitals of central zone of Tigray, Ethiopia 2019. Data were collected using pretested interviewer administered questionnaire. A total of 289 study subjects (96 cases &193 controls) were selected by systematic random sampling. Data were entered to Epi data version 3.1 then exported to SPSS version 23 for analysis. Bivariate logistic regression was employed to examine the statistical association between dependent and independent variables. Variables with p value < 0.25 in binary logistic regression were entered to multivariable logistic regression model and variables with p value < 0.05 was taken as significant determinants of the outcome variable.ResultA total of 96 adult asthmatic patients who have acute asthma attack (cases) and 193 adult asthmatic patients without attack (controls)) with 100% response rate were participated in this study. Upper Respiratory tract Infection [AOR = 6.835,95% CI = 3.285,14.222], Season [AOR =2.204,95% CI = 1.011,4.805] kitchen smoke [AOR = 2.307,95%CI1.010,5.272]& sleep apnea [AOR = 9.254, 5%CI =3.563,25.460] were significantly associated with acute asthma exacerbation.
| S-EPMC7118945 | biostudies-literature
Project description: Not available
| S-EPMC9530212 | biostudies-literature
Project description:In asthma, most of the identified biomarkers pertain to the Th2 phenotype and no known biomarkers have been verified for severe asthmatics. Therefore, identifying biomarkers using the integrative phenotype-genotype approach in severe asthma is needed. The study aims to identify novel biomarkers as genes or pathways representing the core drivers in asthma development, progression to the severe form, resistance to therapy, and tissue remodeling regardless of the sample cells or tissues examined. Comprehensive reanalysis of publicly available transcriptomic data that later was validated in vitro, and locally recruited patients were used to decipher the molecular basis of asthma. Our in-silicoanalysis revealed a total of 10 genes (GPRC5A, SFN, ABCA1, KRT8, TOP2A, SERPINE1, ANLN, MKI67, NEK2, and RRM2) related to cell cycle and proliferation to be deranged in the severe asthmatic bronchial epithelium and fibroblasts compared to their healthy counterparts. In vitro, RT qPCR results showed that (SERPINE1 and RRM2) were upregulated in severe asthmatic bronchial epithelium and fibroblasts, (SFN, ABCA1, TOP2A, SERPINE1, MKI67, and NEK2) were upregulated in asthmatic bronchial epithelium while (GPRC5A and KRT8) were upregulated only in asthmatic bronchial fibroblasts. Furthermore, MKI76, RRM2, and TOP2A were upregulated in Th2 high epithelium while GPRC5A, SFN, ABCA1 were upregulated in the blood of asthmatic patients. SFN, ABCA1 were higher, while MKI67 was lower in severe asthmatic with wheeze compared to nonasthmatics with wheezes. SERPINE1 and GPRC5A were downregulated in the blood of eosinophilic asthmatics, while RRM2 was upregulated in an acute attack of asthma. Validation of the gene expression in PBMC of locally recruited asthma patients showed that SERPINE1, GPRC5A, SFN, ABCA1, MKI67, and RRM2 were downregulated in severe uncontrolled asthma. We have identified a set of biologically crucial genes to the homeostasis of the lung and in asthma development and progression. This study can help us further understand the complex interplay between the transcriptomic data and the external factors which may deviate our understanding of asthma heterogeneity.
| S-EPMC8178351 | biostudies-literature