Estimation of salivary Candida albicans counts in asthmatic adult patients taking anti-asthmatic medication for 3-5 years.
ABSTRACT: Background:Bronchial asthma is a chronic inflammatory disease of airways. The disease itself along with the principal medication used makes the oral cavity susceptible to most common opportunistic infection, i.e., oral candidiasis. There are many species of Candida causing oral candidiasis, but the most prevalent among them is Candida albicans. Hence, assessing C. albicans count in response to disease and its treatment is necessary. This enables us to educate asthma patients about side effects of medication and highlight the necessity for oral health care, thereby improving their quality of life. Aims:The present study aims to evaluate the effects of asthma and its medication on C. albicans count in saliva samples of asthmatic adult patients taking medication for 3-5 years and compare C. albicans count in saliva samples among cases and controls. Materials and Methods:Thirty asthmatic adults taking medication for asthma since 3-5 years' age ranging from 20 to 50 years and equal number of age- and sex-matched healthy participants were included in the study. In both groups, saliva was collected and inoculated on Sabouraud Dextrose Agar culture plates for estimation of C. albicans counts. C. albicans counts were assessed in colony-forming unit/milliliter. Statistical Analysis:Mann-Whitney U-test and Fisher's exact t-test were used. Results:The C. albicans count is significantly higher among asthmatics than healthy individuals. Conclusions:The present study concludes that there is increased candidal growth among asthmatics as compared to their normal healthy counterpart.
Project description:Objectives:To assess the association between different factors in saliva and dental caries experience in children with bronchial asthma. Materials and methods:A total of 60 asthmatic children and 60 healthy controls of both genders with age ranging from 4- to 12-year-old. The asthmatics were grouped according to disease severity into mild, moderate, or severe asthma. All the children were clinically examined to assess their dental caries experience (deft/DMFT), and stimulated saliva samples were collected to measure the saliva pH, flow rate, ?-amylase, and secretory immunoglobulin A (sIgA)-level changes. The data were statistically analyzed using the SPSS program (v. 23) to test for significance at p ? 0.05. Results:Asthmatic children presented significantly higher deft mean value (6.77 ± 1.69), as well as significantly reduced stimulated saliva flow (0.82 ± 0.2) and sIgA (29.42 ± 6.31) when compared to healthy control. The sIgA of asthmatics showed statistically significant negative correlation with deft and DMFT. Severe asthmatics presented significantly the lowest sIgA mean level (23.61 ± 5.33) and the most reduced saliva flow rate (0.64 ± 0.20). Conclusion:The reduction in saliva flow rate and secretory immunoglobulin A render asthmatic children more prone to increased dental caries progression mainly of primary dentition. How to cite this article:Arafa A, AlDahlawi S, Hussien A, et al. Impact of Secretory Immunoglobulin A Level on Dental Caries Experience in Asthmatic Children. Int J Clin Pediatr Dent 2019;12(5):414-418.
Project description:Exposure to fragranced consumer products, such as air fresheners and cleaning supplies, is associated with adverse health effects such as asthma attacks, breathing difficulties, and migraine headaches. This study investigated the prevalence and types of health problems associated with exposure to fragranced products among asthmatic Australians. Nationally representative cross-sectional data were obtained in June 2016 with an online survey of adult Australians (n?=?1098), of which 28.5% were medically diagnosed with asthma or an asthma-like condition. Nationally, 55.6% of asthmatics, and 23.9% of non-asthmatics, report adverse health effects after exposure to fragranced products. Specifically, 24.0% of asthmatics report an asthma attack. Moreover, 18.2% of asthmatics lost workdays or a job in the past year due to fragranced products in the workplace. Over 20% of asthmatics are unable to access public places and restrooms that use air fresheners. Exposure to fragranced products is associated with health problems, some potentially serious, in an estimated 2.2 million asthmatic adult Australians. Asthmatics were proportionately more affected than non-asthmatics (prevalence odds ratio 3.98; 95% confidence interval 3.01-5.24). Most asthmatics would prefer workplaces, healthcare facilities, and environments that are fragrance-free, which could help reduce adverse effects.
Project description:BACKGROUND:Adrenal suppression is a side effect of long-term use of inhaled corticosteroids (ICS). Hair cortisol concentration (HCC) measurement is a noninvasive tool for measuring adrenal function that may be useful for asthmatic patients who are on long-term ICS treatment. The aim of this study was to compare HCC between children with and without asthma and to explore the association between HCC and ICS dose in asthmatic children. METHODS:A cross-sectional observational study in subjects with or without asthma (n?=?72 and 226, respectively, age 6-21 years). Hair samples were obtained from the posterior vertex for each subject and data on medication use were collected using questionnaires. HCC was analyzed by liquid chromatography-mass spectrometry in the most proximal 3?cm of hair. RESULTS:Median HCC was significantly lower in subjects with asthma than in subjects without asthma: 1.83?pg/mg and 2.39?pg/mg, respectively (P value after adjustment for age, sex, and body mass index: .036). Median HCC was 1.98?pg/mg in asthmatics using no ICS, 1.84?pg/mg in those using a low dose, 1.75?pg/mg in those on a medium dose, and 1.46 in those using a high ICS dose (P?=?.54). CONCLUSION:We observed a significantly lower HCC in asthmatics than in healthy controls and a nonsignificant trend of lower HCC with increasing ICS dose. Whether HCC measurement may be used to detect individuals at risk for hypocortisolism and may be useful to monitor adrenal function in asthmatic children using ICS needs to be further investigated.
Project description:A rich microbial environment in infancy protects against asthma ,  and infections precipitate asthma exacerbations . We compared the airway microbiota at three levels in adult patients with asthma, the related condition of COPD, and controls. We also studied bronchial lavage from asthmatic children and controls.We identified 5,054 16S rRNA bacterial sequences from 43 subjects, detecting >70% of species present. The bronchial tree was not sterile, and contained a mean of 2,000 bacterial genomes per cm(2) surface sampled. Pathogenic Proteobacteria, particularly Haemophilus spp., were much more frequent in bronchi of adult asthmatics or patients with COPD than controls. We found similar highly significant increases in Proteobacteria in asthmatic children. Conversely, Bacteroidetes, particularly Prevotella spp., were more frequent in controls than adult or child asthmatics or COPD patients.The results show the bronchial tree to contain a characteristic microbiota, and suggest that this microbiota is disturbed in asthmatic airways.
Project description:Ghrelin is a peptide hormone with direct or indirect effects on obesity and asthma. More data are required to understand the effect of ghrelin on the control and pathogenesis of these diseases. The aim of this study was to evaluate ghrelin levels in selected groups of children to identify the association between serum ghrelin, obesity, and the severity of asthma. The study included 401 school children selected from the Najran area and grouped into non-obese asthmatics, obese asthmatics, obese non-asthmatics and controls (non-obese non-asthmatics). Blood levels of ghrelin, interleukin (IL)-4, IL-5 and IL-21 were determined by ELISA. The mean ghrelin values were insignificantly increased in obese children compared with non-obese children. The highest blood ghrelin values were in the non-obese asthmatic group. Serum ghrelin, IL-4 and IL-21 levels were significantly increased in asthmatic children compared with non-asthmatic children (p < 0.05), and there were significant positive correlations between ghrelin and IL-4, IL-5, and IL-21 in asthmatic children. Furthermore, ghrelin, IL-4, and IL-21 levels were significantly higher in uncontrolled asthmatics compared with controlled-asthmatic children (p < 0.05). Asthma was the only significant risk factor for high ghrelin values. This study provides evidence supporting the anti-inflammatory role of ghrelin in the pathogenesis of asthma. Asthma might be considered as an important determinant of high ghrelin values in children.
Project description:Member RAS oncogene family (RAB1A), a member of the RAS oncogene family, cycles between inactive GDP-bound and active GTP-bound forms regulating vesicle transport in exocytosis. Thus, functional alterations of the RAB1A gene may contribute to aspirin intolerance in asthmatic sufferers. To investigate the relationship between single-nucleotide polymorphisms (SNPs) in the RAB1A gene and aspirin-exacerbated respiratory disease (AERD), asthmatics (n=1197) were categorized into AERD and aspirin-tolerant asthma (ATA). All subjects were diagnosed as asthma on the basis of the Global Initiative for Asthma (GINA) guidelines. AERD was defined as asthmatics showing 15% or greater decreases in forced expiratory volume in one second (FEV(1)) or naso-ocular reactions by the oral acetyl salicylic acid (ASA) challenge (OAC) test. In total, eight SNPs were genotyped. Logistic regression analysis identified that the minor allele frequency of +14444 T>G and +41170 C>G was significantly higher in the AERD group (n=181) than in the ATA group (n=1016) (p=0.0003-0.03). Linear regression analysis revealed a strong association between the SNPs and the aspirin-induced decrease in FEV(1) (p=0.0004-0.004). The RAB1A gene may play a role in the development of AERD in asthmatics and the genetic polymorphisms of the gene have the potential to be used as an indicator of this disease.
Project description:The clinical response to inhaled corticosteroids (ICS) is associated with single nucleotide polymorphisms (SNPs) in various genes. This study aimed to relate variations in genes in the steroid pathway and asthma susceptibility genes to exacerbations in children and young adults treated with ICS.We performed a meta-analysis of three cohort studies: Pharmacogenetics of Asthma Medication in Children: Medication with Anti-Inflammatory effects (n = 357, age: 4-12 years, the Netherlands), BREATHE (n = 820, age: 3-22 years, UK) and Paediatric Asthma Gene Environment Study (n = 391, age: 2-16 years, UK). Seventeen genes were selected based on a role in the glucocorticoid signalling pathway or a reported association with asthma. Two outcome parameters were used to reflect exacerbations: hospital visits and oral corticosteroid (OCS) use in the previous year. The most significant associations were tested in three independent validation cohorts; the Childhood Asthma Management Programme (clinical trial, n = 172, age: 5-12 years, USA), the Genes- environment and Mixture in Latino Americans II- study (n = 745, age: 8-21, USA) and the Pharmacogenetics of adrenal suppression cohort (n = 391, age: 5-18, UK) to test the robustness of the findings. Finally, all results were meta-analysed.Two SNPs in ST13 (rs138335 and rs138337), but not in the other genes, were associated at a nominal level with an increased risk of exacerbations in asthmatics using ICS in the three cohorts studied. In a meta-analysis of all six studies, ST13 rs138335 remained associated with an increased risk of asthma-related hospital visits and OCS use in the previous year; OR = 1.22 (P = 0.013) and OR = 1.22 (P = 0.0017), respectively.A novel susceptibility gene, ST13, coding for a cochaperone of the glucocorticoid receptor, is associated with exacerbations in asthmatic children and young adults despite their ICS use. Genetic variation in the glucocorticoid signalling pathway may contribute to the interindividual variability in clinical response to ICS treatment in children and young adults.
Project description:Asthma is associated with airway narrowing in response to bronchoconstricting stimuli and increased airway smooth muscle (ASM) mass. In addition, some studies have suggested impaired ?-agonist induced ASM relaxation in asthmatics, but the mechanism is not known.To characterize the potential defect in ?-agonist induced cAMP in ASM derived from asthmatic in comparison to non-asthmatic subjects and to investigate its mechanism.We examined ?(2)-adrenergic (?(2)AR) receptor expression and basal ?-agonist and forskolin (direct activator of adenylyl cyclase) stimulated cAMP production in asthmatic cultured ASM (n?=?15) and non-asthmatic ASM (n?=?22). Based on these results, PDE activity, PDE4D expression and cell proliferation were determined.In the presence of IBMX, a pan PDE inhibitor, asthmatic ASM had ?50% lower cAMP production in response to isoproterenol, albuterol, formoterol, and forskolin compared to non-asthmatic ASM. However when PDE4 was specifically inhibited, cAMP production by the agonists and forskolin was normalized in asthmatic ASM. We then measured the amount and activity of PDE4, and found ?2-fold greater expression and activity in asthmatic ASM compared to non-asthmatic ASM. Furthermore, inhibition of PDE4 reduced asthmatic ASM proliferation but not that of non-asthmatic ASM.Decreased ?-agonist induced cAMP in ASM from asthmatics results from enhanced degradation due to increased PDE4D expression. Clinical manifestations of this dysregulation would be suboptimal ?-agonist-mediated bronchodilation and possibly reduced control over increasing ASM mass. These phenotypes appear to be "hard-wired" into ASM from asthmatics, as they do not require an inflammatory environment in culture to be observed.
Project description:Introduction:The proper use of serum periostin (POSTN) as a biomarker for asthma is hindered by inconsistent performance in different clinical settings. Objective:To explore patient's factors that may affect POSTN expression locally and systematically and its utility as a biomarker for asthma development. Materials and Methods:Here we used bioinformatics analysis of publicly available transcriptomics data to confirm that POSTN is an asthma specific gene involved in core signaling pathways enriched in the bronchial epithelium during asthma. We then explored a large number of datasets to identify possible confounders that may affect the POSTN gene expression and consequently, its interpretation as a reliable biomarker for asthma. Plasma and saliva levels of POSTN were determined in locally recruited asthmatic patients (mild, moderate and severe) compared to healthy controls to confirm the bioinformatics findings. Results:Our bioinformatics results confirmed that POSTN was consistently upregulated in the bronchial epithelium in asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) bronchial epithelium. In asthma, its mRNA expression was affected by gender, sample anatomical site and type, steroid therapy, and smoking. In our cohort, plasma POSTN was upregulated in severe and non-severe asthmatic patients. Saliva POSTN was significantly higher in non-severe asthmatic patients compared to healthy and severe asthmatic patients (specifically those who are not on Xolair (omalizumab)). Patients' BMI, inhaled steroid use and Xolair treatment affected POSTN plasma levels. Conclusion:Up to our knowledge, this is the first study examining the level of POSTN in the saliva of asthmatic patients. Both plasma and saliva POSTN levels can aid in early diagnosis of asthma. Saliva POSTN level was more sensitive than plasma POSTN in differentiating between severe and non-severe asthmatics. Patients' characteristics like BMI, the use of inhaled steroids, or Xolair treatment should be carefully reviewed before any meaningful interpretation of POSTN level in clinical practice.
Project description:Background:Glucocorticoid (GC) is the first-line therapy for asthma, but some asthmatics are insensitive to it. Glucocorticoid-induced transcript 1 gene (GLCCI1) is reported to be associated with GCs efficiency in asthmatics, while its exact mechanism remains unknown. Methods:A total of 30 asthmatic patients received fluticasone propionate for 12 weeks. Forced expiratory volume in 1 s (FEV1) and GLCCI1 expression were detected. Asthma model was constructed in wild-type and GLCCI1 knockout (GLCCI1-/-) mice. Glucocorticoid receptor (GR) and mitogen-activated protein kinase phosphatase 1 (MKP-1) expression were detected by polymerase chain reaction and Western blotting (WB). The phosphorylation of p38 mitogen-activated protein kinase (MAPK) was also detected by WB. Results:In asthmatic patients, the change of FEV1 was well positively correlated with change of GLCCI1 expression (r = 0.430, P = 0.022). In animal experiment, GR and MKP-1 mRNA levels were significantly decreased in asthmatic mice than in control mice (wild-type: GR: 0.769 vs. 1.000, P = 0.022; MKP-1: 0.493 vs. 1.000, P < 0.001. GLCCI1-/-: GR: 0.629 vs. 1.645, P < 0.001; MKP-1: 0.377 vs. 2.146, P < 0.001). Hydroprednisone treatment significantly increased GR and MKP-1 mRNA expression levels than in asthmatic groups; however, GLCCI1-/- asthmatic mice had less improvement (wild-type: GR: 1.517 vs. 0.769, P = 0.023; MKP-1: 1.036 vs. 0.493, P = 0.003. GLCCI1-/-: GR: 0.846 vs. 0.629, P = 0.116; MKP-1: 0.475 vs. 0.377, P = 0.388). GLCCI1-/- asthmatic mice had more obvious phosphorylation of p38 MAPK than wild-type asthmatic mice (9.060 vs. 3.484, P < 0.001). It was still higher even though after hydroprednisone treatment (6.440 vs. 2.630, P < 0.001). Conclusions:GLCCI1 deficiency in asthmatic mice inhibits the activation of GR and MKP-1 and leads to more obvious phosphorylation of p38 MAPK, leading to a decremental sensitivity to GCs. Trial Registration:ChiCTR.org.cn, ChiCTR-RCC-13003634; http://www.chictr.org.cn/showproj.aspx?proj=5926.