OBJECTIVE: To determine the association and diagnostic ability of serum and tissue eosinophils in the diagnosis of asthma among CRS patients.
METHODS: A cross-sectional study was conducted involving 24 CRS patients with asthma and without asthma, respectively, from the Otorhinolaryngology clinic of two tertiary hospitals located on the East Coast of Peninsular Malaysia. Serum and tissue eosinophils (obtained from nasal polyp) levels between both groups were compared. Association between serum and tissue eosinophils with asthma was evaluated using logistic regression analysis, adjusting for important sociodemographic characteristics. The diagnostic ability of serum and tissue eosinophil was then evaluated by assessing the receiver operating characteristic curve.
RESULTS: A total of 48 CRS patients with a mean [SD] age of 47.50 [14.99] years were included. Patients with asthma had significantly higher serum [0.48 vs 0.35 × 109/L] and tissue eosinophil [100 vs 8.5 per HPF] levels. Tissue eosinophils were found to be an independent predictor of asthma with adjusted OR 1.05, p 0.375 × 109/L and tissue eosinophil > 58 per HPF.
METHODS: We developed mouse models representing three different phenotypes of allergic airway inflammation-eosinophilic, mixed, and neutrophilic asthma via different methods of house dust mite sensitization and challenge. Transcriptomic analysis of the lungs, followed by the RT-PCR, western blot, and confocal microscopy, was performed. Primary human bronchial epithelial cells cultured in air-liquid interface were used to study the mechanisms revealed in the in vivo models.
RESULTS: By whole-genome transcriptome profiling of the lung, we found that airway tight junction (TJ), mucin, and inflammasome-related genes are differentially expressed in these distinct phenotypes. Further analysis of proteins from these families revealed that Zo-1 and Cldn18 were downregulated in all phenotypes, while increased Cldn4 expression was characteristic for neutrophilic airway inflammation. Mucins Clca1 (Gob5) and Muc5ac were upregulated in eosinophilic and even more in neutrophilic phenotype. Increased expression of inflammasome-related molecules such as Nlrp3, Nlrc4, Casp-1, and IL-1β was characteristic for neutrophilic asthma. In addition, we showed that inflammasome/Th17/neutrophilic axis cytokine-IL-1β-may transiently impair epithelial barrier function, while IL-1β and IL-17 increase mucin expressions in primary human bronchial epithelial cells.
CONCLUSION: Our findings suggest that differential expression of TJ, mucin, and inflammasome-related molecules in distinct inflammatory phenotypes of asthma may be linked to pathophysiology and might reflect the differences observed in the clinic.
MATERIALS AND METHODS: A cross-sectional study done in Baghdad on 112 patients who attended Al-Zahraa Allergic Center. Their demographic characteristics, total IgE, eosinophil counts and PCR result for COVID-19 were determined.
RESULTS: The means for IgE and eosinophils were 245.7±260.1IU/ml and 444.5±117.1cells/microliter sequentially. Around 32.1% had high IgE level (i.e., atopic) and 11.6% had COVID-19. Among the atopic patients, 33.3%, 30.5% and 36.2% had atopic dermatitis, allergic rhinitis and asthma respectively. More than half (58.3%) of them were male, 55.5% aged <45 years, 36.2% were retired or had no job, 69.5% were graduated from secondary school or more and 88.8% lived in urban areas. There is no significant association in IgE level between those with and without COVID-19, which means that exposure to SARS Cov2 virus could not be a trigger or exacerbation for atopic diseases. Also, there was no association between atopic patients with COVID-19 and those without it regarding type of atopy, age, sex, occupation, education, type of living area.
CONCLUSIONS: Atopy is not a risk factor for COVID-19.
METHODS: A cross-sectional study was undertaken among secondary school students in eight suburban and urban schools in the district of Hulu Langat, Selangor, Malaysia. The survey was completed by 96 students at the age of 14 by using the International Study of Asthma and Allergies in Children (ISAAC) and European Community Respiratory Health Survey (ECRHS) questionnaires. The fractional exhaled nitric oxide (FeNO) was measured, and an allergic skin prick test and sputum induction were performed for all students. Induced sputum samples were analysed for the expression of CD11b, CD35, CD63, and CD66b on eosinophils and neutrophils by flow cytometry. The particulate matter (PM2.5 and PM10), NO2, CO2, and formaldehyde were measured inside the classrooms.
RESULTS: Chemometric and regression results have clustered the expression of CD63 with PM2.5, CD11b with NO2, CD66b with FeNO levels, and CO2 with eosinophils, with the prediction accuracy of the models being 71.88%, 76.04%, and 76.04%, respectively. Meanwhile, for neutrophils, the CD63 and CD66b clustering with PM2.5 and CD11b with FeNO levels showed a model prediction accuracy of 72.92% and 71.88%, respectively.
CONCLUSION: The findings indicated that the exposure to PM2.5 and NO2 was likely associated with the degranulation of eosinophils and neutrophils, following the activation mechanisms that led to the inflammatory reactions.
OBJECTIVE: To determine a standardised algorithm to reassess and personalise the treatment COPD patients based on the available evidence.
METHODS: A consensus statement was agreed upon by a panel of pulmonologists in from 11 institutes in Malaysia whose members formed this consensus group.
RESULTS: According to the consensus, which was unanimously adopted, all COPD patients who are currently receiving an ICS-based treatment should be reassessed based on the presence of co-existence of asthma or high eosinophil counts and frequency of moderate or severe exacerbations in the previous 12 months. When that the patients meet any of the aforementioned criteria, then the patient can continue taking ICS-based therapy. However, if the patients do not meet the criteria, then the treatment of patients need to be personalised based on whether the patient is currently receiving long-acting beta-agonists (LABA)/ICS or triple therapy.
CONCLUSION: A flowchart of the consensus providing a guidance to Malaysian clinicians was elucidated based on evidences and international guidelines that identifies the right patients who should receive inhaled corticosteroids and enable to switch non ICS based therapies in patients less likely to benefit from such treatments.