ArticleClinical and translational allergy2013
Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children.
Article in Clinical and translational allergy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Alterations in innate immune responses of patients with chronic rhinosinusitis related to cystic fibrosis.PloS one · 2022Article
- Bacteriophage: A new therapeutic player to combat neutrophilic inflammation in chronic airway diseases.Frontiers in medicine · 2022Review
- Long-term exposure to low-doseOncotarget · 2018Article
- Enhanced neutrophil phagocytic capacity in rheumatoid arthritis related to the autoantibodies rheumatoid factor and anti-cyclic citrullinated peptides.BMC musculoskeletal disorders · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCorticosteroids are the first-line therapy for asthma; however, the effect of corticosteroids on the innate immune system remains unclear. This study's objective was to evaluate the effect of inhaled corticosteroid therapy (ICT) on phagocytic functions.
methodsTo evaluate the impact of ICT, the phagocytosis of Saccharomyces cerevisiae by blood monocytes and neutrophils and the production of superoxide anions were assessed before and after three and six months of ICT treatment in 58 children with persistent asthma and 21 healthy controls.
resultsWe showed that the phagocytic capacity of monocytes and neutrophils that occurred via pattern recognition receptors or was mediated by complement and immunoglobulin receptors in asthmatic children before treatment was significantly lower than in healthy controls (p<0.05, Mann-Whitney test) and was not influenced by the severity of the clinical form of the disease. Although there was clinical improvement with treatment, ICT for 6 months was not sufficient to normalize phagocytosis by the phagocytes. Superoxide anion production was also decreased in the asthmatic children before treatment, and ICT normalized the O- production only for children with mild persistent asthma when assessed at baseline but caused this function to decrease after stimulation (p<0.05, Kruskal-Wallis test).
conclusionsOur data suggest that an immunodeficiency in phagocytes remained even after treatment. However, this immunodeficiency does not appear to correspond with the clinical evolution of asthma because an improvement in clinical parameters occurred.
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Registered trials
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