Responsiveness to oral prednisolone in severe asthma is related to the degree of eosinophilic airway inflammation

Abstract

SummaryBackground: Patients with severe asthma appear relatively corticosteroid resistant.Corticosteroid responsiveness is closely related to the degree of eosinophilic airway inflammation. The extent to which eosinophilic airway inflammation in severe asthma responds to treatment with systemic corticosteroids is not clear.Objective: To relate the physiological and inflammatory response to systemic corticosteroids in asthma to disease severity and the baseline extent of eosinophilic inflammation. Methods:Patients with mild/moderate and severe asthma were investigated before and after 2 weeks of oral prednisolone (Clintrials.gov NCT00331058 and NCT00327197). We pooled the results from two studies with common protocols.The US study contained two independent centres and the UK one independent centre. The effect of oral corticosteroids on FEV 1 , Pc20, airway inflammation and serum cytokines was investigated. Baseline measurements were compared with healthy subjects.Results: Thirty-two mild/moderate asthmatics, 50 severe asthmatics and 35 healthy subjects took part. At baseline, both groups of asthmatics had a lower FEV 1 and Pc20 and increased eosinophilic inflammation compared to healthy subjects. The severe group had a lower FEV 1 and more eosinophilic inflammation compared to mild/moderate asthmatics. Oral prednisolone caused a similar degree of suppression of eosinophilic inflammation in all compartments in both groups of asthmatics. There were small improvements in FEV 1 and Pc20 for both mild/ moderate and severe asthmatics with a correlation between the baseline eosinophilic inflammation and the change in FEV 1 . There was a~50% reduction in the serum concentration of CXCL10 (IP-10), CCL22 (MDC), CCL17(TARC), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after oral corticosteroids.Conclusions and Clinical Relevance: Disease severity does not influence the response to systemic corticosteroids. The study does not therefore support the concept that severe asthma is associated with corticosteroid resistance. Only baseline

Developments in the field of allergy in 2017 through the eyes of Clinical and Experimental Allergy

“…17 Following a two-week course of oral prednisolone, both groups experienced a similar degree of suppression of blood and airway eosinophilia and serum cytokines. Sousa and colleagues have explored this amongst a group of moderate and severe asthmatics.…”

“…Sousa and colleagues have explored this amongst a group of moderate and severe asthmatics. 17 Following a two-week course of oral prednisolone, both groups experienced a similar degree of suppression of blood and airway eosinophilia and serum cytokines. Even in patients on high doses of inhaled steroids, many showed a suppressive eosinophil response.…”

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“…Prednisolone, one of the glucocorticoids, acts as endogenous cortisol that is released from the hypothalamic-pituitary-adrenal (HPA) axis, particularly in the case of stress or injury [9]. Prednisolone fights inflammation via the regulation of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) etc, thus, widely applied to treating various inflammation diseases or states, such as allergies, asthma, dermatitis, rheumatic disorders, systemic lupus erythematosus, and autoimmune disorders [10][11][12]. Recently, Baudoux et al demonstrated that cluster of differentiation CD4 + and CD8 + T-cells regulate immune responses in AA-induced acute tubular necrosis [13].…”

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“…Predictors of successful reduction were younger age and low blood eosinophils. There are interesting parallels with predictors of response to oral corticosteroids …”