Do corticosteroids induce apoptosis in nasal polyp inflammatory cells? in vivo and in vitro studies

Saunders, M. W.; Wheatley, A H; George, Sarah J.; Lai, Teresa; Birchall, MA

doi:10.1097/00005537-199905000-00019

Cited by 49 publications

(34 citation statements)

References 18 publications

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“…Eosinophil apoptosis can be induced or accelerated by ligation of membrane receptors by specific mAb for Fas (CD95) (Matsumoto et al 1995, Druilhe et al 1996, CD69 (Walsh et al 1996) and CD45 (Blaylock et al 1999). Glucocorticoids rapidly induce apoptosis in peripheral blood and tissue eosinophils (Saunders et al 1999). Nasal polyposis is an inflammatory disorder characterised by an intense infiltration of the respiratory mucosa by eosinophils that is often refractory to treatment with corticosteroids.…”

Section: Eosinophil Apoptosismentioning

confidence: 99%

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

Walsh¹,

Sexton²,

Blaylock³

2003

Journal of Endocrinology

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Anti-inflammatory therapy in asthma is reliant on corticosteroids, particularly in their inhaled form. However, steroids are rather non-specific in their actions and they also raise concerns regarding compliance and side-effect issues. Furthermore, a small proportion of patients with asthma fail to respond to oral glucocorticoids even at high doses. This article will review the role that steroids and membrane receptor ligation play in the induction of eosinophil apoptosis together with the mechanisms by which corticosteroids enhance the disposal of apoptotic eosinophils by both professional and non-professional phagocytes. Eosinophils are thought to be the major pro-inflammatory effector cell in asthma and their persistence in the airways is probably enhanced by the presence of several asthma-relevant cytokines that prolong eosinophil survival by inhibition of apoptosis (interleukin (IL)-3, IL-5, granulocyte-macrophage colony-stimulating factor,

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Section: Eosinophil Apoptosismentioning

confidence: 99%

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

Walsh¹,

Sexton²,

Blaylock³

2003

Journal of Endocrinology

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“…Eosinophil apoptosis was previously shown to be induced early by topical or systemic corticosteroids in vivo and in vitro [19]. Therefore, tissue eosinophil infiltration appears to be suppressed after corticosteroid treatments; however, the clinical changes induced in tissue eosinophil counts by oPSL have not yet been clarified, particularly in ECRS.…”

Section: Discussionmentioning

confidence: 99%

Impact of Preoperative Systemic Corticosteroids on the Histology and Diagnosis of Eosinophilic Chronic Rhinosinusitis

Akiyama

Makihara²,

Uraguchi³

et al. 2019

Int Arch Allergy Immunol

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Background: The histological changes corticosteroids induce in nasal polyps, and whether these changes have an impact on the diagnosis of eosinophilic chronic rhinosinusitis (ECRS), currently remain unclear. Objectives: A prospective controlled multicenter trial was conducted to evaluate the efficacy of the low-dose and short-term oral prednisolone (oPSL) treatment for tissue eosinophil infiltrations in ECRS. Methods: Subjects with ECRS diagnosed by previous biopsies received a low dose of oPSL for 3 days (PSL 3) or 7 days (PSL 7) before surgery. Changes in the tissue eosinophil count after these treatments were evaluated. Furthermore, the percent change of tissue eosinophil count from baseline and its impact on the diagnosis defined by the JESREC study were examined. Results: There were 23 and 21 subjects in the PSL 3 and PSL 7 groups, respectively. Polyp scores, clinical symptom scores, and the proportion of blood eosinophils significantly decreased after the treatment, and no significant differences were observed between the groups. The entire tissue eosinophil count tended to be slightly decreased in both groups without reaching a statistically significant value. The median percent change of tissue eosinophil count from baseline was 83.6%, and only the posttreatment proportion of blood eosinophil showed a mild correlation with it. Seven out of 44 nasal polyp specimens collected from the superficial part of the middle meatus showed < 70 eosinophils/high-power field; therefore, the false negative rate was 15.9%, but decreased to 11.4% when other parts were included in the histological evaluation. Conclusions: Low-dose and short-term oPSL did not appear to markedly affect the tissue eosinophil count in ECRS patients; however, the potential for misdiagnoses due to the effects of oPSL cannot be rejected. The diagnosis of ECRS prior to the administration of corticosteroids or tissue evaluations using multiple tissue parts is desirable.

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“…The benefical action of glucocorticoids to reduce eosinophilic inflammation may entail an increase of eosinophil apoptosis [28,32] and ensuing detection and engulfment by alveolar macrophages [33]. Treatment of LAEC and A549 with glucocorticoids enhances the numbers of cells engulfing apoptotic differentiated EoL-1.…”

Section: Role Of Airway Epithelium In Engulfing Apoptotic Eosinophilsmentioning

confidence: 99%

The role of eosinophils in asthma

Alenzi¹,

Alanazi²,

Al-Faim³

et al. 2013

Health

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Do corticosteroids induce apoptosis in nasal polyp inflammatory cells? in vivo and in vitro studies

Abstract: Corticosteroids induce apoptosis in inflammatory cells in human nasal polyps in vitro. This is not reflected by a similar response to FPANS at 14 days in vivo, but may still play a part in regression of polyps with other forms of administration or at other time points.

Cited by 49 publications

References 18 publications

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

Impact of Preoperative Systemic Corticosteroids on the Histology and Diagnosis of Eosinophilic Chronic Rhinosinusitis

The role of eosinophils in asthma

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