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2016 ; 17
(1
): 153
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Impaired anti-inflammatory action of glucocorticoid in neutrophil from patients
with steroid-resistant asthma
#MMPMID27852250
Wang M
; Gao P
; Wu X
; Chen Y
; Feng Y
; Yang Q
; Xu Y
; Zhao J
; Xie J
Respir Res
2016[Nov]; 17
(1
): 153
PMID27852250
show ga
BACKGROUND: Steroid resistant (SR) asthma is characterized by persistent airway
inflammation that fails to resolve despite treatment with high doses of
corticosteroids. Furthermore, SR patient airways show increased numbers
neutrophils, which are less responsive to glucocorticoid. The present study seeks
to determine whether dexamethasone (DEX) has different effect on neutrophils from
steroid sensitive (SS) asthmatics compared to SR asthmatics. METHODS: Adults with
asthma (n?=?38) were classified as SR or SS based on changes in lung FEV1%
following a one-month inhaled corticosteroid (ICS) treatment. Blood samples were
collected from all patients during their first visit of the study. Neutrophils
isolated from the blood were cultured with dexamethasone and/or atopic asthmatic
serum for 18 h. The mRNA expression of mitogen-activated protein kinase
phosphatase-1 (MKP-1), a glucocorticoid transactivation target, and
glucocorticoid-induced transcript 1 (GLCCI1), an early marker of
glucocorticoid-induced apoptosis whose expression was associated with the
response to inhaled glucocorticoids in asthma , was determined by real-time PCR,
and ELISA was used to assess the pro-inflammatory cytokine IL-8 levels in the
supernatant. Constitutive neutrophil apoptosis was detected by flow cytometry.
RESULTS: DEX significantly induced MKP-1 expression in both patients with SS and
SR patients in a concentration-dependent manner, but greater induction was
observed for SS patients at a low concentration (10(-6) M). Asthmatic serum alone
showed no MKP-1expression, and there was impaired induction of MKP-1 by DEX in SR
asthma patients. The expression of GLCCI1 was not induced in neutrophils with DEX
or DEX/atopic asthmatic serum combination. Greater inhibition of IL-8 production
was observed in neutrophils from patients with SS asthma treated with DEX/atopic
asthmatic serum combination compared with SR asthma patients, though DEX alone
showed the same effect on neutrophils from SS and SR asthma patients. Meanwhile,
DEX dependent inhibition of constitutive neutrophil apoptosis was similar between
SS asthma and SR asthma patients. CONCLUSIONS: DEX exerted different effects on
neutrophils from patients with SS asthma and SR asthma, which may contribute to
glucocorticoid insensitivity.
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