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2015 ; 6
(2
): e1632
Nephropedia Template TP
gab.com Text
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English Wikipedia
Induction of eosinophil apoptosis by hydrogen peroxide promotes the resolution of
allergic inflammation
#MMPMID25675292
Reis AC
; Alessandri AL
; Athayde RM
; Perez DA
; Vago JP
; Ávila TV
; Ferreira TP
; de Arantes AC
; Coutinho Dde S
; Rachid MA
; Sousa LP
; Martins MA
; Menezes GB
; Rossi AG
; Teixeira MM
; Pinho V
Cell Death Dis
2015[Feb]; 6
(2
): e1632
PMID25675292
show ga
Eosinophils are effector cells that have an important role in the pathogenesis of
allergic disease. Defective removal of these cells likely leads to chronic
inflammatory diseases such as asthma. Thus, there is great interest in
understanding the mechanisms responsible for the elimination of eosinophils from
inflammatory sites. Previous studies have demonstrated a role for certain
mediators and molecular pathways responsible for the survival and death of
leukocytes at sites of inflammation. Reactive oxygen species have been described
as proinflammatory mediators but their role in the resolution phase of
inflammation is poorly understood. The aim of this study was to investigate the
effect of reactive oxygen species in the resolution of allergic inflammatory
responses. An eosinophilic cell line (Eol-1) was treated with hydrogen peroxide
and apoptosis was measured. Allergic inflammation was induced in ovalbumin
sensitized and challenged mouse models and reactive oxygen species were
administered at the peak of inflammatory cell infiltrate. Inflammatory cell
numbers, cytokine and chemokine levels, mucus production, inflammatory cell
apoptosis and peribronchiolar matrix deposition was quantified in the lungs.
Resistance and elastance were measured at baseline and after aerosolized
methacholine. Hydrogen peroxide accelerates resolution of airway inflammation by
induction of caspase-dependent apoptosis of eosinophils and decrease remodeling,
mucus deposition, inflammatory cytokine production and airway hyperreactivity.
Moreover, the inhibition of reactive oxygen species production by apocynin or in
gp91(phox-/-) mice prolonged the inflammatory response. Hydrogen peroxide induces
Eol-1 apoptosis in vitro and enhances the resolution of inflammation and improves
lung function in vivo by inducing caspase-dependent apoptosis of eosinophils.