Abstract
ABSTRACTThe recovery phase after kidney ischemia/reperfusion (IR) injury is often associated with the suppression of inflammation and the proliferation of tubular epithelial cells (TECs). The duration of this phase is often determined by the suppression of inflammation and the proliferation of TECs. Several lines of evidence suggest that IκB kinase α (IKKα) not only promotes the production of anti-inflammatory factors and/or prevents the production of inflammatory factors, but also induces the accompanying cell differentiation and regeneration, and suppresses inflammation. We therefore hypothesized that IKKα could participate in the kidney repair after IR injury and have used a mouse model of acute kidney injury (AKI) to test this. We found that IKKα mediated the repair of the kidney via infiltrated regulatory T (Treg) cells, which can produce anti-inflammatory cytokine IL10, and that IKKα also increased the proliferation of the surviving TECs and suppressed of inflammation. In addition, the expression of indoleamine 2,3-dioxygenase (IDO) in TECs is consistent with the infiltration of IL10-producing Treg cells. We conclude that IKKα is involved in kidney recovery and regeneration through the Treg cells that can produce IL10, which might be a potential therapeutic target that can be used to promote kidney repair after IR injury.
Highlights
It is well known that ischemia-reperfusion (IR) injury can cause acute kidney injury (AKI) (Bonventre and Weinberg, 2003)
Here, the authors use a mouse model of IR injury to investigate the role of IKKα in kidney repair after IR injury
They show that IKKα mediates the infiltration of Treg cells into the kidney, and that Treg cells are the major source of the anti-inflammatory cytokine IL10, increased levels of which are associated with kidney recovery
Summary
It is well known that ischemia-reperfusion (IR) injury can cause acute kidney injury (AKI) (Bonventre and Weinberg, 2003). The kidney is still able to recover to its normal tissue function and structure after prolonged ischemia (El Sabbahy and Vaidya, 2011; Kulkarni et al, 2014). After the inflammation that follows IR injury, the impaired kidney often heals. Proinflammatory/anti-inflammatory and damage/repair processes are closely intertwined during the entire recovery process (Bonventre and Zuk, 2004; Duffield et al, 2005; Benigni et al, 2010; El Sabbahy and Vaidya, 2011; Kulkarni et al, 2014)
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