Circulating IL-6 upregulates IL-10 production in splenic CD4(+) T cells and limits acute kidney injury-induced lung inflammation
- Authors
- Andres-Hernando, Ana; Okamura, Kayo; Bhargava, Rhea; Kiekhaefer, Carol M.; Soranno, Danielle; Kirkbride-Romeo, Lara A.; Gil, Hyo-wook; Altmann, Chris; Faubel, Sarah
- Issue Date
- May-2017
- Publisher
- Elsevier Inc.
- Keywords
- acute kidney injury; cytokines; ischemic reperfusion
- Citation
- Kidney International, v.91, no.5, pp 1057 - 1069
- Pages
- 13
- Journal Title
- Kidney International
- Volume
- 91
- Number
- 5
- Start Page
- 1057
- End Page
- 1069
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/7616
- DOI
- 10.1016/j.kint.2016.12.014
- ISSN
- 0085-2538
1523-1755
- Abstract
- Although it is well established that acute kidney injury (AKI) is a proinflammatory state, little is known about the endogenous counter-inflammatory response. IL-6 is traditionally considered a pro-inflammatory cytokine that is elevated in the serum in both human and murine AKI. However, IL-6 is known to have anti-inflammatory effects. Here we sought to investigate the role of IL-6 in the counter-inflammatory response after AKI, particularly in regard to the anti-inflammatory cytokine IL-10. Ischemic AKI was induced by bilateral renal pedicle clamping. IL-10-deficient mice had increased systemic and lung inflammation after AKI, demonstrating the role of IL-10 in limiting inflammation after AKI. We then sought to determine whether IL-6 mediates IL-10 production. Wild type mice with AKI had a marked upregulation of splenic IL-10 that was absent in 11-6-deficient mice with AKI. In vitro, addition of 11-6 to splenocytes increased IL-10 production in CD4(+) T cells, B cells, and macrophages. In vivo, CD4-deficient mice with AKI had reduced splenic 11-10 and increased lung myeloperoxidase activity. Thus, IL-6 directly increases IL-10 production and participates in the counter-inflammatory response after AKI.
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