Journal
JOURNAL OF IMMUNOLOGY
Volume 198, Issue 6, Pages 2374-2382Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1601282
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Funding
- Investissements d'Avenir programme [ANR-11-IDEX-0005-02]
- Sorbonne Paris Cite
- Laboratoire d'excellence INFLAMEX
- Departements-Hospitalo-Universitaires FIRE
- COST Action BM1007 (Mast cells and basophils-targets for innovative therapies) of the European Community
- L'Agence Nationale de la Recherche France [ANR-12-ISV3-0006-01]
- Conacyt Mexico [Conacyt-ANR 188565]
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Ischemia-reperfusion injury (IRI) is an important cause of acute kidney injury that can lead to end-stage renal failure. Although the ensuing inflammatory response can restore homeostasis, a consecutive maladaptive repair and persistent inflammation represent important risk factors for postischemic chronic kidney disease development. In this study, we investigated the role of mast cells in both the early and late phases of the inflammatory response in experimental models of acute and chronic renal IRI using our recently developed mouse model that allows conditional ablation of mast cells. Depletion of mast cells prior to IRI resulted in improved renal function due to diminished local inflammatory cytokine/chemokine levels and neutrophil recruitment to the kidneys after the acute injury phase (48 h post-IRI). Furthermore, although not completely protected, mast cell-depleted mice displayed less organ atrophy and fibrosis than did wild-type mice during the chronic phases (2 and 6 wk post-IRI) of disease development. Conversely, mast cell ablation after the acute phase of IRI had no impact on organ atrophy, tubular necrosis, or fibrosis. Thus, our results suggest a deleterious role of mast cells during the acute inflammatory phase of IRI promoting subsequent fibrosis development, but not during the chronic phase of the disease.
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