Tag: injury

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IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury.

IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury.

J Am Soc Nephrol. 2015 Jan 2;

Authors: Huang Q, Niu Z, Tan J, Yang J, Liu Y, Ma H, Lee VW, Sun S, Song X, Guo M, Wang Y, Cao Q

Abstract
IL-25 is an important immune regulator that can promote Th2 immune response-dependent immunity, inflammation, and tissue repair in asthma, intestinal infection, and autoimmune diseases. In this study, we examined the effects of IL-25 in renal ischemic/reperfusion injury (IRI). Treating IRI mice with IL-25 significantly improved renal function and reduced renal injury. Furthermore, IL-25 treatment increased the levels of IL-4, IL-5, and IL-13 in serum and kidney and promoted induction of alternatively activated (M2) macrophages in kidney. Notably, IL-25 treatment also increased the frequency of type 2 innate lymphoid cells (ILC2s) and multipotent progenitor type 2 (MPP(type2)) cells in kidney. IL-25-responsive ILC2 and MPP(type2) cells produced greater amounts of Th2 cytokines that associated with the induction of M2 macrophages and suppression of classically activated (M1) macrophages in vitro. Finally, adoptive transfer of ILC2s or MPP(type2) cells not only reduced renal functional and histologic injury in IRI mice but also induced M2 macrophages in kidney. In conclusion, our data identify a mechanism whereby IL-25-elicited ILC2 and MPP(type2) cells regulate macrophage phenotype in kidney and prevent renal IRI.

PMID: 25556172 [PubMed – as supplied by publisher]

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LSU cross country runner Morgan Schuetz overcomes asthma, injury – LSU The Reveille


LSU The Reveille

LSU cross country runner Morgan Schuetz overcomes asthma, injury
LSU The Reveille
But Schuetz's promising career as a top distance running prospect was nearly cut short when she struggled with asthma during her junior year in high school. Schuetz said running 100 meters became an insurmountable task, and she began reassessing her …

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CXCR4 Antagonism as a Therapeutic Approach to Prevent Acute Kidney Injury.

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CXCR4 Antagonism as a Therapeutic Approach to Prevent Acute Kidney Injury.

Am J Physiol Renal Physiol. 2014 Jul 30;

Authors: Zuk A, Gershenovich M, Ivanova Y, MacFarland RT, Fricker SP, Ledbetter SR

Abstract
We examined whether antagonism of the CXCR4 receptor ameliorates the loss of renal function following ischemia-reperfusion. CXCR4 is ubiquitously expressed on leukocytes, known mediators of renal injury, and on bone marrow hematopoietic stem cells (HSC). Plerixafor (AMD3100, Mozobil ) is a small molecule CXCR4 antagonist that mobilizes HSCs into the peripheral blood and also modulates the immune response in in vivo rodent models of asthma and rheumatoid arthritis. Treatment with plerixafor before and after ischemic clamping ameliorated kidney injury in a rat model of bilateral renal ischemia-reperfusion. Serum creatinine and blood urea nitrogen were significantly reduced 24 hours after reperfusion, as was tissue injury and cell death. Plerixafor prevented the renal increase in the pro-inflammatory chemokines CXCL1 and CXCL5 and the cytokine IL-6. Flow cytometry of kidney homogenates confirmed the presence of significantly fewer leukocytes with plerixafor treatment; additionally, myeloperoxidase activity was reduced. AMD3465, a monocyclam analogue of AMD3100, was likewise renoprotective. Four weeks post-reperfusion, long-term effects included diminished fibrosis, inflammation and ongoing renal injury. The mechanism by which CXCR4 inhibition ameliorates AKI is due to modulation of leukocyte infiltration and expression of pro-inflammatory chemokines/cytokines, rather than a HSC mediated effect. The data suggest that CXCR4 antagonism with plerixafor may be a potential option to prevent AKI.

PMID: 25080523 [PubMed – as supplied by publisher]

View full post on pubmed: asthma