Deficiency of the Interleukin 17/23 Axis Accelerates Renal Injury in Mice With Deoxycorticosterone Acetate+Angiotensin II-Induced Hypertension
Krebs CF, Lange S, Niemann G, Rosendahl A, Lehners A, Meyer-Schwesinger C, Stahl RAK, Benndorf RA, Velden J, Paust HJ, Panzer U, Ehmke H, Wenzel UO (2014)
Publication Type: Journal article
Publication year: 2014
Journal
Book Volume: 63
Pages Range: 565-71
Journal Issue: 3
DOI: 10.1161/HYPERTENSIONAHA.113.02620
Abstract
T cells participate in angiotensin II (Ang II)-induced hypertension. However, the specific subsets of T cells that are important in the end-organ damage are unknown. T-helper 17 cells are a recently identified subset that produces interleukin 17 (IL-17) and requires interleukin 23 (IL-23) for expansion. To evaluate the role of the T-helper 17 immune response in hypertensive renal and cardiac end-organ damage, hypertension was induced with deoxycorticosterone acetate (DOCA)+Ang II in wild-type (n=39) and IL-17-deficient (n=31) mice. The injury was evaluated at day 4 and day 14. To inactivate the IL-17/IL-23 axis at a different point, DOCA+Ang II hypertension was also induced in IL-23p19-deficient mice. Renal infiltration by T-helper 17 cells was increased in hypertensive wild-type mice. Systolic blood pressure did not differ between hypertensive IL-17-deficient and wild-type mice. Three days after induction of hypertension, a significantly higher albuminuria was found in IL-17-deficient than in wild-type mice (196±64 versus 58±16 mg/mg albumin/creatinine). Histology revealed significantly more glomerular injury (1.04±0.06 versus 0.67±0.05) and renal infiltration of ?? T cells in IL-17-deficient than in wild-type mice after 14 days. Similarly, significantly higher albuminuria, glomerular injury, and ?? T cell infiltration were found in IL-23p19-deficient mice with DOCA+Ang II-induced hypertension. DOCA+Ang II also induced cardiac damage as assessed by heart weight, cardiac fibrosis, as well as expression of fetal genes and matrix components, but no significant differences were found among IL-17(-/-), IL-23p19(-/-), and wild-type mice. IL-17/IL-23 deficiency accelerates DOCA+Ang II-induced albuminuria and hypertensive renal but not cardiac end-organ damage.
Involved external institutions
Universitätsklinikum Hamburg-Eppendorf (UKE)
Germany (DE)
Martin-Luther-Universität Halle-Wittenberg (MLU)
Germany (DE)
Germany (DE)
Martin-Luther-Universität Halle-Wittenberg (MLU)
Germany (DE)
How to cite
APA:
Krebs, C.F., Lange, S., Niemann, G., Rosendahl, A., Lehners, A., Meyer-Schwesinger, C.,... Wenzel, U.O. (2014). Deficiency of the Interleukin 17/23 Axis Accelerates Renal Injury in Mice With Deoxycorticosterone Acetate+Angiotensin II-Induced Hypertension. Hypertension, 63(3), 565-71. https://doi.org/10.1161/HYPERTENSIONAHA.113.02620
MLA:
Krebs, Christian F., et al. "Deficiency of the Interleukin 17/23 Axis Accelerates Renal Injury in Mice With Deoxycorticosterone Acetate+Angiotensin II-Induced Hypertension." Hypertension 63.3 (2014): 565-71.
BibTeX: Download