Adiba Hasnat

Introduction.  Angiotensin II hypertension is strongly linked to the immune system since many of the detrimental effects are caused by the inflammatory response mediated by immune cells such as Th17 cells⁷. Th17 have been shown to augment and not just be a secondary response to hypertension by promoting oxidative stress and sodium reabsorption in the kidneys⁴. Inflammatory cytokines such as IL-17A produced by Th17 play a major role in the pathophysiology of Angiotensin II hypertension leading to inflammation induced renal and vascular dysfunction resulting in damage to essential organs such as the heart, brain, kidneys. Methods. All studies used mouse models that were infused with angiotensin II to simulate angiogenin II induced HTN. Some of the mouse models had IL17A knock out². Some of the mouse models were treated with SGKI inhibitor¹, normal saline challenge², and skin mesenchymal stem cells (S-MSC)³. Systolic blood pressure (SBP), serum th17 cells and serum IL17A were measured¹.  Tissues samples from kidneys, heart and aorta of angII infused mice were taken and analyzed for the level of Th17 cells and IL17A using RT-PCR, flow cytometry, ELISA⁴. Renal transporter profiling was performed on ang II infused mice and IL17A knockout mice⁵. Results.  AngII infused mice treated with SGK1 inhibitor had decreased levels of Th17 and IL17A expression in renal and kidney tissue¹. IL17A knock out mice had decreased SBP and higher excretion of injected sodium compared to WT mice when infused with angII². IL17A knock out mice infused with angII had decreased renal sodium transporters compared to WT mice⁵. Culture of mouse distal convolute tubule cells treated with IL17A had higher sodium transporter activity than untreated cells⁵. AngII infused mice treated with S-MSCs had decreased SBP, serum th17, serum IL17A, aortic hypertrophy and aortic fibrosis compared to untreated mice³.  Conclusions.  Ang-II induced hypertension is highly linked to the actions of Th17 Cells and their cytokine IL-17A. IL-17A maintains elevated blood pressure in response to angiogenin II by upregulating sodium transporters⁵. IL-17A knock out results in loss of elevated BP response². SGK1 causes overexpression of Th17 in response to angiotensin II¹. Inhibition of SGK1 results in decreased differentiation of Th17¹. Skin mesenchymal stem cells decrease SBP and vascular damage due to angiotensin II by inhibiting differentiation of Th17³.

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