Key result
IL-1Ra deficiency exacerbated Angiotensin II-induced systolic blood pressure increases (197 vs 169 mmHg, P<0.05) and renal damage, whereas anti-IL-1β antibody treatment attenuated these effects.
Why the study?
Clinical hypertension is associated with renal inflammation, and inhibition of IL-1 was hypothesized to modulate the Ang II-induced hypertensive response and renal injury.
Does anti-IL-1β antibody reduce Angiotensin II-induced hypertension and renal damage in mice?
Does anti-IL-1β antibody reduce Angiotensin II-induced hypertension and renal damage in mice?
Answers are grounded in this paper and cite their sources.
Inhibition of IL-1 suppresses Angiotensin II-induced hypertension and renal damage in a mouse model, highlighting a potential anti-inflammatory strategy for hypertensive renal injury.
Clinical hypertension (HT) is associated with renal inflammation and elevated circulating levels of proinflammatory cytokines. Interleukin (IL)-1 receptor antagonist (IL-1Ra) is one of the most important anti-inflammatory cytokines and plays a crucial role in inflammation. Inhibition of IL-1 may contribute to modulation of the Angiotensin II (Ang II)-induced HT response. The present study aimed to elucidate the effects of IL-1Ra and anti-IL-1β antibody (01BSUR) on Ang II-induced renal injury. To determine the contribution of IL-1Ra to Ang II-induced renal inflammation, male wildtype (WT) and IL-1Ra-deficient (IL-1Ra-/-) mice were infused with Ang II (1000 ng/kg/min) using subcutaneous osmotic pump for 14 days. We checked renal function, histological change, and several mRNA expressions 14 days after infusion. Fourteen days after infusion, systolic blood pressure (197 ± 5 vs 169 ± 9 mmHg, P<0.05) in IL-1Ra-/- mice significantly increased compared with WT mice. Furthermore, on day 14 of Ang II infusion, plasma IL-6 was 5.9-fold higher in IL-1Ra-/- versus WT mice (P<0.001); renal preproendothelin-1 mRNA expression was also significantly higher in IL-1Ra-/- mice (P<0.05). In addition, renal histology revealed greater damage in IL-1Ra-/- mice compared with WT mice 14 days after infusion. Finally, we administrated 01BSUR to both IL-1Ra-/- and WT mice, and 01BSUR treatment decreased Ang II-induced HT and renal damage (glomerular injury and fibrosis of the tubulointerstitial area) in both IL-1Ra-/- and WT mice compared with IgG2a treatment. Inhibition of IL-1 decreased Ang II-induced HT and renal damage in both IL-1Ra-/- and WT mice, suggesting suppression of IL-1 may provide an additional strategy to protect against renal damage in hypertensive patients.
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Akita et al. (2021) studied Angiotensin II-induced renal injury and hypertension. IL-1Ra deficiency and anti-IL-1β antibody (01BSUR) vs. Wildtype mice and IgG2a treatment was evaluated on Systolic blood pressure (p=<0.05). IL-1Ra deficiency exacerbated Angiotensin II-induced systolic blood pressure increases (197 vs 169 mmHg, P<0.05) and renal damage, whereas anti-IL-1β antibody treatment attenuated these effects.
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