期刊
KIDNEY INTERNATIONAL
卷 74, 期 -, 页码 S55-S59出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2008.513
关键词
lymphocytes; heat shock proteins; salt-dependent hypertension; autoimmunity; renal tubulointerstitium
资金
- NIH
- CONDES, Maracaibo, Venezuela [CC-0455-05]
- FONACYT, Venezuela [F-200500283]
- Asociacion de Amigos del Rinon, Maracaibo, Venezuela
Renal tubulointerstitial inflammation is a constant feature of experimental models of hypertension and likely plays a role in the pathogenesis of salt-sensitive hypertension. We have previously raised the possibility that the immune cell infiltration is driven by a low grade autoimmune reactivity directed to or facilitated by renal heat shock protein over expression. The present studies were done to gain insight on possible cell-mediated immune mechanisms in experimental hypertension by determining the renal expression of HSP70 and the proliferation index of T lymphocytes cultured with HSP70. We studied male Sprague-Dawley rats with inhibition of nitric oxide (NO) synthase (n = 6), protein overload (PO) proteinuria (n = 7) and short-term angiotensin II (Ang II) infusion (n = 5), and their corresponding control groups. Each model was associated with 2 to 4 fold increase (P < 0.05-0.001) in renal HSP70 expression. T cells isolated from the spleens demonstrated a significant two-to nine-fold response compared to controls (P < 0.05 or lower for each comparison) when cultured with HSP70. These studies suggest that autoimmunity to stress proteins is involved in the sustained low-grade inflammatory infiltration that occurs in the tubulointerstitial areas of the hypertensive kidney.
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