ArticleAmerican journal of physiology. Renal physiology2026
A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.
Article in American journal of physiology. Renal physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Viral priming refers to the host's recognition of viral components, triggering an antiviral response, and upregulating pathogen recognition receptors. When followed closely by bacterial infection, this immune activation can provoke a hyperinflammatory response, increasing the risk for secondary hemophagocytic lymphohistiocytosis (sHLH), multiorgan failure, and death. We developed a novel murine two-hit model of viral-primed sepsis-associated acute kidney injury using polyinosinic-polycytidylic acid [poly(I:C)] for viral mimicry and lipopolysaccharide (LPS) for bacterial stimulation. Male 8-wk-old C57BL/6J mice were primed with poly(I:C) [2.5 mg/kg, intraperitoneal (ip) injection] at 24 h before low-dose LPS (0.5 mg/kg, ip) (time = 0 h) and compared with vehicle-treated controls for up to 48 h. Poly(I:C) + LPS mice exhibited a significant reduction in glomerular filtration rate at 4 h post-LPS and elevated serum creatinine and urinary kidney injury molecule-1 (KIM-1) at 48 h, indicating sustained kidney injury. These mice also showed marked increases in plasma ferritin, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) at 8 h post-LPS versus nonprimed LPS-treated mice, consistent with a hyperinflammatory state. Poly(I:C) alone induced a rapid type I interferon (IFN) response, with elevated plasma IFNα, IFNβ, and renal
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