Activation of the immunoregulatory transcription factors NF-κB1 and -2 in HUS

Participation of canonical and non-canonical NF-κB signaling pathway in renal damage in hemolytic-uremic syndrome


The hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy that can occur as a severe systemic complication following infection with shiga toxin-producing Escherichia coli (STEC). The HUS is the most common cause of acute renal failure in childhood and adolescence, with a lethality rate of one to three percent. In a murine in vivo model, researchers of the AG Translational Septomics demonstrated for the first time by means of protein and gene expression analyses that in the HUS both canonical and non-canonical NF-κB signaling pathways are activated by shiga toxin in kidney tissue. Furthermore, an increased translocation of NF-κB1 and -2 into the cell nucleus, an increased expression of activating receptors of both signaling pathways and an increased expression of cytokines of the canonical NF-κB signaling pathway were shown. This activation of both NF-κB signalling pathways could at least partially contribute to the development of acute renal failure in HUS.

Original publication:

Sobbe IV, Krieg N, Dennhardt S, Coldewey SM (2020) Involvement of NF-κB1 and the Non-Canonical NF-κB Signaling Pathway in the Pathogenesis of Acute Kidney Injury in Shiga-Toxin-2-Induced Hemolytic-Uremic Syndrome in Mice. Shock, DOI: 10.1097/SHK.0000000000001558

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