Analysis Tools
immune system
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• mice exhibit decreased IL1beta production in response to LPS challenge
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• in an LPSinduced sepsis model of acute kidney injury, mice show attenuated renal tubular injury and interstitial inflammation with markedly less renal tubular epithelial cell (RTEC) swelling and vacuolization, less brush border loss, lower protein levels of HAVCR1 (a renal tubular injury marker, aka KIM-1), and reduced macrophage infiltration relative to LPS-challenged wild-type controls
• however, mice exhibit a normal renal phenotype under control conditions
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homeostasis/metabolism
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• mice exhibit significantly reduced serum creatinine levels in response to LPS challenge
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• mice exhibit significantly reduced serum BUN levels in response to LPS challenge
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cellular
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• renal tubular epithelial cells (RTECs) isolated from LPS-challenged mice show no morphological signs of cell swelling, vacuolation or membrane pore formation, and display lower levels of pyroptosis-related proteins (NLRP3, IL1B and cleaved GSDMD) than LPS-treated wild-type RTECs, indicating reduced activation of the NLRP3 inflammasome and decreased pyroptosis in the LPS-induced sepsis model
• increase in LPS-induced expression of KLF5 protein levels in kidney tissues is attenuated, consistent with downregulation of the KLF5/NFB pathway
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renal/urinary system
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• mice exhibit a significant reduction in LPS-induced expression of KLF5 protein in the renal cortex relative to LPS-treated wild-type controls
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