HOT OFF THE PRESS!!! A new article published in Frontiers in Immunology (impact factor: 4.72) utilized B-CHP to evaluate how the Zika virus influences renal function. The authors monitored fibrosis changes and collagen deposition in healthy and Zika infected mouse kidneys. The authors clearly link the Zika virus infection to kidney injury and elucidated the underlying molecular mechanisms for the first time. B-CHP enabled them to image the amount of damaged collagen in the kidneys of newborn mice (C), and track the damage up to 28 days post-infection in adult mice (D-F). It was a very interesting read for all the immunologists out there as well as those interested in kidney fibrosis.

Abstract: Zika virus (ZIKV) is a newly emerging flavivirus that broadly exhibits in various bodily tissues and fluids, especially in the brain, and ZIKV infection often causes microcephaly. Previous studies have been reported that ZIKV can infect renal cells and can be detected in the urine samples of infected individuals. However, whether ZIKV infection causes renal diseases and its pathogenic mechanisms remains unknown. Here, we identified that ZIKV infection resulted in acute kidney injury (AKI) in both newborn and adult mouse models by increasing the levels of AKI-related biomarkers [e.g., serum creatinine (Scr), kidney injury molecular−1 (Kim-1), and neutrophil gelatinase-associated lipocalin (NGAL)]. ZIKV infection triggered the inflammatory response and renal cell injury by activating Nod-like receptor 3 (NLRP3) inflammasome and secreting interleukin-1β (IL-1β). IL-1β inhibited aquaporins expression and led to water re-absorption disorder. Furthermore, ZIKV infection induced a decreased expression of B-cell lymphoma-2 (Bcl-2) in the kidney. Overexpression of Bcl-2 attenuated ZIKV-induced NLRP3 inflammasome activation in renal cells and down-regulated PARP/caspase-3-mediated renal apoptosis. Overall, our findings demonstrated that ZIKV infection induced AKI by activating NLRP3 inflammasome and apoptosis through suppressing Bcl-2 expression, which provided potential therapeutic targets for ZIKV-associated renal diseases.


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