renal epithelial cells
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Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3522
Author(s):  
Ashok Kumar Kumawat ◽  
Geena Varghese Paramel ◽  
Kartheyaene Jayaprakash Demirel ◽  
Isak Demirel

Understanding how uropathogenic Escherichia coli (UPEC) modulates the immune response in the kidney is essential to prevent UPEC from reaching the bloodstream and causing urosepsis. The purpose of this study was to elucidate if renal fibroblasts can release IL-1β during a UPEC infection and to investigate the mechanism behind the IL-1β release. We found that the UPEC strain CFT073 induced an increased IL-1β and LDH release from renal fibroblasts, but not from renal epithelial cells. The UPEC-induced IL-1β release was found to be NLRP3, caspase-1, caspase-4, ERK 1/2, cathepsin B and serine protease dependent in renal fibroblasts. We also found that the UPEC virulence factor α-hemolysin was necessary for IL-1β release. Conditioned medium from caspase-1, caspase-4 and NLRP3-deficient renal fibroblasts mediated an increased reactive oxygen species production from neutrophils, but reduced UPEC phagocytosis. Taken together, our study demonstrates that renal fibroblasts, but not renal epithelial cells, release IL-1β during a UPEC infection. This suggest that renal fibroblasts are vital immunoreactive cells and not only structural cells that produce and regulate the extracellular matrix.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marta Albertyńska ◽  
Hubert Okła ◽  
Krzysztof Jasik ◽  
Danuta Urbańska-Jasik ◽  
Przemysław Pol

AbstractBabesiosis is one of the most common infections in free-living animals and is rapidly becoming significant among human zoonoses. Cases of acute renal failure in humans caused by Babesia spp. have been described in the literature. The kidneys are characterised by intense blood flow through the blood vessels, which increases the likelihood of contact with the intra-erythrocyte parasite. The aim of this study was to observe the influence of B. microti (ATCC 30221) on renal epithelial cells in vitro cultured (NRK-52E line) and Wistar rats’ kidney. Both NRK-52E cells and rats’ kidney sections were analysed by light microscopy, transmission electron microscopy (TEM) and fluorescence in situ hybridization (FISH). Necrotic changes in renal epithelial cells have been observed in vitro and in vivo. In many cross-sections through the rats’ kidney, adhesion of blood cells to the vascular endothelium, accumulation of erythrocytes and emboli were demonstrated. In NRK-52E culture, elements with a distinctly doubled cell membrane resembling B. microti were found inside the cytoplasm and adjacent to the cell layer. The study indicates a chemotactic tendency for B. microti to adhere to the renal tubules' epithelium, a possibility of piroplasms entering the renal epithelial cells, their proliferation within the cytoplasm and emboli formation.


Author(s):  
Yash R. Mehta ◽  
Spencer A. Lewis ◽  
Kirby T. Leo ◽  
Lihe Chen ◽  
Euijung Park ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Wei-Bo Huang ◽  
Guo-Jun Zou ◽  
Gu-Hua Tang ◽  
Xin-Yuan Sun ◽  
Jian-Ming Ouyang

The original Laminaria polysaccharide (LP0) was sulfated using the sulfur trioxide-pyridine method, and four sulfated Laminaria polysaccharides (SLPs) were obtained, namely, SLP1, SLP2, SLP3, and SLP4. The sulfated (–OSO3–) contents were 8.58%, 15.1%, 22.8%, and 31.3%, respectively. The structures of the polysaccharides were characterized using a Fourier transform infrared (FT-IR) spectrometer and nuclear magnetic resonance (NMR) techniques. SLPs showed better antioxidant activity than LP0, increased the concentration of soluble Ca2+ in the solution, reduced the amount of CaOx precipitation and degree of CaOx crystal aggregation, induced COD crystal formation, and protected HK-2 cells from damage caused by nanometer calcium oxalate crystals. These effects can inhibit the formation of CaOx kidney stones. The biological activity of the polysaccharides increased with the content of –OSO3−, that is, the biological activities of the polysaccharides had the following order: LP0 < SLP1 < SLP2 < SLP3 < SLP4. These results reveal that SLPs with high –OSO3− contents are potential drugs for effectively inhibiting the formation of CaOx stones.


2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Kristoffer Bernhem ◽  
Jacopo M. Fontana ◽  
Daniel Svensson ◽  
Liang Zhang ◽  
Linnéa M. Nilsson ◽  
...  

AbstractActivation of the apoptotic pathway is a major cause of progressive loss of function in chronic diseases such as neurodegenerative and diabetic kidney diseases. There is an unmet need for an anti-apoptotic drug that acts in the early stage of the apoptotic process. The multifunctional protein Na+,K+-ATPase has, in addition to its role as a transporter, a signaling function that is activated by its ligand, the cardiotonic steroid ouabain. Several lines of evidence suggest that sub-saturating concentrations of ouabain protect against apoptosis of renal epithelial cells, a common complication and major cause of death in diabetic patients. Here, we induced apoptosis in primary rat renal epithelial cells by exposing them to an elevated glucose concentration (20 mM) and visualized the early steps in the apoptotic process using super-resolution microscopy. Treatment with 10 nM ouabain interfered with the onset of the apoptotic process by inhibiting the activation of the BH3-only protein Bad and its translocation to mitochondria. This occurred before the pro-apoptotic protein Bax had been recruited to mitochondria. Two ouabain regulated and Akt activating Ca2+/calmodulin-dependent kinases were found to play an essential role in the ouabain anti-apoptotic effect. Our results set the stage for further exploration of ouabain as an anti-apoptotic drug in diabetic kidney disease as well as in other chronic diseases associated with excessive apoptosis.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hao Ding ◽  
Linda Xiaoyan Li ◽  
Peter C. Harris ◽  
Junwei Yang ◽  
Xiaogang Li

AbstractAutosomal dominant polycystic kidney disease (ADPKD) is caused by germline mutations of PKD1 or PKD2 on one allele and a somatic mutation inactivating the remaining normal allele. However, if and how null ADPKD gene renal epithelial cells affect the biology and function of neighboring cells, including heterozygous renal epithelial cells, fibroblasts and macrophages during cyst initiation and expansion remains unknown. Here we address this question with a “cystic extracellular vesicles/exosomes theory”. We show that cystic cell derived extracellular vesicles and urinary exosomes derived from ADPKD patients promote cyst growth in Pkd1 mutant kidneys and in 3D cultures. This is achieved by: 1) downregulation of Pkd1 gene expression and upregulation of specific miRNAs, resulting in the activation of PKD associated signaling pathways in recipient renal epithelial cells and tissues; 2) the activation of fibroblasts; and 3) the induction of cytokine expression and the recruitment of macrophages to increase renal inflammation in cystic kidneys. Inhibition of exosome biogenesis/release with GW4869 significantly delays cyst growth in aggressive and milder ADPKD mouse models, suggesting that targeting exosome secretion has therapeutic potential for ADPKD.


Author(s):  
Anke Schumann ◽  
Véronique Belche ◽  
Kristin Schaller ◽  
Sarah C. Grünert ◽  
Andres Kaech ◽  
...  

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