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304 results on '"Zhou, Wuding"'

2. Collectin 11 has a pivotal role in host defense against kidney and bladder infection in mice.

Author

Wu, Kun-Yi, primary, Cao, Bo, additional, Chen, Wan-Bing, additional, Wu, Weiju, additional, Zhao, Shujuan, additional, Min, Xiao-Yun, additional, Yang, Jurong, additional, Han, Jin, additional, Dong, Xia, additional, Wang, Na, additional, Wu, Yi, additional, Garred, Peter, additional, Sacks, Steven, additional, Zhou, Wuding, additional, and Li, Ke, additional

Published
2023
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3. Collectin-11 promotes cancer cell proliferation and tumor growth

Author

Wang, Jia-Xing, primary, Cao, Bo, additional, Ma, Ning, additional, Wu, Kun-Yi, additional, Chen, Wan-Bing, additional, Wu, Weiju, additional, Dong, Xia, additional, Liu, Cheng-Fei, additional, Gao, Ya-Feng, additional, Diao, Teng-Yue, additional, Min, Xiao-Yun, additional, Yong, Qing, additional, Li, Zong-Fang, additional, Zhou, Wuding, additional, and Li, Ke, additional

Published
2023
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8. Protective role for C3aR in experimental chronic pyelonephritis

Author

Zhao, Shu‐Juan, primary, Wu, Kun‐Yi, additional, Min, Xiao‐Yun, additional, Wang, Chun‐Xuan, additional, Cao, Bo, additional, Ma, Ning, additional, Yang, Xue‐Ling, additional, Zhu, Zhuo‐Ran, additional, Fu, Rong‐Guo, additional, Zhou, Wuding, additional, Yang, Ju‐Rong, additional, and Li, Ke, additional

Published
2022
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11. Collectin-11 detects stress-induced L-fucose pattern to trigger renal epithelial injury

Author

Farrar, Conrad A., Tran, David, Li, Ke, Wu, Weiju, Peng, Qi, Schwaeble, Wilhelm, Zhou, Wuding, and Sacks, Steven H.

Subjects
Proteases -- Analysis, Lectins -- Analysis, Kidney diseases -- Diagnosis -- Research, Biological markers -- Analysis, Health care industry
Abstract

Physiochemical stress induces tissue injury as a result of the detection of abnormal molecular patterns by sensory molecules of the innate immune system. Here, we have described how the recently discovered C-type lectin collectin-11 (CL-11, also known as CL-K1 and encoded by COLEC11) recognizes an abnormal pattern of L-fucose on postischemic renal tubule cells and activates a destructive inflammatory response. We found that intrarenal expression of CL-11 rapidly increases in the postischemic period and colocalizes with complement deposited along the basolateral surface of the proximal renal tubule in association with L-fucose, the potential binding ligand for CL-11. Mice with either generalized or kidney-specific deficiency of CL-11 were strongly protected against loss of renal function and tubule injury due to reduced complement deposition. Ex vivo renal tubule cells showed a marked capacity for CL-11 binding that was induced by cell stress under hypoxic or hypothermic conditions and prevented by specific removal of L-fucose. Further analysis revealed that cell-bound CL-11 required the lectin complement pathway-associated protease MASP-2 to trigger complement deposition. Given these results, we conclude that lectin complement pathway activation triggered by ligand-CL-11 interaction in postischemic tissue is a potent source of acute kidney injury and is amenable to sugar-specific blockade., Introduction Innate immune factors produced by epithelial cells serve defensive and homeostatic functions and also regulate the inflammatory response following physical and biochemical tissue stress (1, 2). Collectin-11 (CL-11, also [...]

Published
2016
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17. Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis

Author

Wang, Na, primary, Wu, Weiju, additional, Qiang, Cui, additional, Ma, Ning, additional, Wu, Kunyi, additional, Liu, Dan, additional, Wang, Jia‐Xing, additional, Yang, Xiao, additional, Xue, Li, additional, Diao, Teng‐Yue, additional, Liu, Jia‐Yu, additional, Li, Ang, additional, Zhang, Baojun, additional, Li, Zong‐Fang, additional, Farrar, Conrad A., additional, Banda, Nirmal K., additional, Bayarri‐Olmos, Rafael, additional, Garred, Peter, additional, Zhou, Wuding, additional, and Li, Ke, additional

Published
2021
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31. Influence of Donor C3 Allotype on Late Renal-Transplantation Outcome

Author

Brown, Katherine M., Kondeatis, Elli, Vaughan, Robert W., Kon, Sui P., Farmer, Christopher K.T., Taylor, John D., He, Xiang, Johnston, Atholl, Horsfield, Catherine, Janssen, Bert J.C., Gros, Piet, Zhou, Wuding, Sacks, Steven H., and Sheerin, Neil S.

Published
2006

47. Synergy between type 1 fimbriae expression and C3 opsonisation increases internalisation of E. coli by human tubular epithelial cells

Author

Sacks Steven H, Hong Yuzhi, Zhou Wuding, Li Ke, and Sheerin Neil S

Subjects
Microbiology, QR1-502
Abstract

Abstract Background Bacterial infection of the urinary tract is a common clinical problem with E. coli being the most common urinary pathogen. Bacterial uptake into epithelial cells is increasingly recognised as an important feature of infection. Bacterial virulence factors, especially fimbrial adhesins, have been conclusively shown to promote host cell invasion. Our recent study reported that C3 opsonisation markedly increases the ability of E. coli strain J96 to internalise into human proximal tubular epithelial cells via CD46, a complement regulatory protein expressed on host cell membrane. In this study, we further assessed whether C3-dependent internalisation by human tubular epithelial cells is a general feature of uropathogenic E. coli and investigated features of the bacterial phenotype that may account for any heterogeneity. Results In 31 clinical isolates of E. coli tested, C3-dependent internalisation was evident in 10 isolates. Type 1 fimbriae mediated-binding is essential for C3-dependent internalisation as shown by phenotypic association, type 1 fimbrial blockade with soluble ligand (mannose) and by assessment of a type 1 fimbrial mutant. Conclusion we propose that efficient internalisation of uropathogenic E. coli by the human urinary tract depends on co-operation between type 1 fimbriae-mediated adhesion and C3 receptor -ligand interaction.

Published
2009
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49. The complement factor 5a receptor 1 has a pathogenic role in chronic inflammation and renal fibrosis in a murine model of chronic pyelonephritis

Author

Choudhry, Naheed, Li, Ke, Zhang, Ting, Wu, Kun-Yi, Song, Yun, Farrar, Conrad A., Wang, Na, Liu, Cheng-Fei, Peng, Qi, Wu, Weiju, Sacks, Steven H., and Zhou, Wuding

Subjects
Inflammation, Mice, Knockout, chronic inflammation, Pyelonephritis, Macrophages, Complement C5a, Epithelial Cells, Kidney, Fibrosis, Peptides, Cyclic, renal fibrosis, Bacterial Load, Monocytes, Disease Models, Animal, Mice, Basic Research, C5aR1, Nephrology, Chronic Disease, Leukocytes, Animals, Antigens, Ly, Uropathogenic Escherichia coli, Receptor, Anaphylatoxin C5a, Escherichia coli Infections
Abstract

Complement factor 5a (C5a) interaction with its receptor (C5aR1) contributes to the pathogenesis of inflammatory diseases, including acute kidney injury. However, its role in chronic inflammation, particularly in pathogen-associated disorders, is largely unknown. Here we tested whether the development of chronic inflammation and renal fibrosis is dependent on C5aR1 in a murine model of chronic pyelonephritis. C5aR1-deficient (C5aR1-/-) mice showed a significant reduction in bacterial load, tubule injury and tubulointerstitial fibrosis in the kidneys following infection, compared with C5aR1-sufficient mice. This was associated with reduced renal leukocyte infiltration specifically for the population of Ly6Chi proinflammatory monocytes/macrophages and reduced intrarenal gene expression of key proinflammatory and profibrogenic factors in C5aR1-/- mice following infection. Antagonizing C5aR1 decreased renal bacterial load, tissue inflammation and tubulointerstitial fibrosis. Ex vivo and in vitro studies showed that under infection conditions, C5a/C5aR1 interaction upregulated the production of proinflammatory and profibrogenic factors by renal tubular epithelial cells and monocytes/macrophages, whereas the phagocytic function of monocytes/macrophages was down-regulated. Thus, C5aR1-dependent bacterial colonization of the tubular epithelium, C5a/C5aR1-mediated upregulation of local inflammatory responses to uropathogenic E. coli and impairment of phagocytic function of phagocytes contribute to persistent bacterial colonization of the kidney, chronic renal inflammation and subsequent tubulointerstitial fibrosis.

Published
2016

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