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Acute kidney injury,dendritic cells

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https://www.readbyqxmd.com/read/28898406/dc-sign-reacts-with-tlr4-and-regulates-inflammatory-cytokine-expression-via-nf-%C3%AE%C2%BAb-activation-in-renal-tubular-epithelial-cells-during-acute-renal-injury
#1
Danying Feng, Yanping Wang, Yan Liu, Liping Wu, Xiao Li, Yufan Chen, Yuanyuan Chen, Yafeng Chen, Chundi Xu, Ke Yang, Tong Zhou
In the pathological process of acute kidney injury (AKI), innate immune receptors are essential in inflammatory response modulation; however, the precise molecular mechanisms are still unclear. Our study sought to demonstrate the inflammatory response mechanisms in renal tubular epithelial cells via Toll-like receptor 4 (TLR4) and dendritic cell-specific ICAM-3-grabbing non-integrin 1 (DC-SIGN) signaling. We found that DC-SIGN exhibited strong expression in renal tubular epithelial cells of human acute renal injury tissues...
September 12, 2017: Clinical and Experimental Immunology
https://www.readbyqxmd.com/read/28878768/natural-igm-and-tlr-agonists-switch-murine-splenic-pan-b-to-regulatory-cells-that-suppress-ischemia-induced-innate-inflammation-via-regulating-nkt-1-cells
#2
Peter I Lobo, Kailo H Schlegel, Amandeep Bajwa, Liping Huang, Mark D Okusa
Natural IgM anti-leukocyte autoantibodies (IgM-ALAs) inhibit inflammation by several mechanisms. Here, we show that pan-B cells and bone marrow-derived dendritic cells (BMDCs) are switched to regulatory cells when pretreated ex vivo with IgM. B cells are also switched to regulatory cells when pretreated ex vivo with CpG but not with LPS. Pre-emptive infusion of such ex vivo induced regulatory cells protects C57BL/6 mice from ischemia-induced acute kidney injury (AKI) via regulation of in vivo NKT-1 cells, which normally amplify the innate inflammatory response to DAMPS released after reperfusion of the ischemic kidney...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28801723/a-review-of-the-role-of-immune-cells-in-acute-kidney-injury
#3
REVIEW
Anthony Bonavia, Kai Singbartl
Acute kidney injury (AKI) is a systemic disease occurring commonly in patients who are critically ill. Etiologies of AKI can be septic or aseptic (nephrotoxic, or ischemia-reperfusion injury). Recent evidence reveals that innate and adaptive immune responses are involved in mediating damage to renal tubular cells and in recovery from AKI. Dendritic cells, monocytes/macrophages, neutrophils, T lymphocytes, and B lymphocytes all contribute to kidney injury. Conversely, M2 macrophages and regulatory T cells are essential in suppressing inflammation, tissue remodeling and repair following kidney injury...
August 11, 2017: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
https://www.readbyqxmd.com/read/28676864/innate-immune-response-in-kidney-ischemia-reperfusion-injury-potential-target-for-therapy
#4
REVIEW
Aleksandra Kezić, Natasa Stajic, Friedrich Thaiss
Acute kidney injury caused by ischemia and subsequent reperfusion is associated with a high rate of mortality and morbidity. Ischemia/reperfusion injury in kidney transplantation causes delayed graft function and is associated with more frequent episodes of acute rejection and progression to chronic allograft nephropathy. Alloantigen-independent inflammation is an important process, participating in pathogenesis of injurious response, caused by ischemia and reperfusion. This innate immune response is characterized by the activity of classical cells belonging to the immune system, such as neutrophils, macrophages, dendritic cells, lymphocytes, and also tubular epithelial cells and endothelial cells...
2017: Journal of Immunology Research
https://www.readbyqxmd.com/read/28433199/glycoprotein-non-metastatic-melanoma-protein-b-gpnmb-is-highly-expressed-in-macrophages-of-acute-injured-kidney-and-promotes-m2-macrophages-polarization
#5
Letian Zhou, Hui Zhuo, Huiyu Ouyang, Yexin Liu, Fang Yuan, Lin Sun, Fuyou Liu, Hong Liu
Acute kidney injury (AKI) is an increasingly common disorder that is strongly linked to short- and long-term morbidity and mortality. During AKI process, macrophages, one of the important immune response cells, can polarize into M1 and M2 subtype from M0 subtype. It is well-known that M1 macrophages play a pro inflammatory role while M2 macrophages play an anti-inflammatory role. Glycoprotein non-metastatic melanoma protein b (Gpnmb) is a glycosylated transmembrane protein highly expressed in numerous cells, including osteoblasts, dendritic cells and macrophages...
June 2017: Cellular Immunology
https://www.readbyqxmd.com/read/28291548/the-role-of-interleukin-17a-in-the-pathogenesis-of-kidney-diseases
#6
REVIEW
Charlotte Cortvrindt, Reinhart Speeckaert, Alena Moerman, Joris R Delanghe, Marijn M Speeckaert
Being a member of the IL-17 family, comprising six structurally related ligands, IL-17A is a cytokine, produced by multiple cell types, such as CD4(+)αβ T cells, γδ T cells, natural killer cells, neutrophils, macrophages, dendritic cells, lymphoid tissue inducer cells, mast cells and plasma cells. IL-17A participates in tissue inflammation by inducing the expression of chemokines, proinflammatory cytokines and matrix metalloproteases. Besides its role in host defence against infectious diseases, IL-17A is involved in different autoimmune and inflammatory diseases...
April 2017: Pathology
https://www.readbyqxmd.com/read/28284381/mechanisms-of-drug-induced-interstitial-nephritis
#7
REVIEW
Rajeev Raghavan, Saed Shawar
Drug-induced acute interstitial nephritis (DI-AIN) is a drug hypersensitivity reaction (DHR) that manifests 7 to 10 days after exposure to the culprit drug. DHRs account for fewer than 15% of reported adverse drug reactions. The kidneys are susceptible to DHR because: (1) the high renal blood flow whereby antigens are filtered, secreted, or concentrated, and (2) it is a major site of excretion for drugs and drug metabolites. More than 250 different drugs from various classes have been incriminated as causative agents of DI-AIN, the third most common cause of acute kidney injury in the hospital...
March 2017: Advances in Chronic Kidney Disease
https://www.readbyqxmd.com/read/27745702/il-4-il-13-mediated-polarization-of-renal-macrophages-dendritic-cells-to-an-m2a-phenotype-is-essential-for-recovery-from-acute-kidney-injury
#8
Ming-Zhi Zhang, Xin Wang, Yinqiu Wang, Aolei Niu, Suwan Wang, Chenhang Zou, Raymond C Harris
Cytokines IL-4 and IL-13 play important roles in polarization of macrophages/dendritic cells to an M2 phenotype, which is important for recovery from acute kidney injury. Both IL-4 and IL-13 activate JAK3/STAT6 signaling. In mice with diphtheria toxin receptor expression in proximal tubules (selective injury model), a relatively selective JAK3 inhibitor, tofacitinib, led to more severe kidney injury, delayed recovery from acute kidney injury, increased inflammatory M1 phenotype markers and decreased reparative M2 phenotype markers of macrophages/dendritic cells, and development of more severe renal fibrosis after diphtheria toxin administration...
February 2017: Kidney International
https://www.readbyqxmd.com/read/27732750/activin-inhibition-limits-early-innate-immune-response-in-rat-kidney-allografts-a-pilot-study
#9
Niina K Palin, Johanna Savikko, Arja Pasternack, Jukka M Rintala, Bhanu Kalra, Shivani Mistry, Ajay Kumar, Marie-Paule Roth, Heikki Helin, Olli Ritvos
Activins are members of the transforming growth factor-beta (TGF-β) superfamily of cytokines. They play critical roles in the onset of acute and chronic inflammatory responses. The aim of this study was to investigate how activin inhibition affects acute kidney injury and inflammation after transplantation. The study was carried out in kidney transplantation and renal ischemia-reperfusion models in the rat. Soluble activin type 2 receptor (sActRIIB-Fc) was used to inhibit activin signaling. Transplantation groups were as follows: (i) cyclosporine A (CsA) (ii) CsA + sActRIIB-Fc, (iii) CsA+ inactive protein control Fc-G1...
January 2017: Transplant International: Official Journal of the European Society for Organ Transplantation
https://www.readbyqxmd.com/read/27027358/paeonol-protects-endotoxin-induced-acute-kidney-injury-potential-mechanism-of-inhibiting-tlr4-nf-%C3%AE%C2%BAb-signal-pathway
#10
Hua-Ying Fan, Dong Qi, Chen Yu, Feng Zhao, Tao Liu, Zuo-Kai Zhang, Ming-Yan Yang, Lei-Ming Zhang, Da-Quan Chen, Yuan Du
STUDY DESIGN AND METHODS: In order to determine the therapeutic effect and mechanism of paeonol on acute kidney injury induced by endotoxin, an acute kidney injury model was established by intraperitoneal administration of lipopolysaccharide in mice in vivo and on LPS-induced dendritic cells in vitro. Renal tissues were used for histologic examination. Concentrations of blood urea nitrogen and serum creatinine were detected, inflammatory cytokines were determined by ELISA. The relative proteins' expression of TLR4-NF-κB signal pathway was assessed by Western blot, the localization and expression of phospho-NF-κB p65 in kidney was monitored by immunohistochemistry...
June 28, 2016: Oncotarget
https://www.readbyqxmd.com/read/27011059/the-nlrp3-inflammasome-in-kidney-disease-and-autoimmunity
#11
REVIEW
Holly L Hutton, Joshua D Ooi, Stephen R Holdsworth, A Richard Kitching
The NLRP3 inflammasome is an intracellular platform that converts the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 to their active forms in response to 'danger' signals, which can be either host or pathogen derived, and mediates a form of inflammatory cell death called pyroptosis. This component of the innate immune system was initially discovered because of its role in rare autoinflammatory syndromes called cryopyrinopathies, but it has since been shown to mediate injurious inflammation in a broad range of diseases...
September 2016: Nephrology
https://www.readbyqxmd.com/read/26890577/donor-brain-death-leads-to-differential-immune-activation-in-solid-organs-but-does-not-accelerate-ischaemia-reperfusion-injury
#12
Paul Viktor Ritschl, Muhammad Imtiaz Ashraf, Rupert Oberhuber, Vanessa Mellitzer, Cornelia Fabritius, Thomas Resch, Susanne Ebner, Martina Sauter, Karin Klingel, Johann Pratschke, Katja Kotsch
A comparative analysis of inflammation between solid organs following donor brain death (BD) is still lacking and the detailed influence of BD accelerating ischaemia-reperfusion injury (IRI) post-transplantation remains to be addressed. Applying a murine model of BD, we demonstrated that 4 h after BD organs were characterized by distinct inflammatory expression patterns. For instance, lipocalin 2 (LCN2), a marker of acute kidney injury, was selectively induced in BD livers but not in kidneys. BD further resulted in significantly reduced frequencies of CD3(+) CD4(+) , CD3(+) CD8(+) T cells and NKp46(+) NK cells in the liver, whereas BD kidneys and hearts were characterized by significantly lower frequencies of conventional dendritic cells (cDCs)...
May 2016: Journal of Pathology
https://www.readbyqxmd.com/read/26764483/acute-kidney-injury-tubular-markers-and-risk-for-chronic-kidney-disease-and-end-stage-kidney-failure
#13
REVIEW
Hon Liang Tan, John Q Yap, Qi Qian
Acute kidney injury (AKI) is a common clinical syndrome directly related to patient short-term and long-term morbidity and mortality. Over the last decade, the occurrence rate of AKI has been increasing, and there has also been a growing epidemic of chronic kidney diseases (CKD) and end-stage kidney disease (ESRD) linked to severe and repeated episodes of AKIs. The detection and management of AKI are currently far from satisfactory. A large proportion of AKI patients, especially those with preexisting CKD, are at an increased risk of non-resolving AKI and progressing to CKD and ESRD...
2016: Blood Purification
https://www.readbyqxmd.com/read/26610206/a-novel-cyclic-helix-b-peptide-inhibits-dendritic-cell-maturation-during-amelioration-of-acute-kidney-graft-rejection-through-jak-2-stat3-socs1
#14
C Yang, Y Zhang, J Wang, L Li, L Wang, M Hu, M Xu, Y Long, R Rong, T Zhu
We recently synthesized a novel proteolysis-resistant cyclic helix B peptide (CHBP) that exhibits promising renoprotective effects. Dendritic cells (DCs) play an activation role in acute rejection (AR). Thus, the present study was designed to investigate the effects of CHBP on DCs in a rat renal transplantation model. The left kidney was harvested from male Lewis rats and then transplanted into male Wistar rats with or without CHBP treatment. Five successive treatment doses of CHBP after transplantation significantly ameliorated AR with lower histological injury, apoptosis and CD4(+) and CD8(+) T-cell infiltration in renal allografts...
2015: Cell Death & Disease
https://www.readbyqxmd.com/read/26607974/beneficial-immune-effects-of-myeloid-related-proteins-in-kidney-transplant-rejection
#15
N V Rekers, I M Bajema, M J K Mallat, B Petersen, J D H Anholts, G M J S Swings, P P M C van Miert, C Kerkhoff, J Roth, D Popp, M C van Groningen, D Baeten, N Goemaere, M D Kraaij, M Zandbergen, S Heidt, C van Kooten, J W de Fijter, F H J Claas, M Eikmans
Acute rejection is a risk factor for inferior long-term kidney transplant survival. Although T cell immunity is considered the main effector in clinical acute rejection, the role of myeloid cells is less clear. Expression of S100 calcium-binding protein A8 (S100A8) and S100A9 was evaluated in 303 biopsies before and after transplantation from 190 patients. In two independent cohorts of patients with acute rejection (n = 98 and n = 11; mostly cellular rejections), high expression of S100 calcium-binding protein A8 (S100A8) and A9 (S100A9) was related to improved graft outcome...
May 2016: American Journal of Transplantation
https://www.readbyqxmd.com/read/26295408/dendritic-cell-protection-from-cisplatin-nephrotoxicity-is-independent-of-neutrophils
#16
Raghu K Tadagavadi, Guofeng Gao, Wei Wei Wang, Manuel Rovira Gonzalez, W Brian Reeves
Cisplatin is a very effective chemotherapeutic agent used against a wide range of solid tumors. A major adverse effect of cisplatin therapy is acute kidney injury (AKI). Neutrophils are reported to infiltrate and exacerbate injury in a wide range of sterile inflammatory models of tissue injury. Here, we studied the kinetics of neutrophil infiltration into kidneys and their role in cisplatin-mediated AKI. Mice treated with cisplatin showed an increase in circulating neutrophils 24 and 48 h after cisplatin administration...
August 2015: Toxins
https://www.readbyqxmd.com/read/25997515/molecular-patterns-of-subclinical-and-clinical-rejection-of-kidney-allograft-quantity-matters
#17
Mariana Wohlfahrtova, Irena Tycova, Eva Honsova, Alena Lodererova, Ondrej Viklicky
BACKGROUND/AIMS: Subclinical rejection diagnosed from protocol biopsies is thought to be a risk factor of long- term allograft dysfunction. The reason why in some patients subclinical rejection does not represent risk for progression is not fully understood. METHODS: The intragraft expression of 376 target genes involved in chemokine defense, apoptosis, inflammation, tolerance and TGF-β signalling pathways was measured using quantitative real-time RT-PCR (2(-)∆∆(Ct)) method in subclinical inflammation (SCI, n=10), clinical inflammation in acute T-cell mediated rejection (CI, n=10) and no rejection samples (n=9)...
2015: Kidney & Blood Pressure Research
https://www.readbyqxmd.com/read/25993317/phospholipase-a2-inhibits-cisplatin-induced-acute-kidney-injury-by-modulating-regulatory-t-cells-by-the-cd206-mannose-receptor
#18
Hyunseong Kim, Hyojung Lee, Gihyun Lee, Hyunil Jang, Sung-Su Kim, Heera Yoon, Geun-Hyung Kang, Deok-Sang Hwang, Sun Kwang Kim, Hwan-Suck Chung, Hyunsu Bae
Previously, we found that Foxp3-expressing CD4(+) regulatory T (Treg) cells attenuate cisplatin-induced acute kidney injury in mice and that bee venom and its constituent phospholipase A2 (PLA2) are capable of modulating Treg cells. Here we tested whether PLA2 could inhibit cisplatin-induced acute kidney injury. As a result of treatment with PLA2, the population of Treg cells was significantly increased, both in vivo and in vitro. PLA2-injected mice showed reduced levels of serum creatinine, blood urea nitrogen, renal tissue damage, and pro-inflammatory cytokine production upon cisplatin administration...
September 2015: Kidney International
https://www.readbyqxmd.com/read/25944235/the-molecular-phenotypes-of-rejection-in-kidney-transplant-biopsies
#19
Philip F Halloran, Konrad Famulski, Jeff Reeve
PURPOSE OF REVIEW: The recent emergence of a system for distinguishing T-cell-mediated rejection (TCMR) from antibody-mediated rejection (ABMR), including C4d-negative ABMR, allows us to map the molecular features of these conditions. RECENT FINDINGS: The TCMR landscape is dominated by molecules expressed in effector T cells, antigen-presenting cells (macrophages, dendritic cells, B cells) and interferon-gamma (IFNG)-induced genes. A surprising finding is the association of transcripts for inhibitory molecules such as CTLA4 and PDL1 with TCMR, indicating that this tubulo-interstitial inflammatory compartment is actively controlled...
June 2015: Current Opinion in Organ Transplantation
https://www.readbyqxmd.com/read/25877257/adenosine-2a-receptors-in-acute-kidney-injury
#20
REVIEW
I S Vincent, M D Okusa
Acute kidney injury (AKI) is an important clinical problem that may lead to death and for those who survive, the sequelae of AKI include loss of quality of life, chronic kidney disease and end-stage renal disease. The incidence of AKI continues to rise without clear successes in humans for the pharmacological prevention of AKI or treatment of established AKI. Dendritic cells and macrophages are critical early initiators of innate immunity in the kidney and orchestrate inflammation subsequent to ischaemia-reperfusion injury...
July 2015: Acta Physiologica
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