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Acute kidney injury,dendritic cells

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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
#1
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...
October 10, 2016: Kidney International
https://www.readbyqxmd.com/read/27732750/activin-inhibition-limits-early-innate-immune-response-in-rat-kidney-allografts-a-pilot-study
#2
Niina K Palin, Johanna Savikko, Arja Pasternack, Jukka M Rintala, Bhanu Kalra, Shivani Mistry, Ajay Kumar, Marie-Paule Roth, Heikki Helin, Olli Ritvos
BACKGROUND: Activins are members of the TGF-beta 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. METHODS: The study was done in kidney transplantation and renal ischemia-reperfusion models in the rat. Soluble activin type 2 receptor (sActRIIB-Fc) was used to inhibit activin signaling...
October 12, 2016: 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
#3
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...
March 25, 2016: Oncotarget
https://www.readbyqxmd.com/read/27011059/the-nlrp3-inflammasome-in-kidney-disease-and-autoimmunity
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
https://www.readbyqxmd.com/read/25599729/drug-induced-acute-interstitial-nephritis-pathology-pathogenesis-and-treatment
#14
REVIEW
Namrata Krishnan, Mark A Perazella
Drug-induced acute interstitial nephritis (DAIN) is a common cause of acute kidney injury and often presents as an unexplained rise in serum creatinine level. Kidney biopsy is therefore frequently required to make a definitive diagnosis. The hallmark pathologic features of DAIN are interstitial edema, interstitial inflammation, and tubulitis with a predominance of CD4+ T lymphocytes and mononuclear cells, with variable numbers of eosinophils. This is a result of a type B idiosyncratic non-immunoglobulin-E-mediated immune reaction marked by cell-mediated immune injury to the renal tubulointerstitium...
January 2015: Iranian Journal of Kidney Diseases
https://www.readbyqxmd.com/read/25568218/dendritic-cells-and-macrophages-sentinels-in-the-kidney
#15
REVIEW
Christina K Weisheit, Daniel R Engel, Christian Kurts
The mononuclear phagocytes (dendritic cells and macrophages) are closely related immune cells with central roles in anti-infectious defense and maintenance of organ integrity. The canonical function of dendritic cells is the activation of T cells, whereas macrophages remove apoptotic cells and microbes by phagocytosis. In the kidney, these cell types form an intricate system of mononuclear phagocytes that surveys against injury and infection and contributes to organ homeostasis and tissue repair but may also promote progression of CKD...
October 7, 2015: Clinical Journal of the American Society of Nephrology: CJASN
https://www.readbyqxmd.com/read/25343821/t-lymphocytes-and-acute-kidney-injury-update
#16
REVIEW
M N Martina, S Noel, S Bandapalle, A R A Hamad, H Rabb
The immune system is among the key pathogenic factors in acute kidney injury (AKI). Various immune cells, including dendritic cells, natural killer T cells, T and B lymphocytes, neutrophils and macrophages are involved. Conventional CD4+ lymphocytes are well established to participate in early injury, and CD4+CD25+FoxP3 regulatory T cells are protective and can accelerate repair. A newly identified kidney T cell receptor + CD4-CD8- (double-negative) T cell has complex functions, including potentially anti-inflammatory roles in AKI...
2014: Nephron. Clinical Practice
https://www.readbyqxmd.com/read/25331787/immune-cells-in-experimental-acute-kidney-injury
#17
REVIEW
Hye Ryoun Jang, Hamid Rabb
Acute kidney injury (AKI) prolongs hospital stay and increases mortality in various clinical settings. Ischaemia-reperfusion injury (IRI), nephrotoxic agents and infection leading to sepsis are among the major causes of AKI. Inflammatory responses substantially contribute to the overall renal damage in AKI. Both innate and adaptive immune systems are involved in the inflammatory process occurring in post-ischaemic AKI. Proinflammatory damage-associated molecular patterns, hypoxia-inducible factors, adhesion molecules, dysfunction of the renal vascular endothelium, chemokines, cytokines and Toll-like receptors are involved in the activation and recruitment of immune cells into injured kidneys...
February 2015: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/24971030/acute-kidney-injury-what-part-do-toll-like-receptors-play
#18
REVIEW
Patricia G Vallés, Andrea Gil Lorenzo, Victoria Bocanegra, Roberto Vallés
The innate immune system plays an important role as a first response to tissue injury. This first response is carried out via germline-encoded receptors. Toll-like receptors (TLRs) are the first identified and best studied family of pattern recognition receptors. TLRs are expressed on a variety of cell types, including epithelial cells, endothelia, dendritic cells, monocytes/macrophages, and B- and T-cells. TLRs initiate innate immune responses and concurrently shape the subsequent adaptive immune response...
2014: International Journal of Nephrology and Renovascular Disease
https://www.readbyqxmd.com/read/24892710/therapeutic-translation-in-acute-kidney-injury-the-epithelial-endothelial-axis
#19
REVIEW
Bruce A Molitoris
Acute kidney injury (AKI) remains a major clinical event with rising incidence, severity, and cost; it now has a morbidity and mortality exceeding acute myocardial infarction. There is also a documented conversion to and acceleration of chronic kidney disease to end-stage renal disease. The multifactorial nature of AKI etiologies and pathophysiology and the lack of diagnostic techniques have hindered translation of preclinical success. An evolving understanding of epithelial, endothelial, and inflammatory cell interactions and individualization of care will result in the eventual development of effective therapeutic strategies...
June 2014: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/24829504/semaphorin-3a-inactivation-suppresses-ischemia-reperfusion-induced-inflammation-and-acute-kidney-injury
#20
Punithavathi Ranganathan, Calpurnia Jayakumar, Riyaz Mohamed, Neal L Weintraub, Ganesan Ramesh
Recent studies show that guidance molecules that are known to regulate cell migration during development may also play an important role in adult pathophysiologic states. One such molecule, semaphorin3A (sema3A), is highly expressed after acute kidney injury (AKI) in mice and humans, but its pathophysiological role is unknown. Genetic inactivation of sema3A protected mice from ischemia-reperfusion-induced AKI, improved tissue histology, reduced neutrophil infiltration, prevented epithelial cell apoptosis, and increased cytokine and chemokine excretion in urine...
July 15, 2014: American Journal of Physiology. Renal Physiology
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