macrophages of kidney are known as

For example, depletion of kidney macrophages using LC at the time of initial injury protected against kidney injury in IRI mice, suggesting that macrophages play a critical role in mediating tissue injury (21, 62). For example, one study revealed that suppression of macrophage recruitment in osteopontin-knockout mice reduces tubulointerstitial fibrosis during the recovery process of IRI (100). 3 317, No. Macrophages in Kidney Injury, Inflammation, and Fibrosis Macrophages are found in normal kidney and in increased numbers in dis- eased kidney, where they act as key players in renal injury, inflammation, and fibrosis. 6, 9 March 2016 | Journal of the American Society of Nephrology, Vol. A: acute kidney injury triggers recruitment of neutrophils and natural-killer (NK) cells within several hours of tissue injury. It is likely that anti-inflammatory (M2) macrophages coexist in small numbers or are absent due to a persistently inflammatory kidney microenvironment. Pro-inflammatory M1 macrophages release inflammatory mediators, including TNF-α and ROS, which cause tissue inflammation and subsequent kidney fibrosis. Macrophage infiltration correlated with kidney structural and functional injury in this model, suggesting that the macrophages may have been responsible for glomerular and interstitial injury (77). Loss of either Pink1 or Prkn promoted renal extracellular … performed experiments; Q.C. ©2015 Int. and Y.W. Adoptive transfer of macrophages that were exposed to a specific Jun amino terminal kinase (JNK) inhibitor significantly reduced proteinuria and glomerular cell proliferation in this model (56). In contrast to the protective effect of macrophage depletion during early phase of kidney I/R, macrophage depletion during the later recovery phase impedes tissue repair and regeneration. Furthermore, specific genes important in regulating possible fibrotic and fibrolytic macrophages have not been defined. Persistent inflammatory and fiborotic factors in chronic kidney disease promote renal fibrosis. Macrophages (MΦ) are highly heterogeneous cells that exhibit distinct phenotypic and functional characteristics depending on their microenvironment and the disease type and stage. Lin found that macrophage-derived Wnt7b also plays a critical role in promoting kidney regeneration via epithelial cell-cycle progression and basement membrane repair after IRI (80). showed that apoptotic cell-derived sphingosine-1-phosphate (S1P) polarized kidney macrophages to a reparative phenotype in the kidney of IRI mice (116). found that targeting IL-18 derived from activated macrophages by a neutralizing binding protein protected against the development of AN, with less interstitial inflammation, tissue injury, and kidney dysfunction (133). These questions need further investigation. These studies also suggest that the novel therapeutic strategies to treat chronic kidney disease should target pro-inflammatory macrophages in vivo. Background Autosomal dominant polycystic kidney disease is caused by genetic mutations in PKD1 or PKD2 . Furthermore, when Wnt7b is somatically deleted in macrophages, … Nikolic-Paterson and his colleagues found that adoptive transfer of IFN-γ-stimulated pro-inflammatory macrophages directly mediated glomerular cell proliferation and proteinuria in acute anti-GBM nephritis (55). Moreover, adoptive transfer of ex vivo activated M1 macrophages or inflammatory macrophages separated from AN kidney exacerbated kidney injury in AN mice (15, 129). 319, No. However, macrophages of type II phenotype (M2b) that express anti-inflammatory molecules IL-10 and osteopontin were identified during disease remission of LN (123). 47 chemokine receptor 1 (CX3CR1)-positive yolk-sac macrophages, also known as pre-macrophages; and ... 74 unappreciated increase in the proportion of yolk-sac-derived macrophages in the kidney with age. Renal macrophages are the most well studied inflammatory cell in the kidney and their involvement in cyst formation has been reported in different animal models and patients with cystic kidney disease. However, the core genes that regulate macrophage phenotype and function are still unclear. Direct evidence for a pathogenic role of macrophages was shown by our group by the protection of macrophages depletion in AN against kidney functional and structural injury (128). Until now, researchers hadn’t known if these macrophages had traveled from elsewhere in the body or if they were produced during embryonic development. approved final version of manuscript. In contrast, the uptake of apoptotic cells and anti-inflammatory cytokines drive macrophage polarization toward an anti-inflammatory M2 phenotype, which in turn promotes renal repair through secretion of trophic factors such as Wnt7b, heme-oxygenase-1 (HO-1), and chitinase-like protein BRP-39. 7, 5 October 2016 | Clinical Kidney Journal, Vol. Recently, Wyburn et al. Macrophage infiltration is a prominent feature of the innate immune response to kidney injury. Kidney macrophages form a functional unit with endothelial cells, rapidly taking up IC transported to them by virtue of their unique position and morphology. Lee found that depletion of macrophages at the time of IRI (when M1 macrophages are predominant) attenuated kidney injury, whereas depletion during the repair phase (when M2 macrophages are predominant) delayed kidney repair (75). 8, 23 May 2017 | Current Pathobiology Reports, Vol. A newly suggested classification may more closely reflect phenotypes of in vivo macrophages; in this classification, macrophages have been defined as pro-inflammatory, anti-inflammatory, fibrotic, and fibrolytic (6). They also showed that embryo-derived renal macrophages have a stronger immune response than their bone marrow-derived counterparts. The methods to target specific genes of macrophages have been made possible by LysMCre mice; for example, deletion of IL-4Ra by LysMCre reveals distinct subsets of M2 macrophages controlling inflammation and fibrosis in chronic schistosomiasis (22, 124). Deletion of CSF-1 significantly reduced macrophage infiltration with a remarkable reduction of tissue injury in MRL/lpr mice (60, 91). They are an essential component of innate immunity and also generate adaptive immune responses by recruiting other immune cells such as lymphocytes. The diversity of macrophage functions has led to several classification systems. More importantly, the applicability of these classification systems, namely the M1/M2 paradigm or the newer system four macrophage phenotypes, needs to be examined in human kidney disease. As mentioned above, macrophages are the predominant infiltrating cells that accumulate in the outer medulla of the postischemic kidney. 784, 28 June 2016 | Frontiers in Immunology, Vol. Several other studies found that rosiglitazone (a PPARγ agonist) and alpha-lipoic acid (an anti-oxidant) decreased infiltration of interstitial macrophages and reduced kidney dysfunction and tubular injury in cisplatin nephrotoxicity (65, 76). More recently, macrophages have been classified as classically activated macrophages (M1 macrophages), wound-healing macrophages (also known as M2a), and regulatory macrophages (also known as M2c) on the basis of their fundamental activation and function (92). Kidney fibrosis is a second-line healing program that only occurs if kidney repair is insufficient or consistently suppressed by ongoing tissue injury and inflammation. Also M1/M2 phenotypes do not fully mirror macrophage phenotypes in vivo. CSF-1 produced by tubular epithelial cells in IRI mice has been shown to polarize resident macrophages toward an M2 phenotype, which partially contributed to kidney repair and regeneration after IRI (2, 90, 137). Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia. Macrophages are involved in the formation of the niches of stem cells and progenitor cells; without macrophage help, stem cells or progenitor cells are not able to proliferate and differentiate in injured tissues (29). Macrophage depletion by clodronate microspheres resulted in greatly reduced TNF-α and IL-1β release in anti-GBM glomerulonephritis, suggesting that inflammatory macrophages mediated glomerular damage through release of pro-inflammatory cytokines (24). Macrophages are present at an early time point of kidney development, and addition of CSF-1 improves development of branch tips and nephrons, suggesting a trophic role of macrophages in embryonic kidney development (102). M1 macrophages may convert to M2 macrophages in response to tissue factors within the kidney during the recovery phase. M2 macrophages predominate at this stage and contribute to resolution of inflammation resolution and tissue repair. 7, No. In the heart, tissue-resident macrophages are known to participate in injury response and support normal physiology (42–44). The reduction of DAMPs and PAMPs as well as the increase of apoptotic cells represent a change in the tissue environment that would promote phenotype change of tissue macrophages (40). Copyright 2020 National Primate Research Centers - All Rights Reserved. Systemic macrophage depletion using LC 1 day before UUO decreased tubular cell apoptosis and kidney fibrosis, suggesting that the initial phase of macrophage infiltration may promote subsequent kidney fibrosis (118). 4, 8 February 2017 | Pflügers Archiv - European Journal of Physiology, Vol. However, it is unknown whether macrophages mainly promote kidney cell regeneration directly through cell fusion, through transformation, or via exosomes, or indirectly by helping stem cells and progenitor proliferation and differentiation. These tissue-specific macrophage subpopulations can change their phenotype and function in response to local microenvironmental signals during tissue infection or injury (94). Union Physiol. Resident macrophages are present during early kidney development, suggesting their role in the process (36, 45). The word macrophage comes from the Greek meaning ‘large eater’. Several other studies confirmed that macrophages are involved in the kidney repair after IRI in that macrophage ablation by either LC or diphtheria toxin 48–72 h after IRI resulted in persistent kidney injury (67, 83, 127). The specific M2 macrophage-dependent pathways or derived molecules that promote kidney repair and regeneration need further investigation. Anti-inflammatory macrophages induced in vivo by IL-25 have been demonstrated to be effective at reducing kidney injury in Adriamycin nephropathy (13). Anti-inflammatory M2 macrophages also suppress kidney inflammation and injury via secretion of anti-inflammatory cytokines such as IL-10 and TGF-β. S1P-dependent neutrophil gelatinase-associated lipocalin (NGAL/Lcn-2) produced by these macrophages was identified as a regenerative mediator enhancing tubular epithelial cell proliferation in the repair phase of IRI. Moreover, early or late treatment with the JNK inhibitor improved kidney function and attenuated glomerular and tubulointerstitial damage in the chronic anti-GBM model (35, 86). 1, 29 January 2019 | American Journal of Physiology-Renal Physiology, Vol. The implications of this discovery are important because while the kidneys help control the volume of blood in the body and maintain the proper concentrations of proteins and electrolytes, they are also subject to infection and disease. The most common form of the disease, autosomal dominant PKD (ADPKD) affects up to 1 in 500 and costs $2 billion/year to care for those afflicted. In contrast, anti-inflammatory M2 macrophages release anti-inflammatory mediators, including IL-10 and TGF-β; the latter suppresses kidney inflammation yet promotes kidney fibrosis. In addition, anti-inflammatory macrophages can be induced by apoptotic cell-derived factors. 5, No. Free full text . Soc. These studies indicate that targeting glomerular macrophages could be a potential approach to treat glomerulonephritis. Macrophages are a type of white blood cell central to the immune system that detect and engulf harmful pathogens, like viruses, bacteria and fungi, serving as helpful scavengers to fight infections. Even though CD11c has traditionally been considered to be a dendritic cell marker, both subsets showed major characteristics and functions of macrophages. demonstrated that mannose receptor 2 (Mrc2)-expressing macrophages displayed a fibrosis-attenuating role through activating a lysosomal collagen turnover pathway in UUO (82). Better strategies to induce reparative macrophages in vivo need to be developed. prepared figures; Q.C. NPRC scientists across the country are working to combat infectious diseases through a variety of research projects. Macrophages acts as sentinel cells; they have a role in destroying bacteria, protozoa and tumour cells, and release substances that act upon other immune cells. They are found everywhere in tissues and organs. Because Wnt7b is known to stimulate epithelial responses during kidney development, these findings suggest that macrophages are able to rapidly invade an injured tissue and reestablish a developmental program that is beneficial for repair and regeneration. We demonstrate downregulation of mitophagy regulators, mitofusin-2 (MFN2) and Parkin, downstream of PINK1 in kidney fibrosis. Macrophages were discovered in 1882 by Eli Mechnikoff and have been widely studied ever since. Steroid-based treatments appear to reduce kidney inflammation and injury by promoting anti-inflammatory macrophages in vivo (58). Triggers of kidney injury cause subsequent recruitment of monocytes that differentiate into different macrophage phenotypes in response to the local microenvironment. Adoptive transfer of netrin-1-treated macrophages suppressed inflammation and protected against kidney injury in IRI mice (105). showed that absence of scavenging receptors on uPAR−/− macrophages led to delayed clearance of pro-fibrotic molecules, resulting in kidney fibrosis in late-stage UUO (136). 312, No. Reparative macrophages also secrete chitinase-like protein BRP-39, which has been shown to promote regeneration in kidney by limiting tubular apoptosis via activation of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling (112). The phenotypic switch of macrophages is determined by microenvironment during the course of acute and chronic kidney disease. However, PAMPs are mostly absent in sterile kidney injury, and, in the sterile kidney inflammatory macrophage, infiltration is driven mostly by DAMPs (20, 69, 107). HO-1-overexpressing macrophages displayed an anti-inflammatory phenotype, with increased phagocytosis of apoptotic cells and increased IL-10 production (32). In contrast, macrophages at the later stage of repair may become profibrotic or fibrolytic to respectively induce or resolve kidney fibrosis directly. In this review … For example, depletion of kidney macrophages by liposomal clodronate (LC) significantly improves kidney injury and function in acute ischemia reperfusion injury (IRI) and unilateral ureteral obstruction (UUO) models (62, 68, 75). We have identified two major subsets of macrophages, which are F4/80+CD11c− and F4/80+CD11c+ cells in murine kidney (15). However, M2 macrophages have been shown to exist in acute kidney injury such as ischemic kidney but not in most chronic kidney diseases (14). In vitro cisplatin induced enhanced expression of TLRs and their associated signaling molecules in macrophages (121). M1 macrophages produce a great amount and a great number of pro-inflammatory mediators and mediate antimicrobial defence and antitumour immunity. For example, biglycan, a small leucine-rich proteoglycan, which is released from kidney resident cells during early stages of IRI, directly activates macrophages through TLR4 and TLR2, which mediate rapid activation of NF-κB and thereby stimulate the expression of inflammatory cytokines (110). In contrast, M2 macrophages have anti-inflammatory functions and are involved in parasite containment, wound healing, and fibrosis (94, 114). Alternatively, macrophages also can be modulated into a protective phenotype to reduce kidney injury in kidney disease. NPRC scientists across the country are working to combat infectious diseases through a variety of research projects. Strikingly, depletion of kidney macrophages by LC suppressed intraglomerular proliferative lesions and abrogated crescent formation in NZB/NZW F1 mice, suggesting that M2b macrophages mediate a dysregulated “tissue repair” program in poly (I:C)-induced LN. Apoptotic cells, anti-inflammatory cytokines, as well as growth factors are likely to predominate in the induction of anti-inflammatory macrophages (FIGURE 2). Cisplatin is a major antineoplastic drug and widely used to treat solid tumors, but it has dose-dependent kidney toxicity characterized by acute tubular necrosis and inflammation. 2, 7 April 2017 | American Journal of Physiology-Renal Physiology, Vol. Classically activated M1-type macrophages promote acute kidney injury, glomerulosclerosis, and renal interstitial fibrosis by exerting proinflammatory effects, while alternatively activated M2 macrophages have an anti-inflammatory effect, promoting wound healing, reducing renal inflammatory response and fibrosis, and reducing kidney damage . 1, 3 October 2017 | Nature Reviews Nephrology, Vol. Macrophages are found in normal kidney and in increased numbers in diseased kidney, where they act as key players in renal injury, inflammation, and fibrosis. Scientists say yes. Moreover, F4/80+CD11c+ macrophages had stronger phagocytic ability and produced more nitric oxide and IL-10 than did F4/80+CD11c− macrophages (15). and resident macrophages reduced survival after AKI (13). These results suggest that these macrophages may have site-specific functions or differing potency for protective or destructive function in kidney diseases. Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. iNOS, inducible nitric oxide synthase; Ym1, a chitinase-like protein; FIZZ1, a resistin-like protein; IGF1, insulin-like growth factor 1; SPHK1, sphingosine kinase 1; SLAM, signaling lymphocytic activation molecule. The anti-inflammatory macrophage-derived reparative molecules in IRI mice are poorly known. Macrophages are well recognized for their pathogenic role in kidney inflammation and fibrosis. They found that the angiotensin II type 1 receptor (Agtr1) on macrophage functions to attenuate kidney fibrosis in vivo. Macrophages and their associated inflammatory cytokines promote cyst progression; however, transcription factors within macrophages that control cytokine production and cystic disease are unknown. Kidney macrophages display phenotypic heterogeneity in kidney disease. Moreover, pro-inflammatory M1 macrophages also induce renal fibrosis by secretion of MMP-9. This review summarizes the role of macrophages with different phenotypes in kidney injury, inflammation, and fibrosis in various acute and chronic kidney diseases. 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Have long known the origins of different types of macrophages do not necessarily reflect true... Second-Line healing program that only occurs if kidney repair and regeneration immune cells such as kidney! Successfully used as a therapeutic in chronic kidney disease should target pro-inflammatory macrophages also kidney. Inflammation is an important feature of cystic kidney disease macrophage infiltration with a remarkable of... Via MMT recent discovery about the body ’ s infectious disease studies this! Injury cause subsequent recruitment of neutrophils and natural-killer ( NK ) cells within several hours of tissue injury in mice! Working to combat infectious diseases through a variety macrophages of kidney are known as research projects health worldwide and cause substantial tissue damage adapt. Improves tissue repair and remodeling, are declared by the author ( )! 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