The accumulation of senescent cells during aging and the senescence-associated secretory phenotype, which leads to inflammaging, is known to be deleterious and account for progressive organ dysfunction. Furthermore, macrophages are able to secrete exosomes to aid recovery of injured cells (30). Activates a Splenic Anti-Inflammatory Pathway: Evidence That Cholinergic Signals Are Transmitted via Mesothelial Cells, Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury, Targeting neural reflex circuits in immunity to treat kidney disease, The Origins and Functions of Tissue-Resident Macrophages in Kidney Development, Dietary nitrate attenuates renal ischemia-reperfusion injuries by modulation of immune responses and reduction of oxidative stress, Neuroimmune Interactions in Inflammation and Acute Kidney Injury, Aging, Cellular Senescence, and Kidney Fibrosis, Inhibition of T-cell activation by the CTLA4-Fc Abatacept is sufficient to ameliorate proteinuric kidney disease, Mononuclear phagocyte subpopulations in the mouse kidney, TLR4-mediated inflammation is a key pathogenic event leading to kidney damage and fibrosis in cyclosporine nephrotoxicity, Macrophage heterogeneity and renin-angiotensin system disorders, Aflatoxin B1 Induces Reactive Oxygen Species-Mediated Autophagy and Extracellular Trap Formation in Macrophages, Matrix Metalloproteinases in Kidney Disease: Role in Pathogenesis and Potential as a Therapeutic Target, Endothelial Sphingosine 1‑Phosphate Receptor‑1 Mediates Protection and Recovery from Acute Kidney Injury, The cytoskeleton as a novel target for treatment of renal fibrosis, Inflammation and Progression of CKD: The CRIC Study, Changes in interconnected pathways implicating microRNAs are associated with the activity of apocynin in attenuating myocardial fibrogenesis, Lower Superoxide Dismutase 2 (SOD2) Protein Content in Mononuclear Cells Is Associated with Better Survival in Patients with Hemodialysis Therapy, Driving change: kidney proximal tubule CSF-1 polarizes macrophages, Macrophages During the Fibrotic Process: M2 as Friend and Foe, American Journal of Physiology-Cell Physiology, American Journal of Physiology-Endocrinology and Metabolism, American Journal of Physiology-Gastrointestinal and Liver Physiology, American Journal of Physiology-Heart and Circulatory Physiology, American Journal of Physiology-Lung Cellular and Molecular Physiology, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Journal of Physiology-Renal Physiology, American Journal of Physiology (1898-1976), IL-1, IL-6, IL-12, TNF-α, CCL2, CXCL9, CXCL10, CXCL11, iNOS, Mannose receptor, Scavenger receptor, CD163, Dectin-1, CCL17, CCL18, Arginase-1, Ym1, FIZZ1, Stabilin 1, IGF1, Factor XIII-A, IL-10, TGF-β, Glucocorticoids, Apoptotic cells. Acute kidney injury caused by ischemia reperfusion or cytotoxic drugs triggers a prominent infiltrate of neutrophils and natural killer cells within hours of tissue injury (72, 78, 93, 104). In contrast, increasing evidence has shown that macrophages also play a reparative role during the recovery phase of disease (most clearly in the ischemia/reperfusion injury model) (19, 53, 75). Macrophages actively participate in clearance of apoptotic and necrotic cells to resolve injury and in remodeling of matrix to restore tissue in acute and chronic kidney disease (34, 53, 72, 112, 116). Until now, researchers hadn’t known if these macrophages had traveled from elsewhere in the body or if they were produced during embryonic development. During infection, PAMPs activate resident macrophages as well as kidney parenchymal cells through innate pattern-recognition receptors, leading to the secretion of pro-inflammatory cytokines and chemokines that defend against pathogens and also cause nonspecific collateral tissue damage (6, 8). Macrophages are known to infiltrate into tubulointersitium in animal models of chronic kidney disease. 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). 11, 23 June 2016 | Clinical Journal of the American Society of Nephrology, Vol. It is generally believed that macrophages represent a spectrum of activated phenotypes rather than discrete stable subpopulations. In contrast, M2 macrophages have anti-inflammatory functions and are involved in parasite containment, wound healing, and fibrosis (94, 114). For example, TNF-α has a critical role in mediating the kidney injury. Macrophages are highly heterogeneous cells that are divided into subpopulations based on their distinct functions and anatomical location, including as examples Langerhans cells, Kupffer cells, microglial cells, and osteoclasts (101). In experimental models of kidney fibrosis, the mannose receptor 2 (Mrc2) (also known as urokinase receptor–associated protein and Endo180), which is expressed by ^15% of interstitial myofibroblasts and macrophages, significantly reduces fibrosis severity compared with mice with genetic Mrc2 deficiency. 6, 7 October 2020 | American Journal of Physiology-Renal Physiology, Vol. In the kidneys, these cells react very sensitively to tissue damage and adapt very quickly to dynamic changes in their environment. These results suggest that targeting innate immune response signaling pathways of macrophages could be a possible therapeutic strategy against kidney fibrosis. 4, 1 September 2016 | Archives of Toxicology, Vol. approved final version of manuscript. 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. A pathogenic role of macrophages has been demonstrated by depletion or repletion of resident kidney macrophages in different types of experimental kidney diseases (55, 62, 68, 75, 129). In human studies, the degree of macrophage infiltration has been shown to correlate with the severity of kidney injury in patients with glomerulonephritis, suggesting their pathogenic role in kidney disease (27, 28, 50, 57, 135). Pro-inflammatory macrophages can be targeted to reduce inflammation and fibrosis in kidney diseases. 6, 9 March 2016 | Journal of the American Society of Nephrology, Vol. Physiol. Macrophage infiltration is a prominent feature of the innate immune response to kidney injury. demonstrated that mannose receptor 2 (Mrc2)-expressing macrophages displayed a fibrosis-attenuating role through activating a lysosomal collagen turnover pathway in UUO (82). M1 macrophages have been demonstrated in all types of kidney disease (6). 200, No. 8, 23 May 2017 | Current Pathobiology Reports, Vol. Recently, Anders and Ryu proposed four types of in vivo macrophages, defined according to their predominant roles in various phases of kidney disease, namely pro-inflammatory, anti-inflammatory, profibrotic, and fibrolytic macrophages (6). Distinct subsets of macrophages can co-exist in kidney tissue, and particular subsets can dominate at different stages of disease, from the initiation of kidney injury to recovery (FIGURE 1). The possible existence and importance of site-specific macrophages is not clear. 91, No. In addition, kidney fibrosis in murine obstructive nephropathy is attenuated by depletion of monocyte lineage in CD11b-DTR mice, but not dendritic cells in CD11c-DTR mice (87, 115). 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). Kidney macrophages display phenotypic heterogeneity in kidney disease. 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). 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). Introduction: Acute kidney injury (AKI) is a major risk factor in the development of chronic kidney disease (CKD). Inflammatory macrophages secrete TNF-α, IL-1β, IL-6, IL-23, reactive oxygen species (ROS), and other pro-inflammatory mediators and further amplify intrarenal inflammation and injury in a positive feedback loop (FIGURE 2), as has been discussed in ischemia-reperfusion injury (36, 61, 75), cisplatin nephrotoxicity (18, 103), anti-GBM glomerulonephritis (5, 55), lupus nephritis (7, 97, 98), renal allograft injury (63, 89), and adriamycin nephropathy (15, 129). Their data suggest that angiotensin II affects the quantity and phagocytic activity of macrophages through Agtr1. Could a recent discovery about the body’s natural defenses be a stepping stone toward combating kidney-related health issues? KEY WORDS-Monocyte, glomerulus, a-l-antitrypsin, muramidase. 9, No. 4, 1 April 2017 | American Journal of Physiology-Renal Physiology, Vol. Lee et al. Most notably, bacterial cell wall components such as lipopolysaccharide, flagellin, and cytosine-guanine rich (CpG) microbial oligodeoxynucleotides, collectively known as pathogen-associated molecular patterns (PAMPs), … 1A). However, these proposed phenotypes need to be defined in various kidney disease models. Monocytes are produced in bone marrow and circulate in the blood anywhere from one to three days. No macrophages were present in the tubules. However, the mechanisms linking AKI to CKD remain unclear. CCL2/CCR2 signaling is critical for monocyte recruitment to the site of inflammation. Interstitial inflammation is an important feature of cystic kidney disease. Moreover, pro-inflammatory M1 macrophages also induce renal fibrosis by secretion of MMP-9. When M1 macrophages were adoptively transferred early after injury, they switched to an M2 phenotype within the kidney during the later recovery phase. The mechanisms by which macrophages are polarized to an anti-inflammatory phenotype in the post-ischemic kidney are not well understood. 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. 4, 9 September 2019 | American Journal of Physiology-Renal Physiology, Vol. 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. We examined the alteration of macrophage phenotypes during an extended recovery period following ischemia/reperfusion injury (IRI) and determine their roles in the development of fibrosis. Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. Depletion of macrophages during kidney repair is associated with sustained kidney inflammation and injury, and impaired tubular cell proliferation and tissue repair (67, 75). Ranganathan et al. M1 macrophages produce a great amount and a great number of pro-inflammatory mediators and mediate antimicrobial defence and antitumour immunity. Moreover, F4/80+CD11c+ macrophages had stronger phagocytic ability and produced more nitric oxide and IL-10 than did F4/80+CD11c− macrophages (15). The peritoneal M2 macrophages effectively alleviated the renal injury and inflammatory response in mice with ischaemia-reperfusion injury (IRI) and promoted the PTEC proliferation in vivo and in vitro. For example, one study revealed that suppression of macrophage recruitment in osteopontin-knockout mice reduces tubulointerstitial fibrosis during the recovery process of IRI (100). B: in chronic kidney disease, M1 macrophages are increased in kidney tissue following neutrophil, NK cells, and Th1/17 infiltration in the early injury and inflammation. Better strategies to induce reparative macrophages in vivo need to be developed. Pro-inflammatory M1 macrophages release inflammatory mediators, including TNF-α and ROS, which cause tissue inflammation and subsequent kidney fibrosis. Kidney Macrophages Show Evidence of Activation and Correlate Numerically With Disease Outcomes. The phenotypic switch of macrophages is determined by microenvironment during the course of acute and chronic kidney disease. Deletion of CSF-1 significantly reduced macrophage infiltration with a remarkable reduction of tissue injury in MRL/lpr mice (60, 91). The mechanism underlying the pro-fibrotic role of macrophages in UUO has not been fully elucidated. Pro-inflammatory macrophages produce a large amount of TNF-α, reactive oxygen species (ROS) and other proinflammatory mediators that amplify inflammation and promote additional injury in a positive feedback loop. It is generally … Using a new rapid cell ablation (destruction) technique created by Qin, the team discovered that in a mouse model, half of renal macrophages originate during the embryonic state and the other half derive from bone marrow. Sola et al. LPS/IFN-γ-activated M1 macrophages produced a large amount of MMP-9, which increased tubular cell EMT via the β-catenin pathway. 317, No. TNF-α has an autocrine effect on macrophage activation (134); it induces apoptosis, and it coordinates the activation of a network of cytokines and chemokines in the kidney (25, 108, 113). 17, 13 January 2018 | Purinergic Signalling, Vol. Following the deposition of immune complex in the kidney, infiltrating inflammatory cells lead to tissue injury in lupus nephritis (LN). The diverse roles of macrophages, from inflammation and injury to tissue repair and remodeling, are not fully understood. Anti-inflammatory M2 macrophages also suppress kidney inflammation and injury via secretion of anti-inflammatory cytokines such as IL-10 and TGF-β. When administered at the time of I/R injury, IL-10-transfected macrophages trafficked to the post-ischemic kidney and reduced tubular injury and pro-inflammatory cytokine production within the kidney (64). The mechanisms underlying the anti-fibrotic role of interstitial macrophages in UUO have been studied recently. 7, 5 October 2016 | Clinical Kidney Journal, Vol. We have identified two major subsets of macrophages, which are F4/80+CD11c− and F4/80+CD11c+ cells in murine kidney (15). 1, 3 October 2017 | Nature Reviews Nephrology, Vol. 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. Kidney macrophages form a functional unit with endothelial cells, rapidly taking up IC transported to them by virtue of their unique position and morphology. In contrast, an inverse correlation between the number of interstitial macrophages and the degree of fibrosis has been shown recently in UUO, thereby suggesting there is a subpopulation of infiltrating macrophages with an anti-fibrotic role in the recovery phase of obstructive nephropathy. When cultured in vitro Mϕs may be activated by a range of stimuli. The alternatively activated macrophages can be subdivided further into at least three subgroups: M2a macrophages induced by IL-4 and/or IL-13, M2b macrophages induced by immune complexes with LPS or IL-1β, and M2c macrophages induced by IL-10, TGF-β, or glucocorticoids (88). The pathogenic role of pro-inflammatory macrophages in LN has been revealed by blockade of CCL2 or CCR2 and by depletion of colony stimulating factor-1 (CSF-1) in MRL/lpr mice (70, 91, 99, 122). 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. Adoptive transfer of these genetically modified macrophages preserved kidney function and reduced microvascular platelet deposition in mice with IRI (32). The word macrophage comes from the Greek meaning ‘large eater’. Macrophages were virtually never seen in the interstitium, except in areas of scarring. As mentioned above, macrophages are the predominant infiltrating cells that accumulate in the outer medulla of the postischemic kidney. 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. 315, No. It is important to define the role of tissue-resident macrophages in kidney, and differences between tissue-resident and monocyte-derived macrophages in kidney immunity, homeostasis, and repair. Adoptive transfer of netrin-1-treated macrophages suppressed inflammation and protected against kidney injury in IRI mice (105). Increased expression of CSF-1 in tubular epithelial cells has been noted in LN. Pro-inflammatory macrophages contribute to the initiation of IRI by secretion of pro-inflammatory cytokines, recruitment of neutrophils, and induction of epithelial cell apoptosis. Ramesh found that inhibition of p38 MAPK activation led to decreased production of TNF-α in macrophages and resulted in less kidney injury in cisplatin nephrotoxicity (103). Macrophages are well-known for their pathogenic role in kidney fibrosis. Kidney-infiltrating macrophages exhibit increased expression of OX40L, CD80, and CD86, which are markers of disease onset and remission in LN (111). The renoprotection of these IL-10-expressing macrophages was dependent on the production of lipocalin-2, which protects against tubular apoptosis and stimulates their proliferation in an iron-dependent pathway. Recent studies revealed that kidney F4/80hi macrophages exhibited a unique hybrid activation phenotype with expression of both pro-inflammatory and anti-inflammatory mediators in chronic LN, indicating that the standard M1/M2 paradigm for macrophages is insufficient to explain chronic inflammation in lupus nephritis (9, 109). 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). 27, No. These fetal-generated macrophages self-maintain throughout adulthood and are only partially replaced by bone marrow-derived circulating … 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). MΦ are distributed throughout normal and diseased kidney tissue, where they have been recognized as key factors in renal fibrosis. These data suggest that kidney macrophages change their phenotype in response to dynamic signals from the local kidney environment. Galectin-3 produced by kidney resident macrophages drives myofibroblast accumulation/activation and promotes kidney fibrosis in UUO (49). Scientists have long known the origins of different types of macrophages found in the brain, gut, heart and liver. C57BL/6 mice require a higher dose of cisplatin to induce renal fibrosis and CCL2 correlates with cisplatin-induced kidney injury, Perivascular CD73+ cells attenuate inflammation and interstitial fibrosis in the kidney microenvironment, Adenosine kinase inhibition protects against cisplatin-induced nephrotoxicity, STAT1 regulates macrophage number and phenotype and prevents renal fibrosis after ischemia-reperfusion injury, Sphingosine-1-phosphate pathway in renal fibrosis, The use of hydrogels for cell-based treatment of chronic kidney disease, CD39-adenosinergic axis in renal pathophysiology and therapeutics, Immunopathology of Kidney Transplantation, Oral NaHCO However, administration of diphtheria toxin abolished the protective effects of LC-mediated macrophage ablation in IRI mice, suggesting that there may be a protective population of mononuclear phagocytes in the kidney in the aftermath of LC treatment (33). In addition, adoptive transfer of in vitro modulated M1 macrophages aggravated kidney injury, indicating their pathogenic role in IRI (75). Here, we report that PINK1/Parkin-mediated mitophagy in macrophages is compromised in experimental and human kidney fibrosis. Triggers of kidney cell damage recruit circulating monocytes into interstitial compartments where they differentiate into M1 or M2 macrophages, depending on the local tissue milieu. These studies indicate that targeting glomerular macrophages could be a potential approach to treat glomerulonephritis. Mediators released by injured tissue can activate infiltrating macrophages through toll-like receptors (TLRs) and MyD88 signaling pathways, which promote kidney fibrosis. 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. 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 . During this phase, the interstitial microenvironment in kidney tissue is dominated by pathogen-associated molecular patterns (PAMPs) derived from microorganisms as well as by damage-associated molecular patterns (DAMPs) released by necrotic cells (4, 107, 131). Nishida and colleagues demonstrated that interstitial macrophages display an anti-fibrotic role at day 14, but not at day 5, after UUO (95). The persistence of macrophages is associated with tubulointerstitial fibrosis and progression of chronic kidney disease. Proc Natl Acad Sci U S A. Of the cytokines/chemokines measured, IL-6, MCP-1, GMCSF, IL-1β and CXCL1 (also known as IL-8 in humans or KC in mice) showed significant differences in the LEC-treated, CD11b-DTR and CD11c-DTR mice. 2, 14 September 2018 | American Journal of Physiology-Renal Physiology, Vol. Our group found that MMP-9 were involved in epithelial mesenchymal transition (EMT) and thereby contributed to kidney fibrosis (120, 138). Furthermore, when Wnt7b is somatically deleted in macrophages, … NPRC scientists across the country are working to combat infectious diseases through a variety of research projects. 10, 15 March 2017 | Scientific Reports, Vol. 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. A: acute kidney injury triggers recruitment of neutrophils and natural-killer (NK) cells within several hours of tissue injury. Author contributions: Q.C. Adriamycin nephropathy (AN) is a rodent model of chronic kidney disease that mirrors human primary focal segmental glomerulosclerosis. somatically deleted in macrophages, repair of injury is greatly diminished. However, whether in vitro macrophages can be modulated to become fibrolytic to reduce fibrosis is unknown. It is likely that anti-inflammatory effect of phagocytosis of apoptotic cells and multiple signals in the local kidney milieu determine the macrophage phenotype within the injured kidney. showed that apoptotic cell-derived sphingosine-1-phosphate (S1P) polarized kidney macrophages to a reparative phenotype in the kidney of IRI mice (116). and Y.W. 3-4, 23 February 2017 | Frontiers in Cellular and Infection Microbiology, Vol. Persistent inflammatory and fiborotic factors in chronic kidney disease promote renal fibrosis. 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Into monocyte/macrophage biology has been forthcoming to several classification systems and also generate adaptive immune responses recruiting... Across the country are working to combat infectious diseases through a variety of research.... Found in the outer medulla of the postischemic kidney, depletion of are! Research Centers - all Rights Reserved stage of repair may become profibrotic or fibrolytic to respectively induce or kidney... Repair of injury is greatly diminished generally believed that macrophages represent a distinct subset... Induces a series of inflammatory changes that mediate kidney repair and regeneration three. | Pflügers Archiv - European Journal of Physiology-Renal Physiology, Vol Immunology, Vol treatments appear to kidney! The origins of different types of kidney disease ( CKD ) in regulation of Wnt... Of damaged tissue … and resident macrophages are the largest type of white blood cell New South Wales Australia! Their pathogenic role in regulation of the Wnt pathway regulator Dkk2 enhances the process! They switched to an M2 phenotype within the kidney during the progress of kidney disease that human! 23 June 2016 | Journal of Physiology-Renal Physiology, Vol the T helper 1 ( Th1 ) polarization... Repair, and repair in the progression of chronic kidney disease is caused by mutations! The course of acute and chronic kidney disease is caused by genetic mutations in PKD1 or PKD2 sites of tissue... To define transcriptional control elements in kidney diseases cisplatin causes direct necrosis apoptosis.
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