Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury

Kim, Myung Gyu; Boo, Chang Su; Ko, Yoon Sook; Lee, Hee Young; Cho, Won Yong; Kim, Hyoung Kyu; Jo, Sang Kyung

doi:10.1093/ndt/gfq183

Cited by 77 publications

(77 citation statements)

References 26 publications

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“…When M1 M⌽ were adoptively transferred early after injury, they switched to an M2 phenotype within the kidney during the later recovery phase (48). These findings are consistent with several other published studies in which M⌽ ablation during the repair phase of IRI resulted in deleterious outcomes (38,52). Lin found that the mechanism underlying M2 promotion of kidney repair involves production of the Wnt pathway ligand Wnt7b, and M⌽ Wnt7b promotes regeneration via epithelial cell-cycle progression and basement membrane repair ( Fig.…”

Section: Pathogenic and Protective Role Of M⌽ In Acute Kidney Diseasesupporting

confidence: 88%

Pathogenic and protective role of macrophages in kidney disease

Cao

Wang

Harris

2013

American Journal of Physiology-Renal Physiology

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Macrophages (MΦ) are located throughout kidney tissue, where they play important roles in homeostasis, surveillance, tolerance, and cytoprotection. MΦ are highly heterogeneous cells and exhibit distinct phenotypic and functional characteristics depending on their microenvironment and the disease type and stage. Recent studies have identified a dual role for MΦ in several murine models of kidney disease. In this review, we discuss the pathogenic and protective roles of the various MΦ subsets in experimental and human kidney diseases and summarize current progress toward the therapeutic use of MΦ in kidney diseases.

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Section: Pathogenic and Protective Role Of M⌽ In Acute Kidney Diseasesupporting

confidence: 88%

Pathogenic and protective role of macrophages in kidney disease

Cao

Wang

Harris

2013

American Journal of Physiology-Renal Physiology

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“…While AM depletion studies in vivo would definitively determine if AMs are the key regulator of the IL-23-mediated inflammatory response to P. aeruginosa infection, the current methodological approaches to AM depletion are inadequate to answer this question. Commonly used approaches, such as clodronate depletion or the use of CD11b Ϫ diphtheria toxin receptor (DTR) mice, do deplete AMs; however, these approaches also deplete DC populations (19,32,50,55). Based on our data, we believe that AMs are capable of driving the IL-23-dependent innate inflammatory response, and more likely than mDCs to do so.…”

Section: Discussionmentioning

confidence: 72%

Interleukin-23-Mediated Inflammation in Pseudomonas aeruginosa Pulmonary Infection

et al. 2012

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Pseudomonas aeruginosa is an opportunistic pathogen that is capable of causing acute and chronic pulmonary infection in the immunocompromised host. In the case of cystic fibrosis (CF), chronic P. aeruginosa infection causes increased mortality by promoting overly exuberant airway inflammation and cumulative lung damage. Identifying the key regulators of this inflammation may lead to the development of new therapies that improve P. aeruginosa-related mortality. We report here that interleukin-23 (IL-23), the cytokine most clearly tied to IL-17-mediated inflammation, also promotes IL-17-independent inflammation during P. aeruginosa pulmonary infection. During the early innate immune response, prior to IL-17 induction, IL-23 acts synergistically with IL-1␤ to promote early neutrophil (polymorphonuclear leukocyte [PMN]) recruitment. However, at later time points, IL-23 also promoted IL-17 production by lung ␥␦ T cells, which was greatly augmented in the presence of IL-1␤. These studies show that IL-23 controls two independent phases of neutrophil recruitment in response to P. aeruginosa infection: early PMN emigration that is IL-17 independent and later PMN emigration regulated by IL-17. Pseudomonas aeruginosa pulmonary infection occurs in immunocompromised hosts and is associated with significant morbidity and mortality. The pathogen induces a robust neutrophil response that causes significant airway damage and does not always eliminate the pathogen. In cystic fibrosis (CF), where infection is chronic, the inflammation causes cumulative airway damage that is a major contributor to morbidity and mortality (41,46,62). Identifying the immune mediators that promote this inflammation is the first step in developing new therapies that can improve outcomes in chronic P. aeruginosa pulmonary infection.We and others have previously shown that airway interleukin-23 (IL-23) and IL-17 levels correlate with infection status and inflammation in individuals with CF (12,15,38) and that lymphocytes from CF-derived draining lymph nodes produce higher levels of IL-17 than non-CF disease controls (3). We have also shown that both IL-23 and IL-17 are critical for neutrophil recruitment in a murine model of chronic P. aeruginosa pulmonary infection (14). While these data demonstrate that the IL-23/ IL-17 proinflammatory axis is active during P. aeruginosa airway infection and in CF, the studies did not isolate the actions of IL-23 from those of IL-17.Historically, IL-17 has been credited with promoting both neutrophil recruitment and granulopoiesis through its induction of neutrophil growth factors and chemokines, including IL-6, granulocyte colony-stimulating factor (G-CSF), keratinocyte chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) (14,24,30,38,49,54,64). IL-23, a recently identified IL-12 family member (42, 60), has been primarily characterized in the context of this Th17 response (1,25,33). Of note, however, IL-23-overexpressing mice have a hyperinflammatory phenotype and notable elevations in serum IL-1␤ and t...

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“…In ischemia reperfusion injury (IRI), an important problem in kidney transplantation, kidney-resident DCs are the first to produce proinflammatory chemokines and cytokines like TNF (59), suggesting a proinflammatory role ( Figure 2B). However, functional studies showed that kidney DCs prevented excess ischemic tissue damage (60,61), which has been linked to anti-inflammatory signaling mechanisms involving IFN regulatory factor 4 and immunosuppressive mediators, like IL-10 and single Ig IL-1-related receptor (62). Protective functions of DCs have also been shown in models of druginduced tubulotoxicity (63) and acute crescentic GN (64), which may be mediated through the inducible costimulatory ligand on DCs (65), a T-cell suppressor.…”

Section: Akimentioning

confidence: 99%

Dendritic Cells and Macrophages

Weisheit¹,

Engel

Kurts

2015

Clinical Journal of the American Society of Nephrology

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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. This review summarizes the general functions and classification of dendritic cells and macrophages in the immune system and recapitulates why overlapping definitions and historically separate research have created controversy about their tasks. Their roles in acute kidney disease, CKD, and renal transplantation are described, and therapeutic strategy to modify these cells for therapeutic purposes is discussed.

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Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury

Abstract: Our results suggest that kidney CD11c(+) F4/80(+) dendritic subset might contribute to the recovery process by dynamic phenotypic change from pro-inflammatory to anti-inflammatory with modulation of immune response.

Cited by 77 publications

References 26 publications

Pathogenic and protective role of macrophages in kidney disease

Pathogenic and protective role of macrophages in kidney disease

Interleukin-23-Mediated Inflammation in Pseudomonas aeruginosa Pulmonary Infection

Dendritic Cells and Macrophages

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