Alternatively activated macrophages in the pathogenesis of chronic kidney allograft injury

Ikezumi, Yohei; Suzuki, Toshiaki; Yamada, Takeshi; Hasegawa, Hideo; Kaneko, Utako; Hara, Masanori; Yanagihara, Toshio; Nikolic-Paterson, David J.; Saitoh, Akihiko

doi:10.1007/s00467-014-3023-0

Cited by 80 publications

(71 citation statements)

References 24 publications

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“…By 28 days, macrophages staining positively for these M2 markers were enlarged, vacuolated, and clustered in thickened alveoli surrounding areas of fibrosis, supporting their profibrotic activity (29,30). Epidemiological evidence, as well as experimental models of idiopathic and chemical-induced fibrosis, have shown that CD163 and CD206 M2 macrophages contribute to fibrogenesis in the lung, kidney, and peritoneum (31)(32)(33)(34)(35). Our findings suggest that they may play a similar role in lung fibrosis after NM exposure; however, this remains to be investigated.…”

Section: Discussionmentioning

confidence: 85%

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

Venosa¹,

Malaviya²,

Choi³

et al. 2016

Am J Respir Cell Mol Biol

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Nitrogen mustard (NM) is an alkylating agent known to cause extensive pulmonary injury progressing to fibrosis. This is accompanied by a persistent macrophage inflammatory response. In these studies, we characterized the phenotype of macrophages accumulating in the lung over time following NM exposure. Treatment of rats with NM (0.125 mg/kg, intratracheally) resulted in an increase in CD11b 1 macrophages in histologic sections. These cells consisted of inducible nitric oxide synthase 1 (iNOS) proinflammatory M1 macrophages, and CD68 1 M1 macrophages and mature CD43 2 M2 macrophages, which increased sequentially. Time-related increases in M1 (iNOS, IL-12a, COX-2, TNF-a, matrix metalloproteinase-9, matrix metalloproteinase-10) and M2 (IL-10, pentraxin-2, connective tissue growth factor, ApoE) genes, as well as chemokines/ chemokine receptors associated with trafficking of M1 (CCR2, CCR5, CCL2, CCL5) and M2 (CX 3 CR1, fractalkine) macrophages to sites of injury, were also noted in macrophages isolated from the lung after NM. The appearance of M1 and M2 macrophages in the lung correlated with NM-induced acute injury and the development of fibrosis, suggesting a potential role of these macrophage subpopulations in the pathogenic response to NM.

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Section: Discussionmentioning

confidence: 85%

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

Venosa¹,

Malaviya²,

Choi³

et al. 2016

Am J Respir Cell Mol Biol

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“…Therefore, interactions with endothelial cells, fibroblasts, and tissue stem cells could be important components of the role of macrophages in angiogenesis and tissue repair. CD163 macrophages are frequently localized to areas of interstitial fibrosis, collagen deposition, and accumulation of SMA-positive myofibroblastic cells in chronic kidney allograft injury [20]. The interactions between endothelial cells, myofibroblasts/SMCs, and CD163 macrophages are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

CD163 macrophage and erythrocyte contents in aspirated deep vein thrombus are associated with the time after onset: a pilot study

Furukoji

Yamashita

et al. 2016

Thrombosis J

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BackgroundThrombolytic therapy is effective in selected patients with deep vein thrombosis (DVT). Therefore, identification of a marker that reflects the age of thrombus is of particular concern. This pilot study aimed to identify a marker that reflects the time after onset in human aspirated DVT.MethodsWe histologically and immunohistochemically analyzed 16 aspirated thrombi. The times from onset to aspiration ranged from 5 to 60 days (median of 13 days). Paraffin sections were stained with hematoxylin and eosin and antibodies for fibrin, glycophorin A, integrin α2bβ3, macrophage markers (CD68, CD163, and CD206), CD34, and smooth muscle actin (SMA).ResultsAll thrombi were immunopositive for glycophorin A, fibrin, integrin α2bβ3, CD68, CD163, and CD206, and contained granulocytes. Almost all of the thrombi had small foci of CD34- or SMA-immunopositive areas. CD68- and CD163-immunopositive cell numbers were positively correlated with the time after onset, while the glycophorin A-immunopositive area was negatively correlated with the time after onset. In double immunohistochemistry, CD163-positive cells existed predominantly among the CD68-immunopositive macrophage population. CD163-positive macrophages were closely localized with glycophorin A, CD34, or SMA-positive cell-rich areas.ConclusionsThese findings indicate that CD163 macrophage and erythrocyte contents could be markers for evaluation of the age of thrombus in DVT. Additionally, CD163 macrophages might play a role in organization of the process of venous thrombus.Electronic supplementary materialThe online version of this article (doi:10.1186/s12959-016-0122-0) contains supplementary material, which is available to authorized users.

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“…For example, the abundance of M2-like Mø in human and mouse polycystic kidney disease (PKD), contribute to the progression of renal disease by promoting cyst growth and fibrosis (50). Similarly, M2-like Mø proliferation and infiltration is associated with tubular injury and progression of fibrosis during inflammation in human kidney transplant allografts (51,52). Moreover, insufficient renal epithelial healing in mice promotes an expansion of M2-like Mø that accelerates fibrogenesis (reviewed in ref.…”

Section: Methodsmentioning

confidence: 99%

IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease

Baek¹,

Zeng²,

et al. 2015

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Alternatively activated macrophages in the pathogenesis of chronic kidney allograft injury

Abstract: Our findings identify a major population of M2-type macrophages in patients with CAI, and suggest that these M2-type macrophages might promote the development of interstitial fibrosis in IF/TA-NOS.

Cited by 80 publications

References 24 publications

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

CD163 macrophage and erythrocyte contents in aspirated deep vein thrombus are associated with the time after onset: a pilot study

IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease

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