Macrophage Subpopulations in Normal and Transplanted Heart and Kidney Tissues in the Rat1,2

Paul, Leendert C.; Grothman, Gary T.; Benediktsson, Hallgrímur; Davidoff, A.; Rozing, Jan

doi:10.1097/00007890-199201000-00032

Cited by 34 publications

(11 citation statements)

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“…A few hypointensity contrast spots are seen in high-resolution MR microscopy images of the native hearts after MPIO injection. This may reflect MPIO taken up by resident-tissue macrophages 27. This mechanism is not likely responsible for MPIO accumulation in our transplant animals because the MPIO injection is 24 hours before surgery and the blood clearance of the MPIO is rapid.…”

Section: Discussionmentioning

confidence: 94%

Longitudinal Tracking of Recipient Macrophages in a Rat Chronic Cardiac Allograft Rejection Model With Noninvasive Magnetic Resonance Imaging Using Micrometer-Sized Paramagnetic Iron Oxide Particles

Wu²,

Foley³

et al. 2008

Circulation

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Background-Long-term survival of heart transplants is hampered by chronic rejection (CR). Studies indicate the involvement of host macrophages in the development of CR; however, the precise role of these cells in CR is unclear. Thus, it is important to develop noninvasive techniques to serially monitor the movement and distribution of recipient macrophages in chronic cardiac allograft rejection in vivo. Methods and Results-We have employed a rat heterotopic working-heart CR model for a magnetic resonance imaging experiment. Twenty-one allograft (PVG.1U3 PVG.R8) and 9 isograft (PVG.R83 PVG.R8) transplantations were performed. Recipient macrophages are labeled via intravenous injection of micron-sized paramagnetic iron oxide particles (0.9 m in diameter) at a dose of 4.5 mg Fe per rat 1 day before transplantation. Serial in vivo magnetic resonance images were acquired for up to 16 weeks. The migration of labeled recipient cells in our CR model, in which cardiac CR is evident at 3 weeks and most extensive by 16 weeks after transplantation, can be assessed with the use of in vivo magnetic resonance imaging for Ͼ100 days after a single micron-sized paramagnetic iron oxide injection. The location and distribution of labeled recipient cells were confirmed with magnetic resonance microscopy and histology. Conclusions-This

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Section: Discussionmentioning

confidence: 94%

Longitudinal Tracking of Recipient Macrophages in a Rat Chronic Cardiac Allograft Rejection Model With Noninvasive Magnetic Resonance Imaging Using Micrometer-Sized Paramagnetic Iron Oxide Particles

Wu²,

Foley³

et al. 2008

Circulation

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“…Third, donor ED1 ϩ macrophages (monocytes/phagocytes) also were depleted in the 100-day heart allografts of all experimental groups, but they were replaced by disproportionate numbers of infiltrating ED1 ϩ host cells, consistent with previous claims that these macrophages are important effector cells in both acute rejection and CR. [51][52][53] Finally, the subpopulation of donor leukocytes in the allograft cell suspensions stained by the LEW MHC class II-specific L21-6 mAb and previously identified as DCs 9,11,54,55 made up only a small fraction of the numerous donor leukocytes contained in the CR-free cardiac allografts of groups 4 and 6. However, when the donor cells were less than 3% of the total leukocytes, the L21-6 ϩ cells made up the majority, raising the possibility that this tiny residual population of migratory cells had lost the ability to mount a GVH reaction, whereas selectively retaining the capacity of antigen presentation.…”

Section: Discussionmentioning

confidence: 99%

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

et al. 2000

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We have attributed organ engraftment to clonal exhaustion-deletion of host-versus-graft and graft-versus-host reactions that are reciprocally induced and governed by migratory donor and recipient leukocytes. The so-called donor passenger leukocytes that migrate from the allograft into the recipients have been thoroughly studied (chimerism), but not the donor leukocytes that remain in, or return to, the transplanted organ. Therefore, using flow cytometry we determined the percentage and lineages of donor leukocytes in cell suspensions prepared from Lewis (LEW) cardiac allografts to 100 days posttransplantation. The LEW hearts were transplanted to naïve untreated Brown Norway (BN) recipients (group 2), to naïve BN recipients treated with a 28-day or continuous course of tacrolimus (TAC) (groups 3 and 4), and to drug-free BN recipients pretolerized by earlier bone marrow cell (BMC) or orthotopic LEW liver transplantation (groups 5 and 6). The findings in the heart cell suspensions were correlated with the results from parallel histopathologic-immunocytochemical studies and other studies of the grafts and of host tissues. Although the LEW heart allografts were rejected in 9.6 days by the unmodified recipients of group 2, all beat for 100 days in the recipients of groups 3 through 6. Nevertheless, all of the long-surviving cardiac allografts (but not the isografts in group 1) were the targets of an immune reaction at 5 days, reflected by dramatic increases in the ratio of leukocytes to nonleukocyte nucleated cells from normal values of 1:5-1:6 to 1:1-5:1 and by manifold other evidence of a major inflammatory event. The acute changes returned to baseline by 100 days in the chronic rejection (CR) free hearts of groups 4 and 6, but not in the CR-afflicted hearts of short-course TAC group 3 or the less-severely damaged hearts of the BMC-prime group 5.The freedom from CR in groups 4 and 6 was associated with a large donor contribution to the intracardiac leukocyte population at 5 days (28.6% and 22% in the respective groups) and at 100 days (30.5% in group 4 and 8.4% in group 6) compared with 2% and 1.2% at 100 days in the CR-blighted allografts of the partially tolerant animals of groups 3 and 5. Whether large or small, the donor leukocyte fraction always included a subset of class II leukocytes that had histopathologic features of dendritic cells. These class II ؉ cells were of mixed myeloid (CD11-b/c ؉ ) and lymphoid lineages; their migration was markedly inhibited by TAC and accelerated by donor-specific priming and TAC discontinuance. Although a large donor leukocyte population and a normal leukocyte/nonleukocyte cell ratio were associated with freedom from CR, these findings and the lineage profile of the intracardiac leukocytes were not associated with tolerance in the animals of groups 3 and 4 under active TAC treatment. The findings in this study, singly and in their entirety, are compatible with our previously proposed leukocyte migration-localization paradigm of organ allograft acceptance and tolerance. (Liver ...

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“…Certain pathogens such as amoebe and schistosomes activate Mϕs, but the pattern of cytokine release is quite distinct with high levels of Tgfβ, IL13, and chemokines such as CCL17, CCl22 being released 35,36. The presence of cell surface ED3 antigen (CD163) in rats or Mac2 (galectin-3) in mice has been implicated as a marker of activated Mϕs in tissues, although expression of NOS2 or IL1β proteins is probably a more reliable marker of activation 37,38.…”

Section: Kidney Macrophages Show Evidence Of Activation and Correlatementioning

confidence: 99%

Macrophages and Immunologic Inflammation of the Kidney

Duffield

2010

Seminars in Nephrology

201

179

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Monocyte derived tissue effector cells, macrophages, are present in large numbers in all forms of kidney disease with inflammation. Their roles in inflammation and the molecular effectors of macrophage function have been difficult to decipher. With the advent of modern genetic tools and mouse models of human disease, great insight into monocyte/macrophage biology has been forthcoming. In this review we will place macrophage study in its historical context, define immunological diseases of the kidney, and broaden its definition to encompass current thinking of the immune response to kidney injury, highlight key advances of the study of monocyte/ macrophages in kidney diseases, and identify new therapeutic pathways and targets that hinge around macrophage function. Here we advance the case that targeting macrophage activation and phenotype is leading to new therapies in treatment of many acute and chronic kidney diseases.

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Macrophage Subpopulations in Normal and Transplanted Heart and Kidney Tissues in the Rat1,2

Cited by 34 publications

References 0 publications

Longitudinal Tracking of Recipient Macrophages in a Rat Chronic Cardiac Allograft Rejection Model With Noninvasive Magnetic Resonance Imaging Using Micrometer-Sized Paramagnetic Iron Oxide Particles

Longitudinal Tracking of Recipient Macrophages in a Rat Chronic Cardiac Allograft Rejection Model With Noninvasive Magnetic Resonance Imaging Using Micrometer-Sized Paramagnetic Iron Oxide Particles

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

Macrophages and Immunologic Inflammation of the Kidney

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