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Quantification and localization of M2 macrophages in human kidneys with acute tubular injury.

Palmer MB, Vichot AA, Cantley LG, Moeckel GW - Int J Nephrol Renovasc Dis (2014)

Bottom Line: M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells.Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells.We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.

ABSTRACT
This study addresses for the first time the question whether there is significant macrophage population in human kidney sections from patients with acute tubular injury (ATI). We examined therefore the interstitial macrophage population in human kidney tissue with biopsy-proven diagnosis of ATI, minimal change disease (MCD), and MCD with ATI. Kidney biopsies from patients with the above diagnoses were stained with antibodies directed against CD68 (general macrophage marker), CD163 (M2 marker), and HLA-DR (M1 marker) and their respective electron microscopy samples were evaluated for the presence of interstitial macrophages. Our study shows that patients with ATI have significantly increased numbers of interstitial CD68(+) macrophages, with an increase in both HLA-DR(+) M1 macrophages and CD163(+) M2 macrophages as compared to patients with MCD alone. Approximately 75% of macrophages were M2 (CD163(+)) whereas only 25% were M1 (HLA-DR(+)). M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells. Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells. We conclude that macrophages accumulate around injured tubules following ATI and exhibit predominantly an M2 phenotype. We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.

No MeSH data available.


Related in: MedlinePlus

Macrophages in human kidney tissue.Notes: (A) Average number per 200× optical field of CD68+, HLA-DR+ and CD163+ macrophages in the interstitium of kidneys from patients with either ATI with MCD, or MCD alone. (B) Average number of CD163+ interstitial macrophages in kidney tissue from patients with ATI, MCD, or MCD with ATI. Values are mean ± SD. N=4–8. *P<0.05.Abbreviations: ATI, acute tubular injury; MCD, minimal change disease; SD, standard deviation; HPF, high power fields.
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f1-ijnrd-7-415: Macrophages in human kidney tissue.Notes: (A) Average number per 200× optical field of CD68+, HLA-DR+ and CD163+ macrophages in the interstitium of kidneys from patients with either ATI with MCD, or MCD alone. (B) Average number of CD163+ interstitial macrophages in kidney tissue from patients with ATI, MCD, or MCD with ATI. Values are mean ± SD. N=4–8. *P<0.05.Abbreviations: ATI, acute tubular injury; MCD, minimal change disease; SD, standard deviation; HPF, high power fields.

Mentions: Interstitial macrophage density was determined by counting CD68+ cells/HPF. Alternatively activated (M2) macrophages were quantified by counting the CD163+ sub-population of CD68+ cells and classically activated (M1) macrophages were quantified by counting HLA-DR+ sub-population of CD68+ cells. Patients with ATI showed higher numbers of macrophages, on average 16.3 CD68+ macrophages/HPF, compared to only five CD68+ macrophages/HPF in patients with MCD alone (Figure 1A). The majority of the CD68+ macrophages was also positive for CD163 in both the patients with ATI and patients with MCD (Figure 1A). HLA-DR+ macrophages accounted for 4.5 cells/HPF in ATI patients’ kidneys and for 1.2 cells/HPF in kidneys of patients with MCD (Figure 1A).


Quantification and localization of M2 macrophages in human kidneys with acute tubular injury.

Palmer MB, Vichot AA, Cantley LG, Moeckel GW - Int J Nephrol Renovasc Dis (2014)

Macrophages in human kidney tissue.Notes: (A) Average number per 200× optical field of CD68+, HLA-DR+ and CD163+ macrophages in the interstitium of kidneys from patients with either ATI with MCD, or MCD alone. (B) Average number of CD163+ interstitial macrophages in kidney tissue from patients with ATI, MCD, or MCD with ATI. Values are mean ± SD. N=4–8. *P<0.05.Abbreviations: ATI, acute tubular injury; MCD, minimal change disease; SD, standard deviation; HPF, high power fields.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4230184&req=5

f1-ijnrd-7-415: Macrophages in human kidney tissue.Notes: (A) Average number per 200× optical field of CD68+, HLA-DR+ and CD163+ macrophages in the interstitium of kidneys from patients with either ATI with MCD, or MCD alone. (B) Average number of CD163+ interstitial macrophages in kidney tissue from patients with ATI, MCD, or MCD with ATI. Values are mean ± SD. N=4–8. *P<0.05.Abbreviations: ATI, acute tubular injury; MCD, minimal change disease; SD, standard deviation; HPF, high power fields.
Mentions: Interstitial macrophage density was determined by counting CD68+ cells/HPF. Alternatively activated (M2) macrophages were quantified by counting the CD163+ sub-population of CD68+ cells and classically activated (M1) macrophages were quantified by counting HLA-DR+ sub-population of CD68+ cells. Patients with ATI showed higher numbers of macrophages, on average 16.3 CD68+ macrophages/HPF, compared to only five CD68+ macrophages/HPF in patients with MCD alone (Figure 1A). The majority of the CD68+ macrophages was also positive for CD163 in both the patients with ATI and patients with MCD (Figure 1A). HLA-DR+ macrophages accounted for 4.5 cells/HPF in ATI patients’ kidneys and for 1.2 cells/HPF in kidneys of patients with MCD (Figure 1A).

Bottom Line: M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells.Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells.We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.

ABSTRACT
This study addresses for the first time the question whether there is significant macrophage population in human kidney sections from patients with acute tubular injury (ATI). We examined therefore the interstitial macrophage population in human kidney tissue with biopsy-proven diagnosis of ATI, minimal change disease (MCD), and MCD with ATI. Kidney biopsies from patients with the above diagnoses were stained with antibodies directed against CD68 (general macrophage marker), CD163 (M2 marker), and HLA-DR (M1 marker) and their respective electron microscopy samples were evaluated for the presence of interstitial macrophages. Our study shows that patients with ATI have significantly increased numbers of interstitial CD68(+) macrophages, with an increase in both HLA-DR(+) M1 macrophages and CD163(+) M2 macrophages as compared to patients with MCD alone. Approximately 75% of macrophages were M2 (CD163(+)) whereas only 25% were M1 (HLA-DR(+)). M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells. Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells. We conclude that macrophages accumulate around injured tubules following ATI and exhibit predominantly an M2 phenotype. We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.

No MeSH data available.


Related in: MedlinePlus