TY  - JOUR
AU  - Petrović-Đergović, D.
AU  - Popović, Milan
AU  - Chittiprol, S.
AU  - Cortado, H.
AU  - Ransom, R. F.
AU  - Partida-Sanchez, S.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/503
AB  - The mechanism responsible for trafficking of monocyte-derived macrophages into kidney in the puromycin aminonucleoside model of nephrotic syndrome in rats (PAN-NS), and the significance of this infiltration, remain largely unknown. CXCL10, a chemokine secreted in many T helper type 1 (Th1) inflammatory diseases, exhibits important roles in trafficking of monocytes and activated T cells. We hypothesized that induction of circulating interferon (IFN)- and glomerular tumour necrosis factor (TNF)- during PAN-NS would stimulate the release of CXCL10 by podocytes, leading to infiltration of activated immune cells and greater glomerular injury. We found that serum IFN-, glomerular Cxcl10mRNA and intra- and peri-glomerular macrophage infiltration were induced strongly during the late acute phase of PAN-NS in Wistar rats, but not in nude (Foxn1(rnu/rnu)) rats lacking functional effector T lymphocytes. Wistar rats also developed significantly greater proteinuria than nude rats, which could be abolished by macrophage depletion. Stimulation of cultured podocytes with both IFN- and TNF- markedly induced the expression of Cxcl10mRNA and CXCL10 secretion. Together, these data support our hypothesis that increased circulating IFN- and glomerular TNF- induce synergistically the production and secretion of CXCL10 by podocytes, attracting activated macrophages into kidney tissue. The study also suggests that IFN-, secreted from Th1 lymphocytes, may prime proinflammatory macrophages that consequently aggravate renal injury.
T2  - Clinical and Experimental Immunology
T1  - CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis
VL  - 180
IS  - 2
SP  - 305
EP  - 315
DO  - 10.1111/cei.12579
ER  - 

@article{
author = "Petrović-Đergović, D. and Popović, Milan and Chittiprol, S. and Cortado, H. and Ransom, R. F. and Partida-Sanchez, S.",
year = "2015",
abstract = "The mechanism responsible for trafficking of monocyte-derived macrophages into kidney in the puromycin aminonucleoside model of nephrotic syndrome in rats (PAN-NS), and the significance of this infiltration, remain largely unknown. CXCL10, a chemokine secreted in many T helper type 1 (Th1) inflammatory diseases, exhibits important roles in trafficking of monocytes and activated T cells. We hypothesized that induction of circulating interferon (IFN)- and glomerular tumour necrosis factor (TNF)- during PAN-NS would stimulate the release of CXCL10 by podocytes, leading to infiltration of activated immune cells and greater glomerular injury. We found that serum IFN-, glomerular Cxcl10mRNA and intra- and peri-glomerular macrophage infiltration were induced strongly during the late acute phase of PAN-NS in Wistar rats, but not in nude (Foxn1(rnu/rnu)) rats lacking functional effector T lymphocytes. Wistar rats also developed significantly greater proteinuria than nude rats, which could be abolished by macrophage depletion. Stimulation of cultured podocytes with both IFN- and TNF- markedly induced the expression of Cxcl10mRNA and CXCL10 secretion. Together, these data support our hypothesis that increased circulating IFN- and glomerular TNF- induce synergistically the production and secretion of CXCL10 by podocytes, attracting activated macrophages into kidney tissue. The study also suggests that IFN-, secreted from Th1 lymphocytes, may prime proinflammatory macrophages that consequently aggravate renal injury.",
journal = "Clinical and Experimental Immunology",
title = "CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis",
volume = "180",
number = "2",
pages = "305-315",
doi = "10.1111/cei.12579"
}

Petrović-Đergović, D., Popović, M., Chittiprol, S., Cortado, H., Ransom, R. F.,& Partida-Sanchez, S.. (2015). CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis. in Clinical and Experimental Immunology, 180(2), 305-315.
https://doi.org/10.1111/cei.12579

Petrović-Đergović D, Popović M, Chittiprol S, Cortado H, Ransom RF, Partida-Sanchez S. CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis. in Clinical and Experimental Immunology. 2015;180(2):305-315.
doi:10.1111/cei.12579 .

Petrović-Đergović, D., Popović, Milan, Chittiprol, S., Cortado, H., Ransom, R. F., Partida-Sanchez, S., "CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis" in Clinical and Experimental Immunology, 180, no. 2 (2015):305-315,
https://doi.org/10.1111/cei.12579 . .