Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury
Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. In this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to f...
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2014-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/291024 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850167680910229504 |
|---|---|
| author | Matheus Correa-Costa Tárcio Teodoro Braga Raphael José Ferreira Felizardo Vinícius Andrade-Oliveira Katia Regina Perez Iolanda Midea Cuccovia Meire Ioshie Hiyane João Santana da Silva Niels Olsen Saraiva Câmara |
| author_facet | Matheus Correa-Costa Tárcio Teodoro Braga Raphael José Ferreira Felizardo Vinícius Andrade-Oliveira Katia Regina Perez Iolanda Midea Cuccovia Meire Ioshie Hiyane João Santana da Silva Niels Olsen Saraiva Câmara |
| author_sort | Matheus Correa-Costa |
| collection | DOAJ |
| description | Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. In this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to fibrosis deposition. Based on this perception, we evaluated the participation of macrophage recruitment in the development of TIN. Initially, we provided adenine-enriched food to WT and searched for macrophage presence and action in the kidney. Also, a group of animals were depleted of macrophages with the clodronate liposome while receiving adenine-enriched diet. We collected blood and renal tissue from these animals and renal function, inflammation, and fibrosis were evaluated. We observed higher expression of chemokines in the kidneys of adenine-fed mice and a substantial protection when macrophages were depleted. Then, we specifically investigated the role of some key chemokines, CCR5 and CCL3, in this TIN experimental model. Interestingly, CCR5 KO and CCL3 KO animals showed less renal dysfunction and a decreased proinflammatory profile. Furthermore, in those animals, there was less profibrotic signaling. In conclusion, we can suggest that macrophage infiltration is important for the onset of renal injury in the adenine-induced TIN. |
| format | Article |
| id | doaj-art-e778ca8b30ac4f89908b230a109b7c08 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-e778ca8b30ac4f89908b230a109b7c082025-08-20T02:21:09ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/291024291024Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney InjuryMatheus Correa-Costa0Tárcio Teodoro Braga1Raphael José Ferreira Felizardo2Vinícius Andrade-Oliveira3Katia Regina Perez4Iolanda Midea Cuccovia5Meire Ioshie Hiyane6João Santana da Silva7Niels Olsen Saraiva Câmara8Laboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, BrazilLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, BrazilLaboratory of Clinical and Experimental Immunology, Nephrology Division, Federal University of São Paulo, 04023-900 São Paulo, SP, BrazilLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, BrazilDepartment of Biophysics, Federal University of São Paulo, 04023-062 São Paulo, SP, BrazilInstitute of Chemistry, Department of Biochemistry, University of São Paulo, 05508-000 São Paulo, SP, BrazilLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, BrazilDepartment of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, BrazilLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, BrazilMacrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. In this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to fibrosis deposition. Based on this perception, we evaluated the participation of macrophage recruitment in the development of TIN. Initially, we provided adenine-enriched food to WT and searched for macrophage presence and action in the kidney. Also, a group of animals were depleted of macrophages with the clodronate liposome while receiving adenine-enriched diet. We collected blood and renal tissue from these animals and renal function, inflammation, and fibrosis were evaluated. We observed higher expression of chemokines in the kidneys of adenine-fed mice and a substantial protection when macrophages were depleted. Then, we specifically investigated the role of some key chemokines, CCR5 and CCL3, in this TIN experimental model. Interestingly, CCR5 KO and CCL3 KO animals showed less renal dysfunction and a decreased proinflammatory profile. Furthermore, in those animals, there was less profibrotic signaling. In conclusion, we can suggest that macrophage infiltration is important for the onset of renal injury in the adenine-induced TIN.http://dx.doi.org/10.1155/2014/291024 |
| spellingShingle | Matheus Correa-Costa Tárcio Teodoro Braga Raphael José Ferreira Felizardo Vinícius Andrade-Oliveira Katia Regina Perez Iolanda Midea Cuccovia Meire Ioshie Hiyane João Santana da Silva Niels Olsen Saraiva Câmara Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury Mediators of Inflammation |
| title | Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury |
| title_full | Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury |
| title_fullStr | Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury |
| title_full_unstemmed | Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury |
| title_short | Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury |
| title_sort | macrophage trafficking as key mediator of adenine induced kidney injury |
| url | http://dx.doi.org/10.1155/2014/291024 |
| work_keys_str_mv | AT matheuscorreacosta macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT tarcioteodorobraga macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT raphaeljoseferreirafelizardo macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT viniciusandradeoliveira macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT katiareginaperez macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT iolandamideacuccovia macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT meireioshiehiyane macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT joaosantanadasilva macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury AT nielsolsensaraivacamara macrophagetraffickingaskeymediatorofadenineinducedkidneyinjury |