ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice

Novel strategies for the prevention and treatment of sepsis-associated acute kidney injury and its long-term outcomes have been required and remain a challenge in critical care medicine. Therapeutic strategies using lipid mediators, such as aspirin-triggered resolvin D1 (ATRvD1), can contribute to t...

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Autores principales:	José Bruno N. F. Silva, Thayanne B. B. Calcia, Cyntia P. Silva, Rafael F. Guilherme, Fernando Almeida-Souza, Felipe S. Lemos, Kátia S. Calabrese, Celso Caruso-Neves, Josiane S. Neves, Claudia F. Benjamim
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	sepsis renal tubulointerstitial injury resolvin ATRvD1 inflammation kidney Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/bc27d461d16249e0bfb505668ad0236d
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spelling	oai:doaj.org-article:bc27d461d16249e0bfb505668ad0236d2021-11-11T17:06:36ZATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice10.3390/ijms2221116341422-00671661-6596https://doaj.org/article/bc27d461d16249e0bfb505668ad0236d2021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11634https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Novel strategies for the prevention and treatment of sepsis-associated acute kidney injury and its long-term outcomes have been required and remain a challenge in critical care medicine. Therapeutic strategies using lipid mediators, such as aspirin-triggered resolvin D1 (ATRvD1), can contribute to the resolution of acute and chronic inflammation. In this study, we examined the potential effect of ATRvD1 on long-term kidney dysfunction after severe sepsis. Fifteen days after cecal ligation and puncture (CLP), sepsis-surviving BALB/c mice were subjected to a tubulointerstitial injury through intraperitoneal injections of bovine serum albumin (BSA) for 7 days, called the subclinical acute kidney injury (subAKI) animal model. ATRvD1 treatment was performed right before BSA injections. On day 22 after CLP, the urinary protein/creatinine ratio (UPC), histologic parameters, fibrosis, cellular infiltration, apoptosis, inflammatory markers levels, and mRNA expression were determined. ATRvD1 treatment mitigated tubulointerstitial injury by reducing proteinuria excretion, the UPC ratio, the glomerular cell number, and extracellular matrix deposition. Pro-fibrotic markers, such as transforming growth factor β (TGFβ), type 3 collagen, and metalloproteinase (MMP)-3 and -9 were reduced after ATRvD1 administration. Post-septic mice treated with ATRvD1 were protected from the recruitment of IBA1<sup>+</sup> cells. The interleukin-1β (IL-1β) levels were increased in the subAKI animal model, being attenuated by ATRvD1. Tumor necrosis factor-α (TNF-α), IL-10, and IL-4 mRNA expression were increased in the kidney of BSA-challenged post-septic mice, and it was also reduced after ATRvD1. These results suggest that ATRvD1 protects the kidney against a second insult such as BSA-induced tubulointerstitial injury and fibrosis by suppressing inflammatory and pro-fibrotic mediators in renal dysfunction after sepsis.José Bruno N. F. SilvaThayanne B. B. CalciaCyntia P. SilvaRafael F. GuilhermeFernando Almeida-SouzaFelipe S. LemosKátia S. CalabreseCelso Caruso-NevesJosiane S. NevesClaudia F. BenjamimMDPI AGarticlesepsisrenal tubulointerstitial injuryresolvinATRvD1inflammationkidneyBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11634, p 11634 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	sepsis renal tubulointerstitial injury resolvin ATRvD1 inflammation kidney Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	sepsis renal tubulointerstitial injury resolvin ATRvD1 inflammation kidney Biology (General) QH301-705.5 Chemistry QD1-999 José Bruno N. F. Silva Thayanne B. B. Calcia Cyntia P. Silva Rafael F. Guilherme Fernando Almeida-Souza Felipe S. Lemos Kátia S. Calabrese Celso Caruso-Neves Josiane S. Neves Claudia F. Benjamim ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
description	Novel strategies for the prevention and treatment of sepsis-associated acute kidney injury and its long-term outcomes have been required and remain a challenge in critical care medicine. Therapeutic strategies using lipid mediators, such as aspirin-triggered resolvin D1 (ATRvD1), can contribute to the resolution of acute and chronic inflammation. In this study, we examined the potential effect of ATRvD1 on long-term kidney dysfunction after severe sepsis. Fifteen days after cecal ligation and puncture (CLP), sepsis-surviving BALB/c mice were subjected to a tubulointerstitial injury through intraperitoneal injections of bovine serum albumin (BSA) for 7 days, called the subclinical acute kidney injury (subAKI) animal model. ATRvD1 treatment was performed right before BSA injections. On day 22 after CLP, the urinary protein/creatinine ratio (UPC), histologic parameters, fibrosis, cellular infiltration, apoptosis, inflammatory markers levels, and mRNA expression were determined. ATRvD1 treatment mitigated tubulointerstitial injury by reducing proteinuria excretion, the UPC ratio, the glomerular cell number, and extracellular matrix deposition. Pro-fibrotic markers, such as transforming growth factor β (TGFβ), type 3 collagen, and metalloproteinase (MMP)-3 and -9 were reduced after ATRvD1 administration. Post-septic mice treated with ATRvD1 were protected from the recruitment of IBA1<sup>+</sup> cells. The interleukin-1β (IL-1β) levels were increased in the subAKI animal model, being attenuated by ATRvD1. Tumor necrosis factor-α (TNF-α), IL-10, and IL-4 mRNA expression were increased in the kidney of BSA-challenged post-septic mice, and it was also reduced after ATRvD1. These results suggest that ATRvD1 protects the kidney against a second insult such as BSA-induced tubulointerstitial injury and fibrosis by suppressing inflammatory and pro-fibrotic mediators in renal dysfunction after sepsis.
format	article
author	José Bruno N. F. Silva Thayanne B. B. Calcia Cyntia P. Silva Rafael F. Guilherme Fernando Almeida-Souza Felipe S. Lemos Kátia S. Calabrese Celso Caruso-Neves Josiane S. Neves Claudia F. Benjamim
author_facet	José Bruno N. F. Silva Thayanne B. B. Calcia Cyntia P. Silva Rafael F. Guilherme Fernando Almeida-Souza Felipe S. Lemos Kátia S. Calabrese Celso Caruso-Neves Josiane S. Neves Claudia F. Benjamim
author_sort	José Bruno N. F. Silva
title	ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
title_short	ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
title_full	ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
title_fullStr	ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
title_full_unstemmed	ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice
title_sort	atrvd1 attenuates renal tubulointerstitial injury induced by albumin overload in sepsis-surviving mice
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/bc27d461d16249e0bfb505668ad0236d
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ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice

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