Immune Cells Are Differentially Modulated in the Heart and the Kidney during the Development of Cardiorenal Syndrome

Imara Caridad Stable Vernier1, Raquel Silva Neres-Santos1, Vinicius Andrade-Oliveira2

  • 1Laboratory of Cardiovascular Immunology, Center of Natural and Human Sciences (CCNH), Federal University of ABC, São Paulo 09210-580, Brazil.

Cells
|February 25, 2023
PubMed

Insights

Acute kidney injury (AKI) triggers immune cell changes in the heart and kidneys, contributing to cardiorenal syndrome type 3 (CRS 3). This study reveals immune system activation linking kidney and cardiac injury.

Area of Science:

  • Immunology
  • Nephrology
  • Cardiology

Background:

  • Cardiorenal syndrome type 3 (CRS 3) involves acute kidney injury (AKI) leading to acute cardiac injury.
  • The immune system's role in CRS 3 pathogenesis is not fully understood.
  • Immune cell dynamics in kidney and heart tissues during AKI-induced CRS 3 require characterization.

Purpose of the Study:

  • To investigate macrophage, T lymphocyte, and B lymphocyte populations in renal and cardiac tissues following AKI induced by renal ischemia-reperfusion (I/R).
  • To elucidate the immune response and inflammatory mediators involved in the development of CRS 3.

Main Methods:

  • Utilized a unilateral renal I/R model in C57BL/6 mice, with reperfusion periods of 3, 8, and 15 days.
  • Employed flow cytometry to identify and quantify immune cell populations.
  • Applied RT-qPCR to assess gene expression profiles of inflammatory mediators.

Main Results:

  • AKI induced by renal I/R significantly increased TCD4+, TCD8+ lymphocytes, and M1 macrophages in renal tissue.
  • A decrease in B cells was observed in cardiac tissue.
  • Renal tissue exhibited a repair response with Foxp3 activation, while cardiac tissue showed an inflammatory profile driven by IL-17RA and IL-1β.

Conclusions:

  • AKI activates and recruits immune cells, including lymphocytes and macrophages, to both renal and cardiac tissues.
  • Pro-inflammatory mediators like IL-17RA and IL-1β contribute to cardiac inflammation in the context of AKI.
  • The immune system acts as a critical link between renal and cardiac dysfunction in CRS 3.

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