April 12, 2018
A new study has shown the role immune cells play in helping prevent further kidney damage and failure after the kidneys are injured when their blood supply is interrupted.
Kidney damage caused by an interrupted blood supply is called renal ischemia-reperfusion injury (IRI). Surgery, such as kidney transplants, and medical conditions including low blood pressure and sepsis can cause a temporary loss of blood in the kidneys, leading to IRI.
After an IRI, the body triggers an immune response that replaces damaged kidney tissue with scar tissue. Excessive scarring and thickening of kidney tissue can cause further kidney damage, and can prevent the kidneys from working effectively.
Innate immune cells, the cells that defend the body against infection, are known to protect kidney tissue in patients with IRI. An international study, led by Dr Qi Cao of the Westmead Institute for Medical Research, investigated how specific immune cells– Interleukin-33 (IL-33) and type 2 innate lymphoid-cells (ILC2)-work to protect the kidneys in humanised mouse models.
“We know innate immune cells such as IL-33 and ILC2 protect our kidneys when blood flow is interrupted. But, we need to understand the specific roles these cells play to prevent IRI,” Dr Qi Cao explained.
The team found that IL-33 causes ILC2 to expand in the kidney, triggering a significant immune response that reduces the scarring and thickening of kidney tissue.
“Mice that received the treatment were found to have a larger number of ILC2 in their kidney, leading to a much greater immune response compared to untreated mice. This means IL-33 and ILC2 play an important role in protecting the kidneys,” Dr Cao said.
IRI is a risk factor for chronic kidney disease (CKD), a condition affecting up to one in ten of the world’s population. CKD is characterised by a gradual loss of kidney function, which can cause high blood pressure, weak bones, heart disease and nerve damage.
“IRI is a key risk factor in chronic kidney disease, a complex, progressive condition affecting millions of the world’s population,” Dr Cao said.
“Currently, there are no treatments available for IRI. Our research is the first to show how IL-33 and ILC2 protect the kidneys in mice with IRI.
“With further study, we believe we could use these cells to develop therapies, helping to reduce the global burden of kidney-related diseases,” Dr Cao concluded.
The paper is available online at the Journal of the American Society of Nephrology: http://jasn.asnjournals.org/content/29/3/961.full.pdf+html?sid=a62268a7-8764-4299-a749-7ca46ca495a4