The kidney can be negatively affected by a range of innate and adaptive immune responses, resulting in alterations in the functions of the kidney and, in some cases, progression to renal failure. In many of these responses, infiltration of blood-borne leukocytes into the kidney is central to the response. In addition, a large population of mononuclear phagocytes resident in the kidney can modulate these responses. A great deal of research has investigated both the mechanisms of leukocyte recruitment to the kidney and the actions of immune cells resident within the kidney. Because of the dynamic nature of the processes whereby leukocytes enter sites of inflammation, in vivo imaging has been one of the key approaches used for understanding leukocyte recruitment as it occurs throughout the body, and this is also true for kidney. However, imaging this organ and its complicated microvasculature during different forms of renal pathology presents a unique set of challenges. In this review, we examine the approaches used for intravital imaging of the kidney and summarize the insights gained from these studies regarding the mechanisms of leukocyte entry into the kidney during inflammation and the actions of immune cells within this organ.
This review describes the analysis of different leukocytes in the kidney using multiphoton intravital imaging, transgenic animals and labelling with antibodies. Leukocytes in the kidney are described in the interstitium, the interstitial microvasculature, and the glomerulus during steady-state conditions, ischemia-reperfusion injury, transplantation, pyelonephritis, ureteric obstruction and glomerulonephritis.
1 Department of Medicine, Centre for Inflammatory Diseases, Monash University Monash Medical Centre, Clayton, Vic, Australia.
2 Departments of Nephrology and Paediatric Nephrology, Monash Medical Centre, Clayton, Vic, Australia.
Received 30 July 2016. Revision received 4 October 2016.
Accepted 13 October 2016.
The work of the authors was supported by funding from the National Health and Medical Research Council (NHMRC), Australia (grants 1045165 and 1064112 to MJH and ARK), the Rebecca L. Cooper Medical Research Foundation and ANZ Trustees. MJH is an NHMRC Senior Research Fellow (grant 1042775). M.F. was supported by an Erwin Schroedinger Fellowship from the Austrian Science Fund (project J 3752-B28).
The authors declare no conflicts of interest.
All authors contributed to the writing of the article.
Correspondence: Michael Hickey, PhD, Department of Medicine, Centre for Inflammatory Diseases, Monash Medical Centre, Monash University, 246 Clayton Road, Clayton, Vic., 3168, Australia. (email@example.com).
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