title: Effect of remote ischemic conditioning on dendritic cell number in blood after renal transplantation--flow cytometry in a porcine model.
abstract: Delayed graft function after transplantation increases the risk of rejection. Remote ischemic conditioning (rIC) consists of repetitive, brief, non-damaging periods of ischemia in a limb. For reasons not fully understood, rIC protects the target organ against subsequent ischemia-reperfusion injury. Because ischemic endothelium attracts dendritic cells (DCs), we hypothesised that rIC protects the organ by "trapping" circulating DCs in the limb exposed to rIC. With fewer DCs thus available to infiltrate the graft, a strong T-cell mediated immune response toward the graft is less likely. To test this hypothesis, we measured the number of circulating DCs in a porcine model of renal transplantation with and without rIC. Brain death was induced in eight 65-kg donor pigs. After 22 h of cold ischemia, the kidneys were transplanted into sixteen 15-kg recipient pigs. The recipients were randomised to either non-rIC or rIC before reperfusion of the graft and observed 10 h after reperfusion. The number of DCs was determined by flow cytometry. DCs were identified on the basis of forward- and side-scatter characteristics of CD14-negative mononuclear cells with expression of CD172a. Dendritic cells were subclassified as either plasmacytoid (pDCs) (CD172a(dim), CD4(+), CD14(-)) or conventional (cDCs) (CD172a(high), CD4(-), CD14(-)). Remote ischemic conditioning did not affect the number of circulating cDCs or pDCs within the 10h after transplantation studied. Regardless of rIC, the number of pDCs decreased after graft reperfusion and then returned to baseline levels. In contrast, the number of circulating cDCs increased after reperfusion and later returned to baseline levels.
authors.affiliation: Department of Nephrology, Aarhus University, Denmark. kristian.ravlo@ki.au.dk
authors.forename: K
authors.initials: K
authors.lastname: Ravlo
authors.forename: P
authors.initials: P
authors.lastname: Koefoed-Nielsen
authors.forename: N
authors.initials: N
authors.lastname: Secher
authors.forename: P
authors.initials: P
authors.lastname: Søndergaard
authors.forename: A K
authors.initials: AK
authors.lastname: Keller
authors.forename: M S
authors.initials: MS
authors.lastname: Petersen
authors.forename: U
authors.initials: U
authors.lastname: Møldrup
authors.forename: E Ø
authors.initials: EØ
authors.lastname: Østraat
authors.forename: B M
authors.initials: BM
authors.lastname: Bibby
authors.forename: T M
authors.initials: TM
authors.lastname: Jørgensen
authors.forename: E
authors.initials: E
authors.lastname: Tønnesen
authors.forename: B
authors.initials: B
authors.lastname: Jespersen
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000097:blood / Q000276:immunology; D002452:Cell Count; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D006084:Graft Rejection / Q000097:blood / Q000276:immunology* / Q000517:prevention & control; D019194:Ischemic Preconditioning; D016030:Kidney Transplantation / Q000276:immunology*; D008954:Models, Biological; D013552:Swine; D013997:Time Factors; D014184:Transplantation, Homologous
chemical_list: D015703:Antigens, CD