Monocytes-macrophages and cytokines/chemokines in fine-needle aspiration biopsy cultures: enhanced interleukin-1 receptor antagonist synthesis in rejection-free kidney transplant patients.
BACKGROUND
Monocytes-macrophages are found within kidney allografts during the first days after surgery, where they perform "housekeeping" tasks, participate in postreperfusion injury, and act as antigen-presenting cells, as well as become involved in the effector phase of acute rejection. They also seem to play a prominent role in chronic rejection. We quantified their presence in fine-needle aspiration biopsies and studied the growth factors that, we hypothesized, would mark the different implications of the presence of monocytes-macrophages.


METHODS
Fine-needle aspiration biopsies were obtained from 56 adult renal transplants and analyzed for CD14+ using the alkaline phosphatase-anti-alkaline phosphatase procedure. Thirty-three patients were studied on the production of interleukin (IL)-1 receptor antagonist (IL-1ra), IL-6, IL-8, macrophage colony-stimulating factor, monocyte chemotactic protein 1, and macrophage inflammatory protein 1alpha by aspiration biopsies cultures using enzyme-linked immunosorbent assay techniques.


RESULTS
CD14+ cells were present at significantly higher numbers in steroid-resistant acute rejections but also during the first days after surgery, especially if acute tubular necrosis was present. We found a significantly higher production of IL-1ra by rejection-free patients compared with acutely rejecting patients, and this difference was already established on day 7 after surgery (10+/-10.5 days before rejection).


CONCLUSIONS
Monocytes-macrophages are present at higher numbers in aspiration biopsies of kidney transplant patients suffering either acute tubular necrosis or steroid-resistant rejections, but they are present during the first days after transplant in stable patients, too. The production of IL-1ra is significantly up-regulated in stable patients, which suggests that monocytes-macrophages may constitute an early key factor in the down-regulation of the anti-allograft immune response.
Oliveira
J G
JG
Renal Department, Hospital S. João, Porto, Portugal.
Xavier
P
P
Neto
S
S
Mendes
A A
AA
Guerra
L E
LE
D000293:Adolescent; D000328:Adult; D001707:Biopsy, Needle; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis; D054407:Chemokine CCL4; D018925:Chemokines / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation; D016173:Macrophage Colony-Stimulating Factor / Q000032:analysis; D019402:Macrophage Inflammatory Proteins / Q000032:analysis; D008264:Macrophages / Q000166:cytology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000166:cytology*; D012795:Sialoglycoproteins / Q000032:analysis
D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018925:Chemokines; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins; D012795:Sialoglycoproteins; D016173:Macrophage Colony-Stimulating Factor