| Literature DB >> 33570750 |
Joanna M Schaenman1, Maura Rossetti2, Emily C Liang1, Erik Lum3, Basmah Abdalla3, Suphamai Bunnapradist3, Phuong Thu Pham3, Gabriel Danovitch3, Elaine F Reed2, Steve W Cole4.
Abstract
After kidney transplantation, infection and death are important clinical complications, especially for the growing numbers of older patients with limited resilience to withstand adverse events. Evaluation of changes in gene expression in immune cells can reveal the underlying mechanisms behind vulnerability to infection. A cohort of 60 kidney transplant recipients was evaluated. Gene expression in peripheral blood mononuclear cells 3 months after kidney transplantation was analyzed to compare differences between patients with infection and those who were infection-free in the first-year post-transplant. Pro-inflammatory genes such as IL1B, CCL4, and TNF were found to be downregulated in post-transplant PBMC from patients who developed infection. In contrast, genes involved in metabolism, HLA genes, and transcripts involved in type I interferon innate antiviral responses were found to be upregulated. Promoter-based bioinformatic analyses implicated increased activity of interferon regulatory factors, erythroid nuclear factor (E2), and CCAAT-enhancer-binding protein (C/EBP) in patients who developed infections. Differential patterns of gene expression were observed in patients who developed infection after kidney transplantation, with patterns distinct from changes associated with patient age, suggesting possible mechanisms behind vulnerability to infection. Assessment of gene expression in blood may offer an approach for patient risk stratification and monitoring after transplantation.Entities:
Keywords: aging; gene expression; infections; inflammation; interferon type I; kidney transplantation
Mesh:
Year: 2021 PMID: 33570750 PMCID: PMC9341289 DOI: 10.1111/ctr.14252
Source DB: PubMed Journal: Clin Transplant ISSN: 0902-0063 Impact factor: 3.456