Publications by authors named "K Hildner"
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation.
View Article and Find Full Text PDFAcute graft-versus-host disease (GvHD) remains the biggest clinical challenge and prognosis-determining complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Donor T cells are acceptedly key mediators of alloreactivity against host tissues and here especially the gut. In support of previous studies, we found that the intestinal intra-epithelial lymphocyte (IEL) compartment was dynamically regulated in the course of MHC class I full mismatch allo-HSCT.
View Article and Find Full Text PDFArticle Synopsis
- Histomorphology is critical for diagnosing acute Graft-versus-host disease (GvHD), but its reproducibility and the effectiveness of current grading systems are debated.
- A study assessed 123 colon biopsies for GvHD, finding high interobserver reproducibility for histological parameters and that simplified sum scores outperformed traditional grading systems in reliability (ICC 0.818-0.896).
- While all grading methods correlated with clinical signs and outcomes, none could stratify patients by the severity of GvHD; further prospective testing of sum scores is recommended.
T cells are considered to be critical drivers of intestinal inflammation in mice and people. The so called intra-epithelial lymphocyte (IEL) compartment largely consist of T cells. Interestingly, the specific regulation and contribution of IELs in the context of inflammatory bowel disease remains poorly understood, in part due to the lack of appropriate analysis tools.
View Article and Find Full Text PDFIntroduction: Macrophages play an important role in intestinal wound healing. However, the trajectories from circulating monocytes to gut macrophages are incompletely understood.
Methods: Taking advantage of mice depleted for non-classical monocytes due to deficiency for the transcription factor Nr4a1, we addressed the relevance of non-classical monocytes for large intestinal wound healing using flow cytometry, in vivo wound healing assays and immunofluorescence.