Patients with Alzheimer's disease display a pro-inflammatory phenotype.

Background: Inflammation plays a pivotal role in amyloid plaque progression thereby contributing to Alzheimer's disease-related neurodegeneration. We hypothesized that patients with Alzheimer's disease have an innate pro-inflammatory phenotype, as compared to control subjects without dementia.

Methods: Patients with a diagnosis of probable Alzheimer's disease (n=12) and control subjects without signs of dementia (n=18) were enrolled.

Interaction of indomethacin with cytokine production in whole blood. Potential mechanism for a brain-protective effect.

Both Alzheimer's disease and vascular dementia are featured by inflammatory responses and it is known that non-steroidal anti-inflammatory drugs (NSAIDs) decrease the risk and severity of these diseases. To study the effect of NSAIDs on PGE2 levels and pro- and anti-inflammatory cytokine levels in the whole blood assay, blood samples from 23 elderly persons aged 85 years were stimulated with thrombin or LPS as primary stimulus. Indomethacin was added in concentrations ranging from 0.

Mechanisms of lymphocyte-mediated cytotoxicity in acute renal allograft rejection.

Background: Graft-infiltrating T-cell (GIC) lines cultured from biopsies obtained during acute renal allograft rejection exhibit donor-specific cytotoxicity toward proximal tubular epithelial cell (PTEC) lines cultured from corresponding biopsies. This system allows for study of the relative contributions of perforin/granzyme B (GrB)- and Fas ligand (FasL)-based cytotoxicity to killing of PTEC.

Methods: Expression of perforin, GrB and FasL was analyzed by immunocytochemical staining of cytocentrifuge preparations of GIC lines cultured from 10 renal allograft biopsies.

Apoptosis of acinar cells in pancreas allograft rejection.

Background: Recently it has been recognized that apoptosis of target cells may occur during liver and kidney allograft rejection and is probably induced by infiltrating cells. Pancreas rejection is also characterized by a cellular infiltrate, however, the occurrence of apoptosis has not been investigated. We assessed whether pancreas rejection was associated with apoptosis of target cells and an influx of granzyme B (GrB)-positive or CD68-positive cells.

Expression and function of Fas (CD95) on human renal tubular epithelial cells.

Renal transplant rejection is characterized by an influx of mononuclear cells in the tubulointerstitial area. Recent studies indicate that tubular damage during graft rejection is dependent, at least in part, on apoptosis. It is thought that apoptosis may be induced by the mononuclear cell infiltrate via the perforin/granzyme or the Fas/Fas ligand pathway.