Interactions of environmental conditions and mechanical loads have influence on matrix turnover by nucleus pulposus cells.

Disc degeneration is associated with several changes in the physicochemical environment of intervertebral disc cells. Nucleus pulposus (NP) cells in the center of degenerated discs are exposed to decreased glucose supply, osmolarity, pH, and oxygen levels. To understand the complexity of these interactions on a cellular level, we designed standardized experiments in which we compared responses to these environmental factors under normal levels with those seen under two different degrees of disc degeneration.

Influence of low glucose supply on the regulation of gene expression by nucleus pulposus cells and their responsiveness to mechanical loading.

Object: Environmental alterations resulting in a decrease in the nutrient supply have been associated with intervertebral disc (IVD) degeneration, particularly of the nucleus pulposus (NP). The goal of the present study was to examine the hypothesis that glucose deprivation alters the metabolism of NP cells and their responsiveness to mechanical loading. A possible interaction of glucose supply and hydrostatic pressure (HP) with gene expression by NP cells has not been investigated.

Mechanical stimulation alters pleiotrophin and aggrecan expression by human intervertebral disc cells and influences their capacity to stimulate endothelial migration.

Study Design: The influence of mechanical load on pleiotrophin (PTM) and aggrecan expression by intervertebral disc (IVD) cells, and the effects of disc cell conditioned medium on endothelial cell migration was investigated.

Objective: To examine possible interactions of mechanical loads and known pro- and antiangiogenic factors, which may regulate disc angiogenesis during degeneration.

Summary Of Background Data: Pleiotrophin expression can be influenced by mechanical stimulation and has been associated with disc vascularization.

The elimination of Anaplasma phagocytophilum requires CD4+ T cells, but is independent of Th1 cytokines and a wide spectrum of effector mechanisms.

Anaplasma phagocytophilum is a Gram-negative, obligate intracellular bacterium that exhibits a striking tropism for neutrophils. When we depleted mice of neutrophils, we found that murine susceptibility to anaplasmal infection was dependent on their presence. While serving as sites of bacterial replication, neutrophils do not seem to act as efficient killer cells in A.