Serum concentrations of monocyte chemoattractant protein-1 in healthy and critically ill dogs.

BACKGROUND: The chemokine monocyte chemoattractant protein-1 (MCP-1) is a primary regulator of monocyte mobilization from bone marrow, and increased concentrations of MCP-1 have been associated with sepsis and other inflammatory disorders in critically ill people. The relationship between MCP-1 and disease in dogs has not been evaluated previously. OBJECTIVE: The purpose of this study was to assess serum concentrations of MCP-1 in healthy dogs, dogs in the postoperative period, and critically ill dogs. We hypothesized that MCP-1 concentrations would be significantly increased in critically ill dogs compared with postoperative or healthy dogs. METHODS: Serum concentrations of MCP-1 were measured in 26 healthy control dogs, 35 postoperative dogs, and 26 critically ill dogs. Critically ill dogs were further subgrouped into dogs with sepsis, parvovirus gastroenteritis, immune-mediated hemolytic anemia, and severe trauma (n=26). MCP-1 concentrations were determined using a commercial canine MCP-1 ELISA. Associations between MCP-1 concentrations and disease status were evaluated statistically. RESULTS: MCP-1 concentration was significantly higher in critically ill dogs (median 578 pg/mL, range 144.7-1723 pg/mL) compared with healthy dogs (median 144 pg/mL, range 4.2-266.8 pg/mL) and postoperative dogs (median 160 pg/mL, range 12.6-560.4 pg/mL) (P<.001). All subgroups of critically ill dogs had increased MCP-1 concentrations with the highest concentrations occurring in dogs with sepsis. However, differences among the 4 subgroups were not statistically significant. CONCLUSION: Critically ill dogs had markedly increased serum concentrations of MCP-1 compared with postoperative and healthy dogs. These results indicate that surgery alone is not sufficient to increase MCP-1 concentrations; thus, measurement of MCP-1 may be useful in assessing disease severity in critically ill dogs.

Amyloid-beta peptide affects viability but not differentiation of embryonic and adult rat hippocampal progenitor cells.

The neurological deficits that are characteristic of Alzheimer's Disease (AD) are ultimately a result of neuronal loss in distinct anatomical regions of the brain. This neuronal loss is thought to be due, in large part to the presence of the neurotoxic beta-amyloid (Abeta) deposits, that are characteristic of the AD brain. Transplantation therapy, in which neural stem cells (NSCs) or neural progenitor cells (NPCs) are introduced into damaged regions of the brain and induced to differentiate into replacement neurons, has been proposed as a possible therapeutic approach to treat AD. However, in the AD brain Abeta plaques, which remain in the area of neuronal degeneration, may affect the viability or differentiation potential of transplanted NSCs. Currently there is contradictory evidence concerning the effect of Abeta on NSCs. To further investigate the effect of Abeta on NSCs, we compared the mitochondrial function, proliferation and cellular differentiation of two populations of hippocampal NSCs (embryonic and adult derived) after Abeta exposure. Our results highlight the heterogeneity between different populations of NSCs even when derived from the same brain region. Our data also demonstrate that while mitochondrial function of NSCs is affected by Abeta, their proliferation and differentiation are not significantly influenced. Considered with previous studies, our results suggest that while NSCs do respond to the presence of Abeta, proliferation and differentiation of certain populations are not affected. Further study of the differences between susceptible vs. resistant populations of NSCs may provide crucial clues for the development of effective therapies to combat AD.