| First Author | Feltis BA | Year | 1994 |
| Journal | Shock | Volume | 2 |
| Issue | 1 | Pages | 29-33 |
| PubMed ID | 7735981 | Mgi Jnum | J:20379 |
| Mgi Id | MGI:68473 | Doi | 10.1097/00024382-199407000-00006 |
| Citation | Feltis BA, et al. (1994) Bacterial translocation and lipopolysaccharide-induced mortality in genetically macrophage-deficient op/op mice. Shock 2(1):29-33 |
| abstractText | Genetically macrophage-deficient op/op mice have a total absence of macrophage colony-stimulating factor (also known as colony-stimulating factor 1 or CSF-1), and therefore an absence of a population of macrophages dependent on CSF-1. op/op mice also have profound secondary deficiencies in certain cytokines secreted by this macrophage population, such as tumor necrosis factor, interleukin-1, and granulocyte colony-stimulating factor. In the present study, op/op mice were used to clarify the role of the macrophage in two clinical processes: (a) bacterial translocation in response to antibiotic-induced intestinal overgrowth, and (b) endotoxin-induced bacterial translocation, morbidity, and mortality. The results were unexpected, in that bacterial translocation and endotoxin-induced morbidity and mortality were similar in op/op mice and their functionally normal littermates. These data indicated either that a specific macrophage population and its cytokines (including tumor necrosis factor and interleukin 1) might not play pivotal roles in the pathogenesis of bacterial translocation and endotoxin-induced septic shock, or alternatively, as yet unknown redundancies in vivo might compensate for the genetic deficiencies associated with the op/op mutation. |
