Chemokines in neurological disease models: correlation between chemokine expression patterns and inflammatory pathology.
We have recently determined chemokine expression profiles in a variety of models of neural trauma and immune-inflammation. The results indicate the following: (1) Chemokine expression in posttraumatic inflammation is generally restricted to the monocyte chemoattractant MCP-1, and occurs before hematogenous cell entry into neural tissues. Therefore MCP-1 is an excellent candidate for a mediator of leukocyte recruitment in these settings. (2) Chemokine expression in immune-inflammation is diverse and includes both alpha- and beta-chemokines. Chemokine production can be attributed to parenchymal and infiltrating cell populations. Early signs of inflammation precede chemokine expression, which is believed to exert the crucial function of amplifying the immune-mediated inflammatory reaction. These observations provide a basis for evaluating model neurological disorders in transgenic mice that express chemokines ectopically or in mice that are deficient in chemokine ligands or receptors as a consequence of gene targeting. Ultimately, a clear definition of roles of chemokines and their receptors in neurological diseases will suggest rational intervention.
Ransohoff
R M
RM
The Lerner Research Institute, Cleveland Clinic Foundation, Ohio 44195, USA.
D000818:Animals; D018925:Chemokines / Q000096:biosynthesis / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D009422:Nervous System Diseases / Q000378:metabolism / Q000473:pathology*
D018925:Chemokines