Experimental lesion of medial frontal cortex mediates inhibition of expression of carbohydrate-binding sites in the spleen macrophages in rat.

The fundamental concept of a neuroimmunological network is well appreciated although detailed description of the individual mechanisms has not yet been attained. In an effort to close this gap, the effect of electrolesion of the frontal medial cortex, a structure with the known "immunoreactivity", on selected phenotypic features of spleen macrophages was studied. Since sugar receptors (lectins) are pivotal for recognition, custom-made tools termed neoglycoproteins were employed to delineate any injury-induced changes of their expression. The total number of macrophages in the spleen red pulp was assessed using the ED-1 monoclonal antibody. The results showed that after lesion of the medial frontal cortex, the extent of expression of carbohydrate-binding sites in red pulp spleen macrophages significantly decreased without affecting the total number of these cells. These data intimate that distinct brain regions are involved in the control of the phenotype of macrophages in the central lymphoid organs by currently elusive biochemical mechanisms.