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Lipopolysaccharide‐induced up‐regulation of activated macrophages in the degenerating taste system
Author(s) -
Cavallin Melissa Ann,
McCluskey Lynnette Phillips
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20438
Subject(s) - taste , lipopolysaccharide , denervation , sodium , immune system , endocrinology , macrophage , medicine , chemistry , immunology , biochemistry , in vitro , organic chemistry
Unilateral chorda tympani (CT) nerve section and maintenance on a sodium‐restricted diet leads to a rapid decrease in neurophysiological taste responses to sodium in the contralateral, intact CT nerve. Up‐regulation of immune function with lipopolysaccharide (LPS; 100 μg i.p.) induces a recovery of normal sodium taste responses, suggesting that the sodium‐deficient diet is immunosuppressive. In fact, there is a bilateral increase in the number of lingual, activated macrophages in control‐fed rats receiving CT nerve section that does not occur in sodium‐deficient rats after sectioning. In the current study, we hypothesized that the LPS‐induced recovery of normal taste function in sodium‐deficient rats is based on an increase in the activated macrophage response to denervation. Rats receiving a unilateral CT nerve section, a sodium‐restricted diet, and/or an injection of LPS (100 μg; i.p.) were overdosed with pentobarbital at day 2 postsectioning, and tongues were rapidly dissected and frozen. Cryosections were then immunohistochemically stained to determine the percentage of ED1 staining for activated macrophages or the number of αβ or γδ T cells. Activated macrophage levels were significantly increased in sodium‐restricted rats that received LPS following unilateral CT nerve section, supporting our hypothesis. These novel findings suggest that LPS overcomes the immunosuppression induced by the sodium‐restricted diet and also indicate that the immune system plays a role in regulating taste function after neural injury. © 2005 Wiley‐Liss, Inc.