Bacterial infection early in life protects against stressor-induced depressive-like symptoms in adult rats.

Journal Article (Journal Article)

Both early-life stress and immune system activation in adulthood have been linked independently to depression in a number of studies. However, the relationship between early-life infection, which may be considered a "stressor", and later-life depression has not been explored. We have reported that neonatal bacterial infection in rats leads to exaggerated brain cytokine production, as well as memory impairments, to a subsequent peripheral immune challenge in adulthood, and therefore predicted that stressor-induced depressive-like symptoms would be more severe in these rats as well. Rats treated on postnatal day 4 with PBS or Escherichia coli were as adults exposed to inescapable tailshock stress (IS), and then tested for sucrose preference, social exploration with a juvenile, and overall activity, 1, 3, 5, and 7 days following the stressor. Serum corticosterone and extracellular 5-HT within the basolateral amygdala were measured in a second group of rats in response to the IS. IS resulted in profound depressive-like behaviors in adult rats, but, surprisingly, rats that suffered a bacterial infection early in life had blunted corticosterone responses to the stressor and were remarkably protected from the depressive symptoms compared to controls. These data suggest that early-life infection should be considered within a cost/benefit perspective, in which outcomes in adulthood may be differentially protected or impaired. These data also suggest that the immune system likely plays a previously unsuspected role in "homeostatic" HPA programming and brain development, which may ultimately lend insight into the often-contradictory literature on cytokines, inflammation, and depression.

Full Text

Duke Authors

Cited Authors

  • Bilbo, SD; Yirmiya, R; Amat, J; Paul, ED; Watkins, LR; Maier, SF

Published Date

  • April 2008

Published In

Volume / Issue

  • 33 / 3

Start / End Page

  • 261 - 269

PubMed ID

  • 18164556

Pubmed Central ID

  • PMC2274778

Electronic International Standard Serial Number (EISSN)

  • 1873-3360

International Standard Serial Number (ISSN)

  • 0306-4530

Digital Object Identifier (DOI)

  • 10.1016/j.psyneuen.2007.11.008


  • eng