More Stress, Less Inflammation

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Science  12 May 2000:
Vol. 288, Issue 5468, pp. 931
DOI: 10.1126/science.288.5468.931c

Early life events commonly are thought to influence physiological and neuronal development directly, but they also may leave lasting impressions. By examining the after-effects of a neonatal challenge of bacterial endotoxin, Shanks et al. add to a growing body of results demarcating the persistent connection between the neuroendocrine and immune systems. They confirm earlier findings that endotoxin evokes increased circulating corticosteroid levels (a marker of stress) and also observe a heightened and more rapid corticosteroid responsiveness to later-in-life stress in comparison to non-endotoxin exposed rats. Furthermore, coupled to this augmented activity of the hypothalamic-pituitary-adrenal system is an apparent suppression of chronic inflammation, as assessed by relative sparing from adjuvant-induced arthritis.—GJC

Proc. Natl. Acad. Sci. U.S.A., in press.

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