Neonatal animals have a proportionately greater risk, relative to the adult animal, of developing a
bacterial infection. Research has revealed that such
infections can influence biological processes long after the actual
infection has been resolved. Indeed, studies examining the long-term alterations induced by early-life
infection, simulated using
endotoxin, have indicated that some aspects of the systemic inflammatory response in the adult animal are susceptible to modification. Available evidence suggests that altered inflammatory activities observed in the neonatally
endotoxin challenged adult may be the result of potentiated hypothalamic pituitary adrenal (HPA) activity, specifically increased
corticosterone production. Few studies, however, have examined whether altered
corticosterone production is actually associated with changes in systemic
inflammation in the neonatally
endotoxin challenged adult animal. The aim, therefore, of the current study was to simultaneously examine the relationship between altered inflammatory activities and
corticosterone production in the neonatally
endotoxin challenged adult rat. Our findings demonstrate no significant differences exist between adults neonatally treated with saline or
endotoxin in terms of their production of
corticosterone following
endotoxin challenge. While not appearing to influence the production of
corticosterone neonatal
endotoxin challenge did result in a marked attenuation in the adult's febrile response following
endotoxin challenge. Interestingly, circulating levels of IL-1beta and
TNF-alpha were found to be equivalent in neonatal treatment groups following
endotoxin administration in adulthood, indicating that the reduction in
fever was unlikely to be the result of altered pro-inflammatory
cytokine production. Further, no differences were found between neonatal treatment groups in net food consumption, water consumption or
weight loss following
endotoxin challenge in adulthood. Collectively, these findings demonstrate that neonatal
endotoxin challenge does not affect a blanket down regulation of inflammatory processes but rather appears to induce highly specific alterations in the adult male Fischer-344 rat.